HX641 23529 
RC341  .M56  A  treatise  on  diseas 


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PLATE  I. 


Opaque  Optic-Nerve  Fibres. — (After  Beard.) — This  is  aeon- 
genital  condition  of  the  fundus  oculi,  in  which  the  medullary 
substance  of  the  optic-nerve  fibres  continues  out  over  the 
retina  instead  of  stopping  at  the  papilla  as  it  normally 
should  do.  In  this  condition  and  location  we  obtain  the  most 
direct  and  complete  observation  of  the  intact  nervous  tissue 
during  life  that  it  is  possible  to  have. 


A  TREATISE 

ON 


DISEASES 


OF  THE 


NERVOUS  SYSTEM 

BY 

L.  HARRISON  METTLER,  A.M.,  M.D. 

Associate  Professor  of  Neurology,  College  of  Medicine  of  the 
University  of  Illinois;  Professor  of  Mental  and  Nervous 
Diseases  in  the  Chicago  Clinical  School;  Con- 
sulting Neurologist  to    the  Norwegian 
Deaconess'  Home  and  Hospital, 
Chicago. 


Complete  in  One  Volume 


grotusjelij  %XlustvaUd 


CLEVELAND  PRESS 
CHICAGO 

1905 


Copyright  1904 

BY    THE 

CI.EVELAXD    PRESS 

CHICAGO 


PREFACE. 


The  Neurone  Doctrine  is  now  an  accepted  fact.  Its  teachings 
have  done  more  to  illuminate  the  dark  places  of  neurology  than  has  any 
single  scientific  generalization  heretofore  promulgated.  In  spite  of  the 
fact  that  in  regard  to  many  of  its  details  much  has  yet  to  be  learned, 
the  main  principles  which  it  lays  down  are  universally  acknowledged 
to  be  scientifically  accurate  and  practically  useful.  The  present  treatise 
has  been  written  with  the  view  of  presenting  the  subject  of  neurology 
in  consonance  with  this  doctrine.  The  diseases  are  classified,  so  far  as 
possible,  upon  that  basis.  The  neuronic  structure  of  the  nervous  sys- 
tem is  given  special  emphasis.  A.nd  the  role  of  the  neurone  in  the 
matter  of  the  pathology  and  symptomatology  of  these  diseases  is  kept 
well  in  view.  The  author  feels  that  the  time  has  arrived  for  the  frank 
recognition  of  this  great  doctrine,  not  merely  in  histology  but  also  in 
the  greater  field  of  neurology.  He  is  convinced  that  one  cannot  acquire 
a  proper  conception  of  modern  neurology  without  an  adequate  knowl- 
edge of  the  neuronic  structure  of  the  nervous  system.  Mistakes  in  the 
diagnosis  and  blunders  in  the  treatment  of  diseases  of  the  nervous  sys- 
tem can  be  minimized  only  by  keeping  well  in  mind  the  facts  taught  in 
the  neurone  theory.  If  the  present  volume  will  enable  the  student  and 
the  practitioner  to  behold  the  entire  field  of  neurology — modern  neu- 
rology— under  the  brilliant  illumination  cast  upon  it  by  this  scientific 
generalization,  the  highest  wish  of  the  author  will  have  been  attained. 

The  unity  of  the  nervous  apparatus  and  its  functions,  the  author 
believes,  is  not  to-day  taught  as  emphatically  as  it  should  be.  In 
some  quarters  the  tendency  is  marked  to  discuss  the  nervous  system 
and  its  diseases  in  such  minute  detail  that  the  universal  working  of  the 
nervous  system  as  a  single,  uniform,  albeit  compound  organ,  seems  to 
have  been  lost  sight  of.  This  is  shown  particularly  in  connection  with 
the  subject  of  the  cerebral  localizations.  Psychology  is  a  science  as 
well  as  neurology  ;  and  as  neurosis  underlies  psychosis,  it  is  incumbent 
that  a  proper  conception  of  modern  psychology  should  be  possessed  to 
fully  comprehend  the  nature  of  the  cerebral  localizations,  the  psychic 
symptoms  of  nearly  all  the  nervous  affections  and  the  entire  psychic 
side  of  neurology.    The  author  has  endeavored  to  make  plain  from  the 


6  PREFACE 

Standpoint  of  modern  psvcholog}-  many  of  the  psycho-physical  manifes- 
tations of  the  nervous  organ. 

In  the  presentation  of  the  individual  diseases,  their  diagnosis  and 
pathology  have  been  especially  dwelt  upon,  the  writer  being  of  the 
firm  opinion  that  treatment  and  general  therapeutics  are  absolutely 
valueless — sometimes  positively  dangerous — in  the  absence  of  a  cor- 
rect or  approximately  correct  diagnosis.  Neurology's  hardest  prob- 
lems are  in  the  diagnostic  sphere.  Given  a  correct  diagnosis,  the  treat- 
ment is  generally  a  very  simple  affair.  Diagnosis  and  pathology  rest 
upon  anatomy  and  physiolog}-,  hence  much  space  has  been  given  to 
normal  as  well  as  abnormal  neurology  in  the  following  work. 

The  proper  classification  of  some  nervous  affections  is  still  a  mat- 
ter of  uncertainty.  One  has  but  to  recall  such  troubles  as  the  myo- 
pathies, the  periodical  paralyses,  Landry's  paralysis,  certain  types  of 
polyneuritis,  exophthalmic  goitre,  progressive  facial  hemiatrophy,  my- 
asthenia gravis.  Bell's  mania,  disseminated  sclerosis,  hypertrophic 
pachymeningitis  and  many  others.  The  author  has  classified  them  in 
accordance  with  his  own  view  and  with  what  he  believes  to  be  the 
general  view  among  the  best  authorities. 

For  valuable  assistance  and  helpful  suggestions  the  author  feels 
his  indebtedness  to  many  friends  and  desires  to  avail  himself  of  this 
opportunity  to  thank  especially  Dr.  Walter  M.  Fitch  for  some  exquisite 
photographic  work :  Dr.  Charles  H.  Beard.  Dr.  Oscar  Dodd  and  Dr. 
Willis  O.  Nance  for  their  ophthalmological  assistance:  Dr.  G.  B. 
Hassin  and  others. 

Grateful  acknowledgment  is  also  extended  to  the  various  publish- 
ing firms  who  have  courteously  permitted  the  use  of  illustrations  from 
works  issued  bv  them. 

L.  H.  M. 


TABLE  OF  CONTENTS. 


SECTION  A. 


IXTRODUCTTOX. 

Peculiarities  of  the  Nervous  System  and  its  diseases 17 

Classification  of  nervous  diseases    : 22 

Etiology  of  the  diseases  of  the  nervous  system  ,  .  . 2^ 

Degeneracy 29 

Patholog}"  of  the  diseases  of  the  nervous  SAStem 35 

Symptomatology  and  Diagnosis  of  the  diseases  of  the  nervous  sys- 
tem   41 

Examination  of  the  patient   42 

Electro-diagnosis   64 

Treatment  of  the  diseases  of  the  nervous  system 75 


SECTION  B. 


THE  XEURONIC  DISEASES. 

The  Neurone  and  the  Neuronic  structure  of  the  nervous  system  .  .   89 

The  Neurone  Doctrine 89 

The  Neuronic  Architecture  of  the  nervous  system 96 

The  Neuroses iot 

a.     The  cerehro-spinal  neuroses 102 

Hysteria 102 

Psychoneuroses  related  to  Sleep  and  Hysteria 138 

Dreams 141 

Pavor  nocturnus    141 

Nightmare 141 

Automatism    142 

Somnambulism 142 

Hypnotism  and  hypnosis 143 

Catalepsy 146 


TABLE  OF   CONTENTS 

Lethargy    146 

Insomnia   146 

Prolonged  sleep  148 

Sleeping  sickness.     Negro  lethargy 148 

Vertigo    149 

Ocular  vertigo 1 52 

Aural  vertigo.    Meniere's  disease 153 

Neurasthenia    157 

Hypochondriasis 173 

The  Traumatic  Neuroses 182 

Epilepsy 188 

Myoclonus-epilepsy   207 

Hemicrania.     Migraine    221 

Headache.     Cephalalgia 234 

The  Neuralgias 242 

Tic  douloureux,  prosopalgia   248 

Glossodynia : 250 

Occipital  neuralgia   250 

Cervico-brachial  neuralgia 251 

Mastodynia  25  r 

Lumbar  neuralgia   251 

Coccydynia    25 1 

Pododynia   252 

Visceral  neuralgia 252 

Spermatic  neuralgia   252 

Urethrodynia 252 

ficlampsia 252 

ficlampsia  infantum 252 

ficlampsia  parturientium .  254 

ficlampsia  ursemica   255 

Tetany.     Tetanilla 256 

Localized  myospasms    262 

Localized  Spasmodic  Tic.     Tic  convulsif 264 

Facial  tic 265 

Masticatory  tic 266 

Hypoglossal  tic 266 

Tic  of  the  trunk  and  extremities 266 

Respiratory  tic 266 

Spasmodic  torticollis 267 

Spasmus  nutans 268 

General  Tic.     Tic  impulsif 269 

"Jumpers,"  Miryachit,  Latah 270 


TABLE  OF   CONTEXTS  t) 

Paramyoclonub  muitipiex 27i 

Occupation  Neuroses    272 

Myotonia  congenita 284 

The  Choreas 286 

Acute  Minor  chorea.     Sydenham's  chorea 287 

Symptomatic  chorea   297 

Chronic  hereditary  (Huntington's)  chorea 297 

Electric  chorea 299 

Paralysis  agitans.     Shaking  palsy 299 

b.     Tlie  syinpathctic   neuroses.  Angioiieuroses  and  trophoiien- 

roses 306 

The  Sympathetic  Nerve ;  anatomy  and  physiology 306 

Symmetrical  gangrene.     Raynaud's  disease 310 

Erythromelalgia 314 

Acroparjesthesia   316 

Angioneurotic  oedema 318 

Chronic  hereditary  trophcedema 321 

Intermittent  articular  hydrops 321 

Exophthalmic  goitre   322 

Athyrea   334 

M3"xoedema   335 

Cretinism „ 337 

Acromegaly 339 

Gigantism    343 

Adiposis  dolorosa    345 

Scleroderma    346 

Progressive  facial  hemiatrophy 348 

Ainhum   350 

The  System  Diseases   350 

Their  nature  and  classification   350 

Diseases  of  the  Afferent  or  Sensory  Systetn 367 

Locomotor  ataxia    367 

Diseases  of  the  Efferent  or  Motor  System .392 

Progressive  muscular  atrophy    392 

Amyotrophic  lateral  sclerosis   401 

Progressive  bulbar  paralysis   406 

Progressive  muscular  dystrophy    409 

Pseudo-hypertrophic   paralysis    416 

Juvenile  dystrophy    418 

Infantile  dystrophy   418 

Spastic  paraplegia  of  adults   421 

Spastic  paraplegia  of  childhood 425 


lO  TABLE  OF   CON^TENTS 

Secondary  spastic  paralyses 426 

Ophthalmoplegia    , 427 

A'lyasthenia  gravis   429 

Occupation  muscular  atrophy.     Craft  palsy  . 430 

Acute  ascending  (Landry's)   paralysis   431 

Periodical  paralysis 43^ 

Diseases  of  the  Afferent  and  Buffer  cut  Systems 437 

Ataxic  paraplegia   439 

liereditary  ataxia 444 

Friedreich's  disease 444 

Amaurotic  family  idiocy    451 

Multiple  neuritis  and  neuromyelitis 454 

Progressive  interstitial  hypertrophic  neuritis   454 


SECTION  C. 


THE  NON-NEURONIC  DISEASES. 

The  Nature  of  the  non-neuronic  diseases   457 

Part  I.    Non-neuronic  diseases  of  the  Spinal  Cord 459 

The  Spinal  Cord ;  its  anatomy  and  physiology   459 

Spinal  localization  and  topography 4S5 

Lumbar  puncture 494 

Diseases  of  the  Spinal  Column 496 

Dislocations  and  fractures  of  the  vertebrae 496 

Caries  of  the  vertebrse.     Tubercular  spondylitis    \  .  .  .499 

Tumors  of  the  vertebra 507 

Syphilitic  disease  of  the  vertebrae 509 

Aneurismal  erosion  of  the  vertebras 509 

Spinal  hydatid  disease 509 

Lateral  curvature  of  the  spine 509 

Arthritis  deformans  of  the  spine  .  .  .  , 510 

Diseases  of  the  Membranes  of  the  Spinal  Cord 511 

Ansemia  and  hyperaemia 511 

Inflammation  of  the  spinal  membranes.     Meningitis 512 

External  pachymeningitis    512 

Chronic  cervical  hypertrophic  pachymeningitis   514 

Acute  spinal  leptomeningitis 516 

Syphilitic  spinal  meningitis.     Spinal  syphilis 519 

Spinal  meningeal  hemorrhage.    Hematorrhachis 524 


TABLE  OF   CONTElv[TS  II 

Diseases  of  the  Spinal  Cord 526 

Anaemia , 527 

Hypergemia   , , , 527 

Embolism.     Thrombosis.     Endarteritis 528 

Spinal  hemorrhage.    Hematomyelia • 528 

MyeHtis   ,. 531 

Acute  anterior  poliomyelitis  of  infants  541 

Poliomyelitis  of  adults 552 

Abscess  of  the  cord 555 

Tumors  of  the  spinal  cord 555 

Cavities  of  the  spinal  cord 562 

Hydromyelia 563 

Syringomyelia  563 

Malformations  of  the  cord.     Spina  bifida 569 

Caisson  disease .570 

Diseases  of  the  Cauda  Equina  and  Filiim  Tenninale 573 

Part  II.    X on-neuronic  diseases  of  the  Peripheral  Nerves  , 576 

The  Peripheral  Nerves;  their  anatomy  and  physiology   576 

Neuritis   S^'^ 

Multiple  neuritis   , 589 

Alcoholic  multiple  neuritis 592 

Lead  multiple  neuritis 595 

Arsenical  multiple  neuritis 597 

Argentic  multiple  neuritis 59'^ 

Mercurial  multiple  neuritis 598 

Diphtheritic  multiple  neuritis 599 

Rheumatic  multiple  neuritis   602 

Puerperal  multiple  neuritis   602 

Beriberi  or  Kakke - 603 

Akatama 603 

Leprous  multiple  neuritis 60J. 

Tumors  of  the  Nerves.     Neuromata 600 

Multiple  neuromata 609 

Fibroma  molluscum  multiplex 6og 

Plexiform  neuroma .  •  6id 

Diseases  of  the  Spina!  Nerves 613 

Phrenic  nerve 613 

The  brachial  plexus • 614 

Erb's  palsy 616 

Klumpke'"s  palsy    616 

Total  plexus  palsy 616 

Obstetrical  palsy 617 


12  TABLE  OF   CONTENTS 

Posterior  or  long  thoracic  nerve .617 

Circumflex  nerve 618 

-  Musculo-cutaneous  nerve 618 

Suprascapular  nerve   618 

Musculo-spiral  nerve 619 

Median  nerve  621 

Ulnar  nerve    622 

The  dorsal  nerves   624 

The  lumbar  plexus 62  x 

Obdurator  nerve    626 

Anterior  crural  nerve 626 

The  sacral  plexus   626 

Sciatic  nerve.    Sciatica 627 

Plantar  nerves   635 

The  muscles  of  the  body,  their  functions  and  nerve  supply 636 

Diseases  of  the  Cranial  Nerves 643 

Oculomotor  or  third  nerve 646 

Trochlear  or  fourth  nerve 648 

Abducens  or  sixth  nerve 64S 

Trifacial  or  fifth  nerve 649 

Facial  or  seventh  nerve 652 

Auditory  or  eighth  nerve 657 

Glossopharyngeal  or  ninth  nerve 658 

Pneumogastric  or  tenth  nerve 659 

Accessorius  or  eleventh  nerve 660 

Hypoglossal  or  twelfth  nerve 661 

Part  III.     Non-neuronic  diseases  of  the  Brain 662 

The  Brain,  its  anatomy   662 

Weight  of  the  brain 664 

Membranes  of  the  brain 665 

Embryological  development 668 

Lobes,  convolutions,  fissures,  sulci 672 

Cranio-cerebral  topography 677 

Minute  structure  of  the  brain 680 

Cortex    681 

Olfactory  lobes    686 

Corpora  striata    689 

Optic  thalami 691 

Optic  tracts  and  retina 692 

Regio  subthalamica 695 

Corpora  quadrigemina    695 

Peduncles  of  the  brain   697 


TABLE  OF  CONTENTS  I 


O 


Cranial  nerve  nuclei 698 

Olivary  bodies    705 

Cerebellum    705 

Cerebellar  cortex   707 

Conducting  tracts  of  the  brain 710 

Circulation  of  the  brain  710 

Brain  physiology  and  cerebral  localisation 714 

Cortex   717 

Internal  capsule  736 

Corpus  callosum    72,6 

Corpora  striata 737 

Optic  thalami  737 

Corpora  quadrigemina,  geniculate  bodies  and  pulvinar 73S 

Red  nucleus,  etc 739 

Corpora  mamillaria 739 

Hypophysis  cerebri   739 

Epiphysis  cerebri 739 

Crura  cerebri 739 

Pons  and  medulla • 740 

Cerebellum 74° 

Olivary  bodies    74i 

Symptoms  of  diseases  of  the  brain   749 

General  symptoms 75^ 

Psychic  symptoms  753 

Disturbances  of  language 7^3 

Motor  symptoms 77^ 

Sensory  symptoms 777 

Olfactory  symptoms    779 

Optic  symptoms •  •  •  .780 

Gustatory  symptoms   ;  ^ '..■.'.  .^' ...  .'• 79^ 

Auditory  symptoms 792 

Diseases  of  the  Membranes  of  the  Brain  .  ........  i  ..........  .  793 

Pachymeningitis 793 

Hsematoma •  ■  •  .......  1  ...  j  ••  ■  -794 

Leptomeningitis    •  •  •  •"•  •  ■    •  •  » -'^  •••i-  • .  •  •  •  •  -790 

Acute  leptomeningitis   ..^u^.i^:. '■■■■•'■■  >j  ■■■■•■  -79^ 

Epidemic  cerebrospinal  meningitis 808 

Tuberculous  meningitis    814 

Chronic  meningitis    820 

Circulatory  diseases  of  the  Brain  821 

Cerebral  anaemia    • °22 

Cerebral  hyperemia °25 


1 4  TABLE  OF   COXreNTS 

Cerebral  hemorrhage    828 

Encephalomalacia.     Embolism  and  thrombosis   845 

Thrombosis  of  the  intracranial  veins  and  sinuses 850 

Infantile  hemiplegia §5^ 

Encephalitis .  : 864 

Acute  hemorrhagic  encephalitis   865 

Acute  suppurative  encephalitis ;  cerebral  abscess 867 

Acute  delirium.     Bell's  mania 874 

Cerebral  syphilis •  •  ■  • 877 

Dementia  paralytica.    General  paresis 888 

^Multiple  sclerosis    ■■  • • 9°^ 

Tumor  of  the  brain • 909 

Intracranial  aneurism '. 93.1. 

Hydrocephalus   : 937 

Serous  meningitis 939 

Acquired  chronic  hydrocephalus  . 941 

Congenital  hydrocephalus 942 

Diseases  of  the  Pons  Varolii  and  Medulla  oblongata. 

Acute  superior  polioencephalitis '. .'. 951 

Acute  inferior  polioencephalitis 952 

Apoplectiform  bulbar  paralysis 952 

Diseases  of  the  Cerehellum .954 

Malformations  of  the  Brain 956 


SECTION  D. 


GENERAL    MALADIES    WITH    LEADING   NEUROLOGICAL 

SYMPTOMS. 

Alcoholism ; .  . gcg 

The  opium  and  kindred  habits 063 

Tetanus g5p 

Hydrophobia 063 

Arthritis  deformans 060 

Other  toxsemic  troubles 071 


SECTION    A. 


INTRODUCTION. 


GENERAL  CONSIDERATIONS  UPON  THE  PECULIARITIES 
OF  THE  NERVOUS   SYSTEM  AND  ITS  DISEASES. 

The  Nervous  System  is  a  unique  and  complex  apparatus  for  the 
performance  of  unique  and  complex  functions.  Neither  its  anatomy  nor 
its  physiology'  is  like  that  of  any  other  organ  of  the  body.  When  rough- 
ly contemplated  as  a  mass  of  tissue,  constituting  the  center,  as  it  were, 
of  the  entire  organism,  it  has  more  or  less  of  a  uniformity  of  structure 
and  a  singleness  of  function.  When  regarded  minutely  in  its  multitu- 
dinous relations  to  all  the  various  parts  of  the  body,  it  is  a  very  com- 
plex, compound  organ  with  a  large  variety  of  functions. 

Nervous  matter  per  se  consists  of  a  single  element  and  its  support- 
ing environment  immensely  multiplied.  The  two  functions  of  this  ele- 
ment are  self-nutrition  and  the  manifestation  of  a  special  form  of  irrita- 
bility. 

A  study  of  nervous  matter,  whether  found  in  the  brain,  the  spinal 
cord  or  the  peripheral  nerves,  exhausts  itself  when  the  nervous  cell 
with  its  processes  is  analyzed.  Its  functions  are  summed  up  in  the  two 
words,  self-nutrition  and  irritability.  Its  supporting  environment  of 
neuroglia,  connective  tissue  and  blood  vessels  is,  strictly  speaking,  extra 
neural,  or  at  least  is  not  primarily  involved  in  the  manifestations  of 
neurility. 

From  this  point  of  view  the  nervous  system  is  a  very  simple  affair. 
It  is  a  point  of  view  to  keep  always  in  mind,  for  in  certain  congenital 
diseases,  inherited  defects  and  degenerative,  systemic  maladies  it  offers 
the  only  clear  explanation. 

It  is  difficult  for  us  to  keep  this  simple,  uniform  conception  of  the 
nervous  apparatus  clearly  before  the  mind's  eye,  because  we  are  accus- 
tomed to  seeing  its  activities  manifested  in  so  many  different  ways. 
Mental,  motor,  sensory,  trophic  are  the  ways  in  which  we  .usually  re- 
mark the  exhibitions  of  nerve  force.  A  moment's  thought,  however, 
will  bring  home  the  fact  that  motion,  sensation,  mentality,  nutrition  are 
not  nervous  phenomena.  Motion  belongs  to  the  muscles,  sensation  to 
particular  end-organs,  nutrition  to  special  embryonic  cells  and  men- 
tality to  the  interplay  of  various  different  processes.  In  other  words, 
the  great  variety  of  outward  presentations  of  nervous  activity  is  due 
not  to  any  variety  in  the  structures  and  functions  of  the  intrinsic  nervous 


l8  GENERAL    COXSIDERATIOXS    UPOX    XERVOUS   DISEASES 

elements  themselves,  but  to  the  different  organs  and  tissues  of  the  body 
with  which  they  are  in  intimate  relationship  and  which  they  bind  to- 
gether in  perfect  harmony  of  action. 

This  also  is  a  most  important  point  of  view  from  which  to  contem- 
plate the  nen-ous  system  and  one  which  emphasizes  the  peculiar  differ- 
ence between  it  and  the  other  organs  of  the  body.  In  the  localization 
of  the  lesion  this  point  of  view  from  which  to  regard  the  entire  nerv-ous 
apparatus  and  its  functions  is  a  very  important  one. 

From  these  standpoints  it  must  be  obvious  to  the  casual  reader 
even  that  a  thorough  knowledge  of  the  histology  and  physiology  both 
of  the  nervous  elements  themselves  and  of  the  nervous  elements  with 
their  various  connections  and  end-organs  must  be  presupposed  before 
anv  profitable  advance  can  be  made  in  the  study  of  ner^'ous  diseases. 
This,  of  course,  is  largely  true  of  all  the  organs  and  tissues  of  the  body, 
but  nowhere  in  the  whole  range  of  medicine,  except  in  neurology,  is  a 
perfect  knowledge  of  normal  structure,  normal  relationships  and  normal 
functions  so  absolutely  necessary  for  the  accurate  appreciation  of  ab- 
normal changes  and  abnormal  manifestations. 

The  oft-quoted  aphorism  that  disease  is  nothing  but  perverted 
physiolog}'  comes  more  nearly  to  expressing  the  whole  truth  in  neu- 
rology than  in  any  other  department  of  medicine.  Much  of  the  pessi- 
mism, lack  of  interest  and  ignorance  in  regard  to  the  diseases  of  the 
nervous  system  spring  out  of  unfamiliarity  with  the  anatomy  and 
physiolog}-  of  the  normal  nervous  system. 

In  many  other  diseases  of  the  body  there  are  new  secretions  formed, 
new  sounds  produced,  new  appearances  presented  that  enable  one  to 
form  a  diagnosis  along  with  the  aid  of  a  good  memor}-.  For  example, 
an  ascitic  fluid,  a  valvular  bruit,  a  crepitant  rale,  a  peculiar  intestinal 
discharge  may  be  so  remote  from  all  normal  physiological  exhibitions 
that  its  existence  alone  will  quite  determine  the  diagnosis.  These  un- 
physiological  symptoms  afford  to  the  examiner  a  most  ready  and  avail- 
able means  of  diagnosing  disease. 

On  the  other  hand,  there  is  not  a  symptom  belonging  to  disease  of 
the  nen^ous  system  that  is  not  in  its  last  analysis  a  simple  perversion  of 
a  physiological  manifestation.  Fagge  was  therefore  right  when  long 
ago  he  declared  that  the  symptoms  of  nervous  disease  were  almost 
without  exception  those  of  perverted  ner^'ous  function.  They  reveal 
themselves  always  as  an  increase,  a  diminution  or  a  modification  of 
what  would  be  a  normal  nervous  exhibition. 

This  is  a  most  important  fundamental  fact  to  grasp  in  beginning 
the  study  of  these  diseases.  It  emphasizes  the  truth  that  a  clear  con- 
ception of  the  normal  anatomy  and  physiology  of  the  entire  apparatus 
is  an  absolute  prerequisite  to  the  further  comprehension  of  its  pathology 
and  symptomatology. 

Another  peculiarity  in  regard  to  the  nervous  system  is  that  most 
of  its  external  manifestations  are  secondary  in  character  and  extraneu- 
ral.  At  no  point  except  at  the  fundus  of  the  eye  do  we  at  any  time 
obtain  a  direct  view  of  normal,  functionating  nerve  tissue.  Hidden 
behind  the  other  organs  and  tissues,  it  reveals  its  own  changes  of  activ- 
ity by  the  changes  of  activity  in  these  organs  and  tissues.     Motor, 


GENERAL    CONSfDEKATIGNS    UPON    NERVOUS    DISEASES  I9 

vasomotor,  sensory  and  trophic  disturbances  may  all  be  directly  due> 
to  nervous  disturbances,  but  all  that  we  can  observe  are  the  functional 
disturbances  of  muscles,  blood  vessels  and  special  cutaneous  end-organs 
and  the  nutritional  changes  in  the  related  tissues.  Occasionally  we  can 
observe  changes  in  the  optic  nerve  at  the  fundus  of  the  eye  to  corre- 
spond with  changes  in  the  vision,  but  more  often  even  visual  dis- 
turbances occur  without  any  discoverable  alterations  in  the  fundus. 
Practically  all  objective  nervous  manifestations  therefore  are  extraneu- 
ral  in  character. 

We  can  only  infer  corresponding  changes  in  the  nervous  matter 
from  the  changes  that  we  see  in  the  non-nervous.  Even  mental  and 
subjective  symptoms  are  practically  non-neural  in  their  manifestation. 
The  changes  in  the  mental  functions  are  recognized  only  by  the  indi- 
vidual himself  as  being  related  to  motion  and  sensation.  A  change  of 
volition,  for  instance,  is  to  the  subject  himself  a  conceptual  change 
of  muscular  movement ;  an  alteration  of  some  special  or  general  sensa- 
tion is  identified  with  the  actual  or  conceptual  alteration  in  the  activity 
of  some  special  end-organ  such  as  the  eye,  ear  or  skin. 

Practically,  therefore,  all  nervous  manifestations,  whether  subjec- 
tive or  objective,  are  secondary  in  character  and  involve  extraneural 
tissues  and  organs. 

This  is  a  startling  and  peculiar  fact  to  remember  always  in  con- 
sidering the  semeiology  of  nervous  diseases. 

So  far  as  we  know,  irritability  and  self-nutrition  are  the  only  pri- 
mary physiological  manifestations  of  unrelated  nervous  matter.  When 
we  speak  of  motor,  sensory  and  trophic  symptoms  we  refer  merely  to 
secondary,  extraneural  phenomena.  Our  analysis  O'f  the  nervous  activ- 
ity involves  only  inference  and  indirect  reasoning. 

There  is  a  third  peculiarity  in  regard  to  the  nervous  apparatus  that 
must  be  noted  by  one  who  wishes  to  understand  its  diseases.  Though 
we  often  speak  of  it  as  a  single  apparatus,  and  though  all  its  parts  usu- 
ally functionate  together  in  harmony,  it  is  really  a  most  complex  and 
compound  organ,  made  up  of  a  great  conglomeration  of  little  organs 
or  deposits  of  nervous  matter,  each  having  its  own  liftle  sphere  of 
activity  and  each  exercising  different  functions  according  to  the  particu- 
lar end-organ  with  which  it  happens  to  be  in  connection.  In  the  brain, 
in  the  spinal  cord  and  in  the  nerves  are  clumps  of  elements  which  sub- 
serve motor,  sensory  and  other  functions,  and  yet  lie  in  the  closest  sort 
of  juxtaposition. 

Many  observations  in  connection  with  the  systemic  diseases,  with' 
the  progressive  degenerations,  and  with  the  changes  that  sometimes  take 
place  in  widely  separated  but  functionally  similar  parts  of  the  nervous 
system,  lead  us  to^  suspect  that  the  nervous  elements  are  not  all  exactly 
alike  in  structure.  Whether  they  differ  chemically,  physically  or  func- 
tionally we  cannot  guess.  That  they  differ  at  all  is  only  a  matter  of 
inference.  So  far  as  our  present  means  of  examination  lead  us,  we  can 
merely  say  that  in  structure  the  nervous  system  seems  to  be  the  same 
everywhere,  though  in  function  it  is  like  a  multicolored  kaleidoscope. 
No  other  organ  in  the  body  is  thus  constructed.  As  a  consequence  the 
localization  of  disease  in  the  nervous  system  is  a  characteristic   and 


20  GENERAL    COXSIDERATIOXS    UPON    NERVOUS   DISEASES 

diagnostic  feature.  The  same  lesion  in  different  parts  creates  very  dif: 
ferent  clinical  pictures,  and  the  mastery  of  the  so-called  selective  action 
of  poisons  and  disease  processes  is  in  part  dissolved. 

Mewed  independently,  then,  the  nervous  organism  is  seen  to  fall 
into  a  category  of  its  own.  Under  the  impulse  of  a  strong  ancestral 
and  biological  influence  it  appears  in  the  embryo.  The  continuation  of 
this  same  prenatal  or  hereditary  influence,  coupled  later  on  with  an 
environmental  and  postnatal  force,  guides  and  directs  its  further  de- 
velopments. In  structure  it  is  made  up  of  innumerable  elements  whose 
chief  powers  seem  to  be  fimctionally  those  of  self-nourishment  and  the 
exhibition  of  a  high  degree  of  irritability. 

Such  is  the  nervous  system  apart  from  all  its  structural  and  func- 
tional cormections.  It  represents  a  mass  of  protoplasmic  cells  evolved 
from  primitive  embryonic  cells  and  differentiated  to  a  high  degree  for 
the  performance  of  special  purposes  in  the  organism  at  large.  It  is 
always  well  to  keep  this  conception  of  the  nervous  apparatus  in  mind, 
for  it  makes  easy  of  comprehension  some  of  the  remarkable  things  that 
are  observed  in  the  nervous  system  in  connection  with  heredity,  de- 
generative influences,  general  infections  and  special'diseases. 

As  a  matter  of  fact,  however,  the  nervous  apparatus  is  practically 
never  an  independent  and  imrelated  organ.  We  have  already  seen  how 
it  is  so  intimately  associated  with  the  other  organs  and  tissues  of  the 
body  that  its  own  changes  of  action  can  only  betray  themselves  by  cor- 
responding changes  of  action  in  these  other  organs  and  tissues.  So 
close  is  the  connection  and  so  mutuall}"  dependent  upon  each  other  are 
the  nervous  elements  and  the  rest  of  the  organic  tissues  that  the  latter 
can  even  react  upon  the  former  almost  as  vigorously  as  the  former  can 
upon  the  latter.  Nervous  lesions  can  produce  muscular  atrophy ;  but 
muscular  disease  often  reacts  in  a  wa}-  to  cause  wasting  of  the  nervous 
elements.  Optic  atrophy  causes  the  visual  organ  to  undergo  marked 
changes,  while  permanent  shutting  out  of  light  from  the  eye  results  in 
a  wasting  of  the  optic  nerve.  This  phrase  mens  saiia  in  cor  pore  sann 
is  expressive  of  the  truth  that  even  mental  and  physical  processes  are 
mutually  interdependent. 

If  the  nerv^ous  apparatus  consists  essentially,  as  I  have  previously 
indicated,  of  a  mass  of  highly  diff'erentiated  cells,  it  is  subject  not  only 
to  the  tissues  and  organs  with  which  these  cells  are  functionally  con- 
nected, but  also  to  the  tissues  and  organs  which  surround  and  support 
them.  The  latter,  as  we  know,  consist  of  neuroglia,  connective  tissue, 
lymphatics  and  blood  vessels.  These,  together  with  the  nervous  ele- 
ments, make  up  what  in  gross  anatomy  is  called  the  nervous  system. 
Sometimes  the  nerve  cells  are  spoken  of  as  the  noble  and  parenchy- 
matous elements,  while  the  nutritive  and  sustentacula  r  structures  that 
surround  them  are  referred  to  as  the  ignoble  or  interstitial. 

A  large  number  of  diseases  of  the  nerv^ous  system  originate  in  these 
sustentacular  tissues  and  secondarily  damage  the  nervous  apparatus  in 
their  way,  just  as  diseases  of  the  functionally  related  organs  and  tis- 
sues do  in  theirs.  These  diseases  are  literally  as  much  extraneural  as 
if  they  w^ere  located  in  the  surrounding  bones  or  membranes.  The 
only  primary  diseases  of  the  nervous  apparatus  are  those  that  originate 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  21 

and  have  their  primary  seat  in  the  noble  or  true  elements ;  all  others 
are  secondary. 

The  terms  primary  and  secondary  used  to  be  employed  in  a  grosser 
sense,  the  former  being  applied  to  all  diseases  that  originated  in  the 
nervous  system  as  distinguished  from  diseases  that  began  in  the  bones, 
membranes  and  other  coarse  structures  in  the  neighborhood. 

From  the  histopathological  standpoint  only  the  primary  diseases 
of  the  nervous  system  are  the  parenchymatous  diseases.  The  vascular 
and  interstitial  diseases  are  literally  as  much  outside  of  the  nervous 
apparatus  as  would  be,  for  mstance,  disease  of  the  spinal,  vertebral  or 
cerebral  membranes.  They  afifect  the  nervous  apparatus  secondarily 
and  cause  the  appearance  of  nervous  symptoms  by  their  pressure  or 
destructive  influence  upon  the  parenchymatous  elements.  Locomotor 
ataxia  is  a  primary  nervous  disease ;  cerebral  syphilis  of  the  gummatous 
type  is  not  a  nervous  disease,  but  a  disease  of  the  blood  vessels.  The 
nervous  changes  in  the  latter  are  all  secondary. 

For  the  proper  appreciation  of  the  intraneural  diseases  and  the 
extraneural  this  conception  of  their  primary  and  secondary  charac- 
teristics should  be  insisted  upon.  Etiologically,  pathologically,  symp- 
tomatically  and  therapeutically  there  is  the  widest  difference  between 
the  two  sets  of  affections. 

The  primary  diseases  are  more  subject  to  hereditary  influences  than 
are  the  secondary.  They  are  degenerative  in  nature  and  are  usually 
provoked  by  toxic,  infective,  cachectic,  nutritional  and  other  depressing 
causes  of  a  general  character.  Their  symptomatology  is  purely  neu- 
rotic and  as  a  rule  is  more  or  less  uniform  and  progressive  from  the 
start.  The  localization  symptoms  are  comparatively  clear  and  well  de- 
fined. Their  prognosis  is  generally  fan*  as  to  life,  but  bad  as  to  recov- 
ery. Their  treatment  is  most  discouraging.  They  are  both  organic  and 
functional,  inherited  and  acquired.  Inherited  defect  is  at  the  bottom 
of  a  good  many  of  them  and  accounts  largely  for  the  unsatisfactory 
character  of  their  treatment. 

The  secondary  diseases  are  the  result  of  traumata  and  various 
noxious  agents.  Heredity  plays  but  an  insignificant  role  here.  The 
primary  seat  of  these  troubles  is  strictly  extraneural,  and  hence  the 
lesions  represent  all  sorts  of  general  and  specific  vascular  and  connec- 
tive tissue  changes. 

Inflammation  is  at  the  foundation  of  most  of  these  troubles  and  by 
pressure  and  otherwise  the  inflammatory  process  damages  the  parenchy- 
matous elements  or  the  true  nervous  apparatus. 

The  symptomatology  of  these  diseases  bears  a  double  countenance 
— namely,  the  symptoms  of  the  vascular  disturbance  and  the  symptoms 
of  the  nervous.  The  former  are  varied  in  character,  are  more  or  less 
febrile  and  are  the  same  wherever  the  lesion  may  be  located ;  the  latter 
are  more  uniform,  reveal  progressive  irritation  and  destruction  of  the 
neighboring  nerve  elements,  and  are  varied  according  to  the  location 
of  the  lesion.  As  these  diseases  are  usually  diffuse,  the  localization  of 
the  lesion  is  not  a  prominent  feature  and  is  possible  only  when  the  lesion 
happens  to  be  of  a  certain  character. 

The  prognosis  of  these  diseases  depends  upon  the  extent  of  the 


22  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

damage  done  to  the  nervous  elements  and  to  some  few  particular  in- 
herent features  of  their  own.    As  a  rule  it  is  hopeful. 

Their  treatment  is  generally  effective  and  sometimes  is  rewarded 
with  most  brilliant  success.  They  are  practically  all  organic  diseases, 
though  the  nervous  elements  for  a  time  may  be  o^nly  functionally  dis- 
turbed. The  minimum'  of  influential  heredity  amongst  them  accounts 
very  largely  for  their  more  hopeful  management. 

"  As  illustrative  of  what  is  meant  by  primary  nervous  diseases  may 
be  mentioned  tabes,  Friedreich's  ataxia,  primary  Little's  disease,  some 
types  of  progressive  muscular  atrophy,  amyotrophic  lateral  sclerosis, 
progressive  bulbar  paralysis  and  most  of  the  so-called  neuroses. 

Among  the  secondary  group  I  would  place  all  of  the  inflammations, 
hemorrhages,  neoplasms,  and  vascular,  connective  tissue  changes, 
whether  they  occur  in  the  tissues  immediately  surrounding  the  nervous 
elements  or  in  the  more  remote  membranes,  bones,  etc.  Myelitis,  en- 
cephalitis and  neuritis  occur  here.  All  forms  of  vascular  diseases,  such 
as  arteritis,  hemorrhage,  embolism,  thrombosis,  must  be  included. 
Tumors  are  all  extraneural  primarily,  even  including  the  unique  glio- 
mata.  Primary  sclerotic  processes  are  extraneural,  being  due  to  con- 
nective tissue  changes.  It  hardly  needs  to  be  mentioned  that  diseases- 
of  the  meninges  and  of  the  osseous  coverings  are  pre-eminently  extra- 
neural. 

These  illustrations  of  wdiat  is  meant  by  primary  and  secondary 
nervous  diseases  do  not  include  all  of  the  known  affections  by  any 
means.  The  principle  underlying  the  distinction  having  once  been  rec- 
ognized, it  will  be  an  easy  matter  when  the  diseases  are  studied  in  detail 
to  assign  them  respectively  to  one  or  the  other  class  as  we  learn  their 
pathology. 

The  Classification  of  the  diseases  of  the  nervous  system  is  still 
in  a  most  chaotic  condition.  There  is  an  obvious  reason  for  this.  Hith- 
erto all  classifications  have  been  based  upon  such  varied  and  hetero- 
geneous factors  as  gross,  arbitrary  anatomical  subdivisions,  upoii  par- 
ticularly prominent  symptoms,  or  upon  strange  etiological  and  thera- 
peutical distinctions.  Some  of  these  classifications  were  so  absurd  that 
they  have  long  passed  into  the  limbo  of  oblivion.  Our  knowledge  of  the 
nervous  system  is  so  incomplete  that  we  still  find  justification  for  the 
calling  of  a  special  symptom  a  disease  and  giving  it  all  the  dignity  of  a 
special  chapter.  Though  we  no  longer  head  a  page  in  our  modern  text- 
books with  such  meaningless  terms  as  paralysis  and  apoplexy,  we  still 
treat  chorea  and  hydrocephalus  and  hemicrania  and  headache  and 
vertigo  as  though  they  were  diseases.  By  the  later  elimination  of  the 
names  Landry's  Paralysis,  Meniere's  Disease  and  others  and  the  proper 
assignment  of  these  diseases  to  the  places  which  their  pathology  indi- 
cates, it  is  seen  that  we  are  steadily  though  slowly  progressing  towards 
a  more  accurate  neurological  nosology.  Some  day  symptoms  will  not  be 
employed  at  all  as  the  basis  of  classification. 

It  was  long  ago  recognized  that  the  pathology  of  a  disease  should 
constitute  the  only  guide  for  its  name  and  classification.  Pathology, 
however,  involves  both  the  location  and  the  character  of  the  lesion. 
Many  authors  adopt  both  factors  in  their  classification.     In  one  part  of 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  23 

the  book  will  be  found  the  discussion  of  the  system  diseases.  Here  the 
location  of  the  lesion  is  the  prominent  feature.  In  another  part  of  the 
book  there  will  be  found  a  discussion  of  tumors  of  the  nervous  system 
and  syphilis.  Here  obviously  the  character  of  the  lesion  is  the  principal 
consideration.  It  must  be  frankly  admitted  that  in  the  present  state  of 
our  knowledge  such  incongruity  is  not  altogether  blameworthy.  In 
fact,  it  has  its  advantages  for  the  present.  Some  day,  however,  this 
also  will  be  avoidable. 

A  very  gross,  yet  convenient,  classification,  based  upon  location,  is 
that  which  divides  the  diseases  into  those  of  the  brain,  spinal  cord  and 
peripheral  nerves.  Modern  histology,  and  especially  its  recent  magnifi- 
cent generalization,  the  Neurone  Doctrine,  has  demonstrated  that  it  is 
coarse  and  arbitrary  to  divide  the  nervous  system  intO'  brain,  spinal 
cord  and  nerves.  It  has  shown  us  that  there  are  no'  lines  of  separation 
between  these  so-called  parts  of  the  nervous  system.  Processes  from 
the  brain  cells  pass  far  into  the  cord  from  above,  while  processes  from 
the  nerves  extend  high  up  into  it  from  below.  From  the  cord  cells  pass, 
in  opposite  directions,  processes  into  the  brain  above  and  into  the  nerves 
below.  In  other  words,  most  of  the  nervous  elements  lie  partly  in  one 
and  partly  in  another  of  these  so-called  divisions  of  the  nervous  system. 
Our  ignorance  of  this  fact  has  hitherto  caused  some  most  erroneous 
conceptions  and  classifications  of  the  nervous  affections  and  the  incubus 
of  it  we  even  yet  find  hard  to  shake  off.  M^e  still  sometimes  refer  to 
locomotor  ataxia  as  a  spinal  cord  disease,  though  its  lesion  is  chiefly 
found  in  nervous  elements  that  extend  farther  outside  of  than  inside  of 
the  spinal  canal.  There  are  certain  bulbar  diseases  that  present  a  symp- 
tomatology more  nearly  related  to  spinal  cord  than  to  brain  phenomena. 
It  is  a  question  in  the  minds  of  some  pathologists  whether  certain  foirms 
of  so-called  peripheral  neuritis  are  not  really^ degenerative  processes  in 
the  peripheral  nerves  due  to  trophic  disturbances  in  the  anterior  horns  of 
the  cord.  Certain  eye  symptoms  have  long  been  recognized  as  attrib- 
utable to  disease  in  the  lower  part  of  the  cervical  cord. 

So  far  as  the  tracts  and  cellular  processes  are  concerned  in  diseases 
of  the  nervous  system,  there  are  no  demarkation  lines  between  the  brain, 
cord  and  peripheral  nerves.  As  we  will  see  when  we  come  to  discuss 
the  neurone  and  neurone  theory,  the  diseases  that  attack  the  true 
nervous  elements  primarily,  the  true  nervous  diseases,  extend  from 
brain  into  cord  and  into  nerves  and  vice  versa.  They  dO'  not  confine 
themselves  to  any  one  of  these  arbitrary  divisions  of  the  anatomists, 
but  follow  the  course  of  the  nervous  elements.  They  may  be  classified, 
therefore,  as  Neuronic  Diseases.  They  are  the  most  truly  nervous  of  all 
the  nervous  diseases.  They  are  organic  and  functional,  the  former  be- 
ing quite  sharply  localized,  the  latter  being  more  difi^use  and  including 
to  a  large  extent  the  so-called  Neuroses  and  Psychoneuroses. 

The  Neuronic  Diseases  and  the  Neuroses,  therefore,  will  be  treated 
of  in  sections  by  themselves  and  no  attempt  will  be  made  to  classify 
them  as  brain,  cord  or  peripheral  nerve  affections. 

An  examination  of  the  gray  matter  of  the  nervous  system  reveals 
the  fact  that  it  is  made  up  of  a  series  of  aggregations  of  cells  extending 
all  along  the  cerebro-spinal  canal.    These  ganglia,  or  little  brains,  as  it 


24  GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES 

were,  are  to  a  certain  extent  independent  in  their  individual  activities 
and  control  without  much  interference  various  related  organs  and  parts 
of  the  bodv.  These  ganglia  are  numerous  and  are  found  everywhere, 
though  regularly  situated"  in  all  parts  of  the  nervous  system.  They  are 
in  the  sympathetic  system,  in  the  posterior  spinal  roots,  and  in  many 
of  the  cranial  nerves.  They  constitute  the  central  gray  matter  of  the 
cord  as  explained  in  the  chapter  on  the  minute  anatomy  of  the  cord. 
They  are  found  in  the  nuclei,  basal  ganglia  and  cortex  of  the  brain. 
Since  their  functions  differ  on  account  of  their  connection  with  differ- 
ent end-organs  and  different  parts  of  the  body,  when  they  are  anywhere 
attacked  by  disease,  the  location  of  the  lesion  can  be  at  once  determined 
by  the  peculiar  symptoms  presented.  When  the  intraspinal  ganglia, 
for  instance,  are  affected,  the  symptoms  are  quite  different  from  what 
they  are  when  any  of  the  intracranial  ganglia  are  miplicated.  There- 
fore, for  obvious  reasons,  we  still  find  it  convenient  to  speak  of  dis- 
eases of  the  brain,  of  the  cord,  of  the  nerves  and  of  the  sympathetic 
system. 

In  each  of  these  divisions  there  are  many  distinct  ganglionic  m.asses 
with  sharply  defined  functions.  This  enables  us  to  carry  the  classifica- 
tion of  diseases  on  the  basis  of  location  to  a  still  higher  point.  W  e 
subdivide  those  of  the  brain,  for  instance,  into  those  of  the  cerebrum, 
the  cerebellum,  the  pons  and  the  medulla.  We  mig-ht  carry  the  division 
even  still  farther,  but  as  a  matter  of  fact  do  not  find  it  specially  con- 
venient to  do  so.  \\'e  might  even  speak  of  the  diseases  of  the  motor 
cortex,  of  the  visual  cortex,  of  the  sensory  cortex,  of  the  cervical  cord, 
of  the  lumbar  cord,  etc.  All  this,  however,  can  better  be  left  to  the  con- 
sideration of  the  cerebral  and  spinal  localizations  in  the  chapters  devoted 
to  the  anatomy  of  the  brain  and  cord. 

In  the  following  work  I  will  adopt  this  provisional  classification  of 
the  diseases  of  the  nervous  system,  believing  it  to  be  justified  by  the 
present  state  of  our  knowledge,  and  realizing  perfectly  that  newer  dis- 
coveries will  from  tim.e  to  time  transfer  some  of  the  diseases  from  one 
group  into  another. 

Neuronic  Diseases. 

(Parenchymatous  Degenerative  Troubles.) 

a.  The  Functional  Neuronic  Diseases. 

1.  Cerebro-spinal. 

2.  Sympathetic. 

b.  The  Organic  Xenronic  Diseases. 

1.  Of  the  Aft'erent  System. 

2.  Of  the  Eff'erent  System. 

3.  Of  Both  the  Aff'erent  and  Efferent  Systems. 
Xon-Xeuronic  Diseases. 

(Interstitial  and  Vascular  troubles  affecting  the  Neurones 
secondarily.) 

a.  Of  the  Spinal  Cord  and  its  ^Membranes. 

b.  Of  the  Peripheral  Nerves. 

c.  Of  the  Brain  and  its  Membranes. 

General  Intoxications  with  Special  Nervous  Symptoms. 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES 


GENERAL  CONSIDERATIONS  UPON  THE  ETIOLOGY  OF 
DISEASES  OF  THE  NERVOUS  SYSTEM. 

It  is  premature  to  formulate  an  exact  etiology  or  classification  of 
the  causes  of  diseases  of  the  nervous  system.  They  are  so  many,  so 
varied  and  so  indistinct  sometimes  that  we  are  quite  at  a  loss  to  give 
to  them  always  their  deserved  valuation. 

For  many  reasons,  however,  an  attempt  should  be  made  tO'  gener- 
alize, so  far  as  known  data  will  warrant,  the  etiology  of  these  affections. 

In  the  first  place,  the  causation  lying  behind  the  pathology  serves 
as  the  guide  to  the  proper  therapy.  Our  management  of  these  dis- 
eases, even  more  so  than  in  others,  cannot  proceed  along  logical 
and  scientific  lines  as  to  the  best  interests  of  the  patient  until  we  have 
a  clear  conception  of  their  etiology  and  pathology.  It  seems  like  a 
truism  to  say  this  and  yet  the  pre-eminence  given  to  therapeutics,  to  the 
neglect  of  etiology  and  pathology-,  is  the  folly  of  the  quack,  the  ignor- 
ance of  the  layman  and  the  weakness  of  the  physician. 

In  the  second  place,  we  are  so  rapidly  eliminating  the  innumer- 
able causative  factors  harped  upon  by  the  writers  of  the  past,  and 
discovering  so  much  more  positively  the  comparatively  few  real  causes, 
that  the  time  is  getting  ripe  for  an  attempt  at  a  systematic  arrange- 
ment of  the  latter. 

In  the  third  place,  our  knowledge  of  the  pathology  of  nervous 
diseases  has  lately  grown  so  and  our  conception  of  its  relationship  to 
all  etiological  antecedents  has  clarified  to  such  a  degree,  that  we  are 
beginning  to  occupy  a  position  to  speak  with  a  high  tone  of  positive- 
ness  of  the  latter  as  being  the  undeniable  causes. 

In  the  fourth  place,  a  study  of  the  etiology  of  these  affections 
points  out  a  line  for  the  classification  of  the  diseases  themselves,  enables 
us  to  calculate  the  possibility  of  the  removal  of  the  cause  and  of  the 
disease,  and  helps  to  determine  the  prognosis  as  well  as  the  hopeful- 
ness or  hopelessness  of  treatment. 

As  all  diseases  of  the  nervous  system  naturally  fall  into  one  or 
the  other  of  the  two  groups — namely,  those  that  start  primarily  in  the 
neurones  and  those  that  start  primarily  outside  of  the  neurones,  we 
must  remember  this  in  studying  their  etiology,  for  the  latter  is  not 
exactly  the  same  in  all  particulars  for  both.  This  will  be  noticed  as 
we  proceed  in  the  discussion  of  the  causes  and  especially  when  the 
particular  diseases  themselves  are  taken  up  for  consideration. 

Another  useful,  because  practical,  division  of  the  causation  of 
nervous  diseases  is  into  those  that  are  endogenous  or  developed  within 
the  body,  and  those  that  are  exogenous  or  exert  their  influence  from 
without. 

An  ansemia  is  an  endogenous  cause  of  nervous  degeneracy ;  a  blow 
on  the  head  is  an  exogenous  cause  of  meningitis. 

It  would  be  perhaps  too  fine  a  distinction  to  speak  of  the  endogen- 
ous and  exogenous  causes  in  relation  to  the  neurones  or  true  nervous 
elements ;  and  yet  such  a  division  would  be  both  scientific  and  prac- 
tical, for  all  of  the  hereditary  diseases  are  practically  due  to  endogenous 


26  GENERAL    COXSIDERATIOXS    UPOX    \LRVOUS    DISEASES 

influences  within  the  neurones,,  while  all  other  diseases,  whether  merely 
congenital  or  prenatal,  natal  or  postnatal,  are  exogenous. 

A  grand  starting  point  for  the  study  of  the  etiology  of  nervous 
diseases  is  the  division  of  the  causes  into  the  predisposing  and  the 
exciting.  The  former  are  inherent,  of  course,  and  include  everything 
that  involves  the  patient's  individual  body  and  personality.  They  there- 
fore take  cognizance  of  his  heredity,  his  intrauterine  development,  his 
birth  and  his  constitutional  state  and  his  subjection  to  other  diseases 
up  to  the  moment  of  examination.  They  are  concerned  with  his  age, 
sex,  nationality,  occupation,  mode  of  life  and  habits,  his  climatic, 
hygienic  and  social  environment.  The  exciting  causes  are  not  neces- 
sarily inherent  in  the  patient.  As  a  matter  of  fact,  they  are  more  fre- 
quently external,  all  more  or  less  temporary,  and  invade  tfn,  organism 
rather  abruptly.  They  include  the  traumata,  the  intoxications  and  the 
infections.  Among  the  reflex  causes  so  much  referred  to  by  many 
writers,  some  are  of  the  nature  of  mere  predisposing  factors,  some  fall 
into  the  category  of  direct  traumata.    I  will  discuss  them  later  on. 

For  convenience  we  may  formulate  the  following  scheme  of  the 
causes  of  the  diseases  of  the  nervous  system : 

1.  Predisposing  causes. 

Heredity. 

Age. 

Sex. 

Nationality. 

Occupation. 

Mode  of  Life  and  Habits. 

Climatic,  Hygienic  and  Social  Environment. 

2.  Exciting  causes. 

Traumata. 

Intoxications. 

Infections. 

3.  Reflex  causes. 

I  will  now  discuss  these  a  little  more  in  detail  and  explain  the 
omission  in  the  schema  grossly  outlined  above,  some  causes,  as,  for 
instance,  tumors,  parasites,  etc. 

As  has  been  long  recognized,  heredity  plays  its  most  brilliant  role 
in  connection  with  the  nervous  tissues.  So  recently  has  the  nervous 
system,  at  least  in  its  highest  and  most  complex  elaboration,  been 
evolved  in  the  course  of  biological  development  that  we  can  trace  an- 
cestral phenomena,  both  anatomical  and  functional,  better  in  it  than 
in  any  other  organ  or  tissue  of  the  body.  Zoologists  recognize  this  so 
forcibly  that  they  are  beginning  to  use  the  nervous  apparatus  for  the 
basis  of  their  higher  classifications  and  to  trace  out  with  its  aid  the 
lines  of  descent  in  the  various  classes  of  animals.  In  neurology  we 
have  come  to  acknowledge  that  heredity  is  the  most  important  factor 
biologically  for  modifying  the  nervous  apparatus  for  good  or  for  evil. 
Note  carefully  here  the  use  of  terms.  I  said  the  nervous  apparatus. 
Strictly  speaking,  this  includes,  we  now  knovr,  only  the  neurones  and 
the  neurosrlia.     It  follows  logicallv  and  it  is  clearlv  demonstrated  em- 


GENERAL    COXSIDERATIOXS    UPON    NERVOUS    DISEASES  2" 

pirically,  that  in  the  neuronic  and  neuroghomatous  diseases  only  do  we 
find  heredity  exerting  the  most  transcendent  force.  2vlanv  of  the  dis- 
eases of  this  class  are  purely  and  entirely  hereditary.  They  are  of 
the  nature  of  inherited  defects.  Such,  for  example,  are  Friedreich's 
disease,  some  of  the  progressive  muscular  atrophies,  the  so-called  con- 
genital neurasthenias,  hysterias,  epilepsies. 

There  are  other  diseases  of  the  neuronic  class,  however,  that  are 
provoked  into  existence  by  one  or  more  exciting  causes,  but  are  local- 
ized and  otherwise  determined  by  the  patient's  heredity.  In  these  there 
is  a  tendency  toward  the  disease,  but  it  remains  latent  until  some  ex- 
traneous cause  starts  the  latent  influence  into  action.  It  is  believed 
that  this  explanation  applies  to  many  of  the  acquired  systemic  diseases 
like  locomotor  ataxia,  to  most  of  the  gliomatous  conditions  and  to  a 
large  number  of  the  acquired  and  secondary  neurasthenias,  hysterias, 
epilepsies  and  other  so-called  functional  neuroses.  It  is  going  too  far, 
however,  to  affirm,  as  some  have  done,  that  a  true  neuronic  disease 
cannot  develop,  whatever  the  exciting  cause  may  be,  unless  there  is 
an  inherited  neuropathic  weakness  of  some  sort  present.  It  is  not  at 
all  improbable  that  monotonous  overexertion,  intoxication  or  infection 
tnay  expose  itself  in  a  disease  of  neurones  that  may  originally  haA'e  been 
endowed  with  perfect  health.  These  cases,  however,  are  not  as  com- 
mon as  is  generally  supposed.  It  is  astonishing  the  amount  of  strain 
the  perfectly  healthy  and  well-developed  nervous  apparatus  will  bear. 
Most  of  the  breakdowns  that  we  observe  in  actual  life,  whether  of  the 
organic  or  functional  type  of  neuronic  disease,  owe  a  large  part  of 
their  misfortune  to  the  inheritance  of  an  madequate  strength  and 
vitality. 

In  the  diseases  that  start  outside  of  the  neurones  heredity  plays 
such  a  small  part  that  it  amounts  to  practically  nothing.  In  certain 
vascular  troubles,  such  as  the  cerebral  hemorrhages  and  possibly  in 
some  of  the  tumors,  there  is  a  bare  trace  of  hereditary  influence.  In 
the  traumatic,  toxic  and  infectious  troubles  that  cause  inflammation 
and  all  its  sequelae,  it  is  practically  nil.  The  diseases  that  occur  as 
the  result  of  hereditary  syphilis  are  not  hereditary  nervous  diseases. 
Hence  what  I  will  say  in  regard  to  heredity  will  apply  more  particu- 
larly to  the  neuronic  degenerations  and  neuroses. 

By  direct  heredity  is  meant  the  transmission  of  the  same  disease 
from  parent  to  child.  Such  heredity  is  not  common.  -]\Iore  frequently 
a  nervous  weakness  or  tendency  is  handed  down.  This  is  known  as 
indirect  heredity.  When  the  hereditary  influence  is  towards  the  pro- 
duction of  the  same  disease  in  the  child  that  was  in  the  parent,  it  is 
spoken  of  as  an  inherited  tendency.  EA'en  this  is  not  so  common. 
Much  more  frequenth'  the  progeny  is  presented  with  a  neuropathic 
taint  merely,  which,  upon  provocation  or  without,  may  develop  a  simi- 
lar or  dissimilar  disease  from  that  observed  in  the  ancestry.  A  neu- 
ropathic diathesis  is  so  frequently  traceable  in  these  cases  that  no  ex- 
amination is  properly  conducted  in  which  it  is  not  promptly  and  most 
persistently  inquired  into. 

It  is  not  always  necessary  that  there  should  be  a  well-defined  dis- 
ease in  the  parentage.     Xervous  strain  may  be  sufficient  to  cause  the 


28  GKXEKAL    CONSIDERA  lldNS    UPON    NERVOUS    DISEASES 

children  to  inherit  a  constitution  that  soon  revels  in  the  most  elaborate 
forms  of  nervous  disease.  I  have  seen  a  girl  go  insane  with  a  primary 
form  of  degenerative  dementia  for  which  no  other  possible  cause  could 
be  detected  than  a  congenital  neuropathic  weakness.  When  she  was 
conceived  and  being  carried  her  mother  was  under  excessive  worr)' 
and  a  physical  and  mental  strain  striving  to  make  a  livmg  for  a  large 
and  healthfully  growing  family.  Hard  brain  workers,  those  who  dis- 
sipate and  indulge  freely  in  alcohol  and  tobacco,  often  transmit  to  their 
children  a  vitiated  nervous  apparatus.  The  latter  suffer  from  neu- 
rasthenia, hysteria,  epilepsy  and  various  psychoses.  If  both  parents  are- 
neurotic  or  subject  themselves  to  causes  that  deteriorate  the  nervous 
system,  the  chances  for  the  children  are  bad.  The  intermarriage  of 
blood  relatives  is  dangerous  for  the  offspring.  I  have  under  observa- 
tion now  a  middle-aged  man,  the  father  of  two  vigorous,  grown-up 
daughters,  who  has  been  the  victim  during  the  last  eight  years  of 
typical  disseminated  sclerosis.  His  habits  have  always  been  exemplary 
and  there  is  no  known  exciting  cause  for  the  disease.  His  paternal 
grandparents,  however,  were  first  cousins.  His  own  father  and  a 
paternal  uncle  and  aunt  were  all  congenital  deaf  mutes.  His  own 
mother  became  a  deaf  mute  from  scarlet  fever  in  childhood.  The  pa- 
tient himself  is  the  younger  and  weaker  of  twins. 

Mental  troubles  not  infrequently  follow  close  blood  intermarriages^ 
Dean  concludes  from  his  examination  of  i8i  cases  of  eye  troubles  in  an 
institution  for  the  blind  that  of  the  congenital  cases  fourteen  per  cent 
were  the  result  of  consanguineous  marriages  of  the  first  degree.  He 
believes  from  his  statistics  that  the  greater  the  inheritability  of  a  con- 
dition the  more  liable  it  is  to  be  the  result  of  consanguineous  marriage. 

Sometimes  the  parent  will  be  afflicted  with  a  typical  disease  while 
the  child  will  reveal  only  a  general  neuropathic  depreciation.  A  mother 
is  epileptic,  her  daughter  becomes  hysterical.  It  may  be  znce  versa. 
A  father  has  all  his  life  had  attacks  of  typical  hemicrania ;  his  child  has 
epileptic  fits  or  becomes  the  victim  of  dementia  prgecox.  Chorea  breaks 
out  in  the  children  of  markedly  neurasthenic  parents.  The  neuroses 
are  more  frequently  transmitted  by  the  mother  than  by  the  father. 

The  heredity  has  been  seen  to  be  direct,  if  I  may  say  so,  in  alter- 
nate generations,  indirect  in  succeeding  -generations.  Epilepsy,  for 
instance,  has  been  among  the  grandparents :  genius  with  some  of  its- 
oddities  and  psychic  peculiarities  appeared  in  the  next  generation ; 
epilepsy  again,  with  terminal  insanity,  reappear  in  the  third  genera- 
tion. This  is  sometimes  called  a  manifestation  of  atavism,  a  reversal 
to  earlier  forms  of  nervous  exhibition. 

Atavism  is  a  remarkable  and  not  such  an  uncommon  phenomenon 
in  the  animal  world.  It  is  not  frequent,  however,  in  connection  with 
nervous  diseases.  Indeed,  it  may  seriously  be  questioned  whether  the 
mere  repetition  of  the  same  disease  back  of  the  preceding  generation 
is  a  true  form  of  atavism.  A  disease  in  the  ancestor  is  not  necessarily 
an  earlier  or  more  primitive  type  of  that  seen  in  the  progeny.  It  is 
really  the  same  disease  probably  occurring  in  the  same  sort  of  a  neu- 
ropathic constitution.  As  a  phenomenon,  however,  this  atavistic  ten- 
dency in  nervous  disease,  whether  real  or  apparent,  is  interesting  and 


GENERAL    COXSIDERATIOXS    UPOX    XERVOUS   DISEASES  29 

■worthy  of  further  study.  The  same  may  be  said  of  those  diseases  that 
:sometimes  appear  in  collateral  branches  or  in  several  members  of  the 
same  family,  so  that  they  are  spoken  of  as  "familial  diseases."  These 
are  largely  of  the  nature  of  developmental  defects  or  anomalies.  Fried- 
reich's disease  and  some  of  the  atrophies  may  be  cited  as  illustrations. 
Glioma  is  a  congenital  defect.  Diseases  that  reappear,  and  the  morbid 
conditions  that  occur,  later  in  life  in  the  descendants  than  thev  did  in 
the  ancestry,  may  be  looked  upon  as  waning  in  the  family. 

Under  the  head  of  heredity  the  modern  doctrines  of  degeneracy 
must  receive  some  consideration.  The  term  is  one  that  is  much  abused 
and  misunderstood. 

Degeneracy  is  the  result  of  a  biological  taint.  It  is  a  product  of 
liereditary  and  congenital  influences.  It  is  not  the  immediate  result  of 
environment.  It  therefore  does  not  mean  a  falling  back  of  the  individ- 
ual from  a  previously  normal  state,  but  a  falling  back  of  the  racial  or 
familial  development,  as  shown  in  the  anomalous  and  primitive  stigmata 
of  the  individual.  A  degenerate  is  what  he  is  because  of  his  ancestry, 
and  not  because  of  anything,  he  himself  has  done.  It  is  therefore  a 
misfortune,  not  a  disgrace.  In  the  physical  sphere  it  shows  itself  by 
various  stigmata,  the  value  of  which  have  not  all  been  positively  estab- 
lished. No  man  is  perfect  physically  and  yet  we  do  not  consider  all 
men  as  degenerates.  Just  where  degeneracy  stops  and  so-called  nor- 
mality begins  is  a  hazy  region ;  hence  the  many  extreme  and  ofttimes 
absurd  notions  put  forth  by  those  who  believe  and  those  who  reject 
the  doctrines  of  Lombroso.  Asymmetry  of  the  skull,  protrusion  of  the 
lower  teeth,  irregularities  about  the  eyes,  anomalies  in  connection  with 
the  ears,  disproportion  between  different  parts  of  the  face  are  all  often 
signs  of  physical  imperfection.  Still  greater  degeneracy  is  seen  in 
such  conditions  as  hare-lip,  cleft  palate,  irregular  teeth,  retinitis  pig- 
mentosa, albinism  perhaps.  And  yet  too  much  must  not  be  inferred 
even  from  such  coarse  defects  as  these.  ]\Iost  epileptics  reveal  more  or 
less  stigmata  of  degeneracy.  Cranks  and  queer  people  very  often  pos- 
sess them.  Genius  has  been  accompanied  by  them.  On  the  street 
scarcely  an  individual  is  seen  who  does  not  exhibit  some  similar  phys- 
ical anomaly  in  greater  or  less  degree. 

There  are  parallel  stigmata  in  the  neurotic  and  psychic  manifesta- 
tions. They  may  range  all  the  way  from  a  slight  eccentricity  of  thought 
and  manner  down  to  gross  mental  debility,  imbecility  and  idiocy.  As 
no  man  is  perfect  physically,  so  no  man  is  perfect  mentally. 

This  is  all  too  obvious  when  a  definition  of  what  is  meant  by  nor- 
mal mentality  is  attempted  in  court  during  a  trial  for  insanity.  So 
many  factors  enter  into  the  make-up  of  one's  mental  manifestations 
that  what  is  craziness  in  one  man  is  perfect  mentality  in  another.  The 
points  of  view  vary.  Hottentots  are  not  insane,  nor  even  degenerate, 
because  they  do  not  think  and  act  as  Englishmen  do.  A  genius,  an 
artist,  may  well  appear  to  be  erratic,  even  crazy,  beside  a  dull  financier 
with  his  one  idea  of  money-getting.  Their  opinions  of  each  other  in 
regard  to  their  mental  exhibitions  will  probably  be  mutually  uncom- 
plimentary. 

"W'e  may,   if  we  please,  call  the  average   man  normal.     Only  in 


30  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

comparatively  coarse  defects,  however,  can  the  positively  abnormal  be 
recognized.  Genius  is  eccentric,  even  crazy  at  times  ;•  so  seems  the 
dull  monotony  occasionally  of  the  average  man. 

It  behooves  the  true  scientist  to  be  conservative  in  his  conceptions 
of  mental  and  nervous  degeneracy,  just  as  he  must  be  conservative  in 
deciding  who  are  afflicted  with  the  stigmata  of  physical  degeneracy. 

Along  coarse  lines  we  can  recognize  both  psychic  and  physical  de- 
generacy. We  can  even  note  a  remarkable  parallelism  running  be- 
tween them.  A  wholesale  slashing  about  of  the  doctrine  as  some  en- 
thusiasts have  made,  attributing  degeneracy  to  all  geniuses  and  bril- 
liant intellects,  and  to  all  deviations  from  their  preconceived  notions  of 
physical  and  mental  perfection,  will  lead,  in  the  present  state  of  our 
knowdedge,  like  a  boomerang,  back  to  their  own  imperfections  and  de- 
generate reasonings. 

The  age  of  the  individual  exercises  a  considerable  influenct  in 
determining  the  nature  of  the  disease.  This  is  partly  on  account  of  the 
differences  in  the  patient's  own  organism  and  in  his  habits  and  en- 
vironment in  dififerent  years.  It  may  even  be  entirely  secondary  so 
far  as  the  nervous  system  itself  is  concerned,  for  the  primary  disease 
may  entirely  determine  the  age  at  which  the  nervous  troubles  appear. 
The  nervous  sequelse  of  scarlet  fever,  for  instance,  occur  in  childhood 
merely  because  scarlet  fever  is  a  childhood  disease.  In  childhood  and 
earlv  life  generally  the  congenital  troubles  that  result  from  prenatal  and 
natal  injuries  usually  declare  themselves.  Hereditary  troubles  also  are 
apt  to  appear  early.  The  infectious  fevers  that  occur  in  children  are 
responsible  for  a  large  number  of  nervous  diseases.  Early  malnutrition 
exerts  its  influence,  as  well  as  unwonted  strains.  The  child's  ner\^ous 
apparatus  is,  of  course,  a  growing  and  immatvire  one.  a  fact  wdiich 
exercises  some  force  in  the  determination  of  the  kind  of  disease,  as 
well  as  of  its  symptomatology  and  prognosis. 

In  middle  and  later  childhood  we  observe  a  predominance  of  motor 
troubles,  such  as  chorea,  paralysis  and  convulsive  seizures.  The  ex- 
cessive use  of  the  motor  apparatus  in  learning  to  talk,  to  walk  and  to 
adjust  the  voung  creature  to  his  environment  is  possibly  the  cause  of 
this. 

About  the  time  of  puberty  the  sensory  and  emotional  disorders  are 
in  the  ascendent.  Under  the  awakening  of  the  sexual  life  and  all  that 
it  means  lx)th  in  the  individual's  inner  sensibilities  and  in  his  relation- 
ship to  his  surroundings,  hysteria,  neurasthenia,  epilepsy,  sleep  troubles,, 
hvpochondriasis  and  inherited  tendencies,  nervous  and  mental,  are  apt 
to  break  out. 

From  puberty  on  to  the  climacteric  the  nervous  system  is  mort  «>r 
less  stationary  and  developed,  but  it  is  subjected  to  all  of  the  strains  of 
an  active  adult  life.  Traumatisms  of  all  sorts  now  come  into  play.  So 
do  the  intoxications  and  infectious  diseases  of  adults. 

After  the  climacteric  the  troubles  of  old  age,  the  degenerations  of 
all  the  tissues,  ner\'ous  and  vascular,  are  to  be  counted  upon.  Hence 
the  senile  weakness,  the  apoplexies,  the  softenings,  the  arteriosclerotic 
and  atheromatous  degenerations,  vertigos,  neuralgias  and  paralyses  are 
common. 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  3 1 

The  influence  of  sex  is  a  knotty  question.  Women  are  more  emo- 
tional than  men  and  are  undoubtedly  subject  to  different  physiological 
influences.  But  they  also  lead  very  different  lives  from  men.  The 
neuroses  and  sensory  disorders  predominate  among-  them,  whereas  the 
organic  and  motor  affections  lead  among  men.  Just  how  much  of  this 
is  to  be  attributed  to  their  difference  oi  organization,  and  how  much 
to  their  difference  of  mode  of  living,  it  is  not  easy  to  say.  More  study 
is  needed  before  the  influence  of  sex  upon  the  development  of  nervous 
disorders  can  be  dogmatically  spoken  upon. 

Nationality  seems  to  have  some  bearing.  Whether  this  is  a  racial, 
a  biological  or  a  mere  geographical  factor  is  not  entirely  known.  The 
neuroses,  for  instance,  are  more  prominent  among  the  Jews  and  the 
Latin  races  of  Europe.  They  are  old  races  and  have  been  historically 
subjected  to  most  unhappy  conditions.  A  degree  of  degeneracy  there- 
fore may  account  in  part  at  least  for  their  proneness  to  the  functional 
troubles.  The  organic  diseases  are  more  common  in  the  Germanic  and 
Anglo-Saxon  peoples.  Locomotor  ataxia  is  a  rarity  in  the  Negro  and 
the  Jap.  The  insanities  of  childhood  are  almost  considered  American 
diseases,  but  they  are  probably  due  to  the  strenuous  lives  we  live  here. 
Certain  immigrant  races,  such  as  the  Bohemians  and  Poles,  probably 
owe  their  susceptibility  to  epilepsy  and  other  neuroses  to  their  de- 
pressed conditions  in  life  as  much  as  to  their  nationality.  France  is 
the  home  of  hysteria ;  as  a  people  the  French  live  a  comparatively 
sensuous,  unrestrained  and  highly  emotional  existence. 

All  occupations  that  are  in  unhygienic  surroundings,  that  are 
monotonously  prolonged,  that  necessitate  irregularity  of  habits,  that 
interfere  with  sufflcient  exercise,  fresh  air  and  relaxation,  that,  in  a 
word,  destroy  the  nice  balance  between  all  the  functions  of  the  body 
necessary  for  its  health,  predispose  towards  the  development  of  nervous 
troubles.  Much  neurasthenia  is  attributed  to  hard  work,  especially 
mental  work,  in  these  strenuous  days,  whereas  it  is  not  the  work  that 
is  to  be  blamed,  but  the  monotony  of  it  and  the  one-sided  development 
which  it  enforces.  Hysteria  is  often  provoked  by  the  narrow  mental 
lives  that  many  women  lead,  as  well  as  by  their  want  of  self-discipline. 

Occupations  of  some  kinds  are  particularly  prone  to  lead  to 
nervous  troubles  on  account  of  the  exposure  to  accidents,  to  intoxica- 
tion and  to  infection.  Bridge  builders  are  liable  to  the  caisson  disease; 
saloonkeepers  suffer  from  alcoholic  degenerations ;  lead  workers  some- 
times develop  lead  palsy;  and  traveling  men  get  syphilis  and  develop 
tertiary  consequences. 

It  is  said  that  the  unmarried  suffer  more  from  nervous  diseases 
than  the  married.  The  freer  life  and  greater  dissipation  of  the  former 
may  be  the  proper  explanation  for  this. 

The  whole  subject  of  occupation,  environment  and  the  special 
dangers  therein  is  a  large  one  and  can  only  be  referred  to  briefly  here. 

The  influence  of  the  mode  of  life  that  an  individual  lives  has 
already  been  hinted  at  in  the  consideration  of  the  age,  sex,  occupation 
and  nationality.  It  is  very  great.  It  involves  the  mental  as  well  as 
the  physical  life.  Overindulgence  in  eating,  in  the  use  of  spirituous 
beverages,  tea,  coffee,  tobacco,  is  a  prolific  source  of  nervous  trouble. 


32  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

Bad  sleeping  arrangements,  bad  bathing  customs,  bad  methods  in 
everything  will  surely  lead  to  misfortune.  It  is  astounding  how  some 
of  the  simplest  intimations  of  nature  are  misinterpreted  and  unheeded 
by  those  who  ought  to  know  better.  A  physician,  in  a  high  degree  an 
irritable  neurasthenic,  came  to  me  and  declared  that  he  did  not  seem 
to  get  well,  but  worse,  though  he  stimulated  himself  up  every  day 
with  a  cold  plunge  bath  in  the  morning,  full  doses  of  strychnia  and 
long,  exhausting  walks.     I  told  him  I  was  not  surprised  i 

Excessive  sexual  indulgence  is  undoubtedly  a  source  of  much 
nervous  breakdown  in  both  married  and  unmarried.  Athletics  and  the 
indulgence  in  outdoor  sports  at  the  present  time  are  so  excessive  that 
they  become  a  source  of  danger  by  putting  unusual  strain  upon  the 
vascular  system. 

On  the  mental  side,  sensational  literature,  narrow  thinking  and 
the  habit  of  flaring  up  in  anger  at  every  trifle  are  highly  conducive  to 
the  development  of  the  neuroses,  as  weU  as  being  often  a  symptom  of 
them.  Why  is  it  so  frequently  forgotten  that  the  mind  is  as  much  in 
need  of  proper  exercise  as  the  muscles  are?  The  mind  is  a  product  of 
brain  activity  and  the  brain  grows  or  wastes  just  as  any  other  tissue 
of  the  body  if  it  is  exercised  or  neglected.  We  do  not  know  what  parts 
of  the  brain  subserve  particular  faculties  of  the  mind,  but  we  do  know- 
that  as  a  sort  of  counterpart  to  the  biceps  and  triceps  and  lumbar  mus- 
cles of  the  body  there  is  a  memory  and  an  imagination,  a  logical  and 
a  speech  faculty.  How  pitifully  lop-sided  is  that  man  who  toils  daily 
after  business  hours  in  the  gymnasium  with  his  dumbbells  and  Indian 
clubs  in  order  to  develop  the  nmscular  system,  but  who  never  once 
thinks  of  exercising  specifically  his  imagination  or  his  memory.  The 
dull  round  of  his  routine  life  does  not  afTord  the  opportunity  for  very 
wide  mental  development. 

I  am  convinced  that  one-sidedness  in  mental  development  as  well  as 
one-sidedness  in  physical  is  responsible  for  some  of  the  neurasthenia 
and  hysteria  which  we  observe  alDOut  us. 

A  volume  could  be  written  upon  the  influence  of  habits  and  the 
mode  of  life  in  the  fostering  of  nervous  affections. 

Climate,  apart  from  mere  racial  and  geographical  influences,  is  not 
an  important  factor  in  the  etiology  of  nervous  .diseases.  The  fact  that 
these  are  more  common  in  the  temperate  zones  is  because  there  the 
strenuous  life  and  extreme  competition  are  found.  This  suggests  the 
truth  that  civilization  is  responsible  for  much  nervous  and  mental  trou- 
ble. Neurologists  and  alienists  would  find  their  services  at  a  discount 
among  barbarous  races.  In  the  centers  where  civilization  is  burning  at 
white  heat,  as  it  were,  namely,  the  great  cities,  there  the  nervous  trou- 
bles are  in  abundance.  In  fact  they  are  on  the  increase.  The  two  great- 
est causes  of  these  affections  were  included  in  that  happy  epigram 
of  Krafift-Ebing,  "syphilization  and  civilization.'''  We  must  be  careful, 
however,  not  to  charge  civilization  with  what  is  to  be  blamed  upon  squal- 
or and  vile  conditions  in  some  of  our  cities.  To  argue  as  Rousseau  did 
that  we  need  to  return  to  barbarism  is  a  bad  mixing  up  of  cause  and 
efifect,  of  separate  and  distinct  forces,  that  is  wholly  inexcusable.  Civi- 
lization in  its  true  sense  means  culture,  refinement,  comfort  and  mental 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  33 

elevation.  Because  ignorance,  stupidity,  greed  and  poverty  happen  to 
loom  up  where  civilization  is  existent,  it  merely  shows  by  the  contrast 
that  much  good  has  been  accomplished  though  much  is  yet  to  be  ac- 
complished. Not  civilization  but  the  abuse  of  the  opportunities  offered 
by  civilization  is  the  cause  of  the  apparent  mcrease  of  nervous  troubles. 

Among  the  predisposing  causes  of  nervous  affections,  certain 
diatheses  must  not  be  overlooked,  especially  the  gouty  and  rheumatic. 
What  passes  under  the  general  name  of  the  litha;mic  condition  is  read- 
ily recognized  clinically,  though  the  nature  of  the  defective  process 
is  not  fully  understood.  Faulty  metabolism  with  faulty  elimination  is 
perhaps  the  real  difficulty.  How  this  reacts  upon  the  nervous  system 
to  produce  functional  and  peripheral  diseases  is  not  clear  but  that  it 
does  do  so  is  amply  demonstrated  both  clinically  and  therapeutically. 

I  come  now  to  the  exciting  causes  of  nervous  diseases,  and  first 
and  foremost  I  place  in  the  list  the  traumata.  These  include  all  kinds 
of  physical  and  mental  insults.  A  terrific  blow  on  the  head  may  pro- 
duce less  serious  eft'ects  than  a  terrible  fright.  Bodily  injuries  of  all 
sorts,  especially  about  the  head,  may  set  up  profound  nervous  and 
mental  deterioration.  Primarily  or  secondarily  the  delicate  neurones 
may  be  disturbed.  From  a  gross  fracture  of  the  skull,  all  the  way 
to  a  mere  concussion,  may  the  traumata  range.  The  former  lacerates, 
compresses,  invades  with  hemorrhage,  inflammation  and  infection  the 
cerebral  tissues;  the  latter  jars  and  disturbs  the  functions  of  the 
neurones  in  such  a  way  as  to  give  rise  to  neurosis.  Exposure  to  cold 
and  damp  is  of  the  nature  of  a  trauma.  So  are  sudden  excitement, 
tmnatural  coitus  and  many  other  causes  given  in  the  books. 

Almost  any  form  of  infection  may  give  rise  tO'  disease  of  the 
nervous  organism.  Usually  it  is  of  the  inflammatory  type  of  disease 
though  in  some  chronic  infections  it  may  be  non-infllammatory  and 
purely  a  neuronic  degeneration.  It  is  generally  believed  that  not  the 
germs  themselves  but  their  toxic  products  are  the  immediate  causes  of 
the  disease  process.  Syphilis,  both  acute  and  chronic,  acquired  and  inher- 
ited, is  hig'hly  blameable.  Scarlet  fever,  measles,  influenza,  pertussis, 
erysipelas,  gonorrhoea,  septicaemia,  pyaemia,  etc.,  all  enter  into  the  etiol- 
ogy of  nervous  affections.  Tuberculosis,  near  and  remote  abscesses  and 
other  germ  troubles  may  provoke  metastatic  lesions  in  the  nerve  cen- 
ters. Some  tumors  and  parasitic  growths  should  probably  be  classed 
here,  though  in  a  way  they  act  more  as  traumatic  causes  by  compress- 
ing and  mechanically  irritating  the  nervous  elements  near  which  they 
are  located.  Until  we  know  more  about  the  pathogenesis  of  these  neo- 
plasms we  can  only  say  that  infection  and  traumatism  are  the  imme- 
diate causes  of  the  nervous  disturbances  when  they  are  present. 

Of  the  intexications  that  provoke  nervous  maladies,  the  alcoholic 
far  outranks  all  the  others.  Lead,  arsenic,  mercury,  aniline,  copper, 
carbon  dioxide,  tea,  coffee  and  tobacco  are  a  few  of  the  intoxicants. 
Here  should  be  mentioned  also  the  drugs  that  are  sometimes  used  as 
a  habit,  morphine,  cocaine,  chloral.  Autointoxication  together  with 
malnutrition  is  probably  the  explanation  of  the  etiological  bases  of  the 
various  cachexias,  of  ansmia,  of  diabetes  mellitus,  of  nephritis  and 
certain  alimentary  troubles. 


34  GENERAL    COXSTDERATIOXS    UPOX    XERVOUS    DISEASES 

Finally,  a  word  must  be  said  upon  the  much-discussed  _  reflex 
causes  of  nervous  diseases.  To  deny  all  etiological  influence  of  a  re- 
flex character  is  to  deny  the  reflex  phenomenon  of  the  normal  nervous 
apparatus.  To  attribute  disease  in  the  otherwise  unaffected  nervous 
centers  to  a  mere  reflex  activity,  which  is  a  normal  function  of  a  nor- 
mal nervous  system,  is  illogical  on  the  face  of  it.  Therefore,  we  as- 
sume that  a  constant  reflex  excitement  of  the  nervous  apparatus  pro- 
duces the  manifestation  of  disease  symptoms  in  only  one  of  two  condi- 
tions ;  either  as  an  excitant  to  an  already  abnormal  and  diseased  nervous 
organism  or  as  an  excitant  to  an  exhausted  and  wearied  one. 

In  the  first  case  the  reflex  is  not  the  primary  cause  of  the  dis- 
ease but  is  clearly  a  mere  irritant  to  it. 

In  the  second  case,  it  may  be  seriously  questioned  w^hether  a  mere 
state  of  exhaustion  ever  becomes  transformed  into  a  specific  type  of 
disease.  Let  me  illustrate.  There  are  ophthalmologists  to-day  who 
attribute  epilepsy  to  eye-strain.  Where  there  is  epilepsy,  eye-strain 
as  well  as  a  painful  corn  on  the  toe,  a  phimosis  or  an  impacted  bowel 
may  provoke  the  attacks.  If  there  is  a  tendency  to  epilepsy  even,  eye- 
strain may  start  the  disease  into  activity.  In  all  cases  of  epilepsy 
therefore  the  eyes  should  be  corrected  if  need  be,  but  don't  charge  the 
eyes  with  the  central  nervous  trouble.  When  it  is  contended  that  eye- 
strain produces  epilepsy  de  novo  in  a  previously  healthy  nervous  appa- 
ratus, it  is  incumbent  upon  the  ophthalmologist  to  explain  how  it  does 
it.  He  declares  that  it  does  it  by  exhausting  the  nervous  centers.  He 
has  been  betrayed  clearly  in  his  pathology  by  the  use  of  the  unfortu- 
nate word  fiinctional.  Epilepsy,  hysteria  and  neurasthenia  we  may 
grant  for  argument's  sake  are  all  alike  in  being  functional  but  their 
very  symptomatology  proves  that  they  are  not  alike  in  their  origin 
and  physical  basis  wherever  and  whatever  that  may  be.  The  eye-strain 
of  the  ophthalmologists'  pathology  acts  always  in  the  one  way,  namely, 
as  an  exhausting  strain,  and  yet  strange  to  say  it  produces  a  variety 
of  distinct  specific  diseases  of  a  different  character  in  different  indi- 
viduals. 

Knowledge  of  the  pathogenesis  of  these  various  diseases  is  not  as 
clear  as  it  should  be  but  it  certainly  is  clear  enough  to  reveal  the  illog- 
ical reasoning  of  those  who  attribute  a  series  of  distinct,  sharply-de- 
fined, different  aft'ections  to  a  mere  peripheral  wearying  reflex  that  is 
always  the  same  in  character  and  points  to  no  direct  connection  between 
these  various  diseases  or  between  them  and  itself.  The  causation  of 
different  distinct  pathological  conditions  in  a  previously  normal  system 
by  the  mere  constant  exercise  of  a  single  and  uniform  reflex  irritation 
is  a  step  backward  and  brings  us  face  to  face  again  with  a  pathology 
that  is  hazy  and  antiquated  and  from  which  we  had  fondly  thought  mod- 
ern neurology-  was  redeemed. 

In  my  opinion,  nervous  diseases  are  not  reflex  diseases  though 
they  may  be  aroused  into  expression,  or  excited  into  greater  activity 
when  so  aroused,  by  a  dozen  or  more  sources  of  peripheral  reflex  stim- 
ulation. 


GENERAL    COXSIDERATIOXS    UPOX    XERVOUS    DISEASES 


6:j 


GEXEE_\L  COXSIDERATIOXS  UPOX  THE  PATHOLOGY  OF 
XER\'OUS  DISEASES. 

In  order  to  have  a  clear  comprehension  of  the  pathology  of  the 
diseases  of  the  nerv^ous  system,  one  must  keep  well  in  mind  the  com- 
plex character  of  the  ner^^ous  tissues  and  their  relationship  to  all  the 
other  tissues.  Alany  diseases  are  secondary  to  extraneous  affections 
that  cause  pressure  or  by  extension  and  metastases  invade  the  neri'ous 
system.  Therefore  in  these  diseases  frequently  there  are  pathological 
findings  of  great  importance  in  other  parts  of  the  body.  For  instance, 
intracranial  embolism  is  usually  associated  with  valvular  heart  dis- 
ease; tuberculous  meningitis  is  accompanied  b}^  tuberculous  foci  in  the 
lungs;  abscess  of  the  brain  is  very  largely  due  to  suppurative  otitis 
media ;  damage  to  the  spinal  cord  frequently  results  from  caries  of 
the  spine;  disease  of  the  muscles  and  various  end-organs  in  direct 
functional  connection  with  the  neurones  not  infrequently  sets  up  de- 
generative changes  in  the  latter. 

It  is  not  our  province  to  refer  to  all  of  these  extraneural  troubles 
but  merely  to  the  pathological  changes  which  the}'  and  other  causes 
set  up  within  the  nervous  apparatus. 

It  will  be  remembered  that  nervous  tissue  consists  of  two  dis- 
tinct sets  of  elements,  developed  from  dift'erent  embryonic  layers  in  the 
ovum.  The  true  nervous  elements  are  the  neurones  and  the  neuroglia 
cells.  Though  these  differ  in  function,  the  former  being  the  excitable 
elements  while  the  latter  are  merely  sustentacular  or  supporting,  both 
are  found  only  in  the  nervous  system,  and  developed  from  the  epiblast 
are  non-vascular. 

The  false  nervous  elements  are  the  connective  tissue  cells,  the 
blood  vessels,  the  lymphatics  and  the  epithelium  lining  the  ventricles. 
The  function  of  these  is  to  nourish  and  furnish  a  matrix  for  the  true 
nen'ous  elements.  They  are  found  in  other  parts  of  the  body  as  well 
as  here,  are  mesoblastic  in  origin  and  are  vascular. 

Pathologically  then  the  nen^ous  system  is  liable  to  two  great  types 
of  change.  The  non-vascular  elements  undergo  degeneration,  the  vas- 
cular elements  undergo  inflammation. 

Degeneration  is  the  only  change  that  tvtv  occurs  in  the  neurones. 
The  neuroglia  cells  may  proliferate,  form  tumors  and  then  undergo 
degeneration. 

Inflammation  with  all  its  attendant  conditions,  hemorrhage,  vas- 
cular obstruction,  infective  processes,  connective-tissue  and  parasitic 
new-growths,  and  sclerotic  changes  may  occur  in  the  vascular  con- 
nective-tissue of  the  nen'ous  system  just  as  they  may  occur  in  the 
vascular  connective-tissue  of  other  organs  and  parts  of  the  body.  Un- 
der such  circumstances  the  true  or  nobler  nervous  elements  are  damaged 
secondarily. 

It  is  doubtful  whether  a  simple,  primary  degeneration  in  the  true 
nervous  elements  ever  sets  tip  inflammation  secondarily  in  tiie  vascu- 
lar structures.  I  knoAv  that  in  locomotor  ataxia,  a  true  degenerative 
disease,  and  in  some  degenerative  forms  of  polyneuritis  inflammation 


36  nFXKRAL    COXSIUKRATIOXS    UPON    XERVOUS   DISEASES 

of  the  meninges  and  of  the  interstitial  tissues  is  often  respectively  ob- 
served but  it" is  a  question  whether  this  inflammation  is  not  due  pri- 
marily to  the  same  general  infection  or  intoxication  that  gives  rise  to 
the  degeneration. 

Degeneration  as  it  is  seen  in  the  nervous  system  is  a  unique  pro- 
cess. It  gives  a  very  characteristic  appearance  to  the  affected  tissues, 
and  its  presence  and  progress  render  the  symptomatology  of  nervous 
lesions  clinically  almost  pathognomonic.  Hence  its  appreciation  is 
most  important.  As  the  distinctive  lesion  of  the  nervous  apparatus,  it 
is  more  important  than  the  grosser  lesions  of  vascular  origin.  When 
a  nervous  element  undergoes  degeneration  it  dies,  wastes  and  dis- 
appears. The  cell-body  swells  up,  then  becomes  granular  and  fatty, 
and  finally  is  absorbed.  The  process  is  sometimes  called  chromatolysis. 
In  the  early  stage  and  temporarily,  if  the  degeneration  is  not  severe 
or  complete,  there  may  be  a  shriveling  up  of  the  cell-body ;  its  edges 
then  become  serrated,  its  nucleolus  disappears,  its  nucleus  shifts  to  one 
side  (decentralization),  the  chromophyllic  particles  diminish  in  amount 
and  closely  hug  the  nucleus  while  open  sp?xes  appear  in  the  substance 
of  the  cell-body  ( vacuolaticn).  Such  cells  sometimes  regenerate,  pass- 
ing through  a  reverse  order  of  events. 

In  acute  and  complete  degeneration  the  neuraxones  participate  in 
the  cellular  destruction.  The  white  substance  of  Schwann  breaks  up 
into  fatty  globules,  the  nuclei  of  the  neurilemma  proliferate,  and  the 
entire  process  becomes  a  hollow  tube  containing  the  axis-cylinder  and 
degenerated  white  substance.  At  length  the  axis-cylinder  breaks  down ; 
absorption  takes  place,  and  nothing  is  left.  Into  the  hollow  space 
vacated  by  the  process,  or  neuraxone,  the  neuroglia  and  connective- 
elements  crowd  and  thus  render  the  tissue  firmer  and  denser,  more 
vascular  and  less  puctuated  from  nerv^e  fibres  on  cross-section  (scler- 
osis) than  it  was  before. 

Degeneration  may  be  an  acute  or  chronic  process,  severe  or  mild, 
partial  or  complete.  Most  important  is  the  fact  that  it  may  be  primary 
or  secondary.  Under  certain  circumstances  it  may  involve  the  entire 
neurone  or  only  a  part  of  it.  It  may  spread  directly  from  one  neurone 
to  the  next  one  in  the  same  nervous  pathway,  provided  the  second  neu- 
rone is  functionally  subordinate  to  the  first.  This  explains  the  morbid 
anatomy  of  the  progressive  system  diseases.  It  probably  never  passes 
directly  from  one  neurone  laterally  across  to  another  lying  beside  it. 
The  simultaneous  degeneration  of  the  two  neurones  under  such  circum- 
stances is  in  all  probability  due  to  the  simultaneous  action  of  the  same 
cause. 

The  origin  of  these  degenerations  lets  a  flood  of  light  in  upon  the 
etiology  of  nervous  diseases.  The  primary  degenerations  may  be  due 
to  hereditary,  congenital,  toxgemic,  nutritional  and  traumatic  influ- 
ences. When  the  vitality  of  the  neurones,  transmitted  from  the  parent 
to  the  child,  is  so  vitiated  that  they  cannot  develop  properly,  function- 
ate normally,  or  resist  the  deleteriou.=  influences  of  life,  they  are  neuro- 
pathic and  break  down  into  the  condition  of  disease.  In  this  way  the 
developmental  and  familial  diseases  are  evolved.  Friedreich's  ataxia 
and  the  progressive  atrophies  furnish  capital  illustrations.    In  all  prob- 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  37 

ability,  it  is  only  degree  that  distinguishes  the  neuroses  such  as  epilepsy, 
migraine,  congenital  neurasthenia  and  hysteria  from  the  cited  ex- 
amples. 

Congenital  primary  degenerations  are  undoubtedly  due  sometimes 
to  shock  and  malnutrition  of  the  mother  and  then  of  the  child  while 
the  latter  is  in  the  uterus.  One  must  not  confuse  with  these  cases 
the  infantile  hemiplegias  in  whom  secondary  degenerations  occur  as 
the  result  of  hemorrhage,  inflammation  and  other  factors.  The  con- 
genital primarv^  degenerations  are  non-hereditary  for  the}^  are  intra- 
uterine in  origin.  Most  of  them,  like  most  of  the  natal,  postnatal  and 
adult  primary  degenerations,  are  due  to  general  or  local  traumatic,  nu- 
tritional and  toxjemic  influences. 

Profound  shocks,  blows  and  concussions,  without  causing  any 
discoverable  lesion,  are  not  unfrequently  seen  to  provoke  degenerative 
troubles,  particularly  of  the  mild  type  of  the  neuroses.  Some  of  these 
even  go  on  to  severe  degenerative  alterations  pronounced  enough  to 
be  manifested  in  permanent  paralysis. 

Malnutrition  as  a  cause  of  degenerative  trouble  needs  but  to  be 
mentioned.  Local  malnutrition  occurs  from  vascular  oibstruction  by 
emboli,  thrombi  and  arteritis  obliterans.  Many  senile  forms  of  nerv- 
ous degeneration  are  due  to  inefficient  nutrition  and  metabolism. 

The  supreme  cause  of  the  primary  degenerations  in  adult  life 
are  the  intoxications  and  infections.  I  might  have  said  only  the  intox- 
ications, for  in  the  infections  it  is  tlie  poisonous  products  of  the  germs 
and  not  the  germis  themselves  that  provoke  the  degenerative  changes. 
Under  the  head  of  etiology  in  the  previous  chapter  I  have  referred 
to  the  various  kinds  of  intoxication.  Just  how  these  intoxications 
act  upon  the  nervous  elements  is  not  clear.  Some  probably  damage 
them  directly ;  others  doubtless  affect  them,  indirectly  by  lowering  the 
nutritive  value  of  the  blood.  Much  has  yet  to  be  learned  upon  this 
question. 

Perhaps  the  greater  number  of  nervous  degenerations  are  sec- 
ondary in  origin.  The  function  of  self-nutrition  for  the  entire  nervous 
element,  seems  tO'  reside  in  the  cell  body.  Therefore  if  the  cell  body  is 
damaged,  all  parts  of  the  neurone  undergo  a  parallel  wasting.  If  a 
part  of  the  neurone,  say  a  part  of  the  neuraxone,  is  severed  from  its 
cell-body,  all  that  part  that  has  been  cut  off  wastes  away. 

The  latter  is  the  well-known  Wallerian  type  of  denegeration. 

Now  the  factors  that  may  damage  the  cell-bodies  of  a  mass  of 
neurones,  or  lacerate  and  sever  their  processes  from  them,  are  innu- 
merable and  as  a  rule  belong  to  the  diseases  and  lesions  of  the  con- 
nective tissue,  the  vascular  and  sustentacular  elements  generally.  It 
is  not  necessary  to^  describe  these  in  detail  but  it  is  important  to  note 
that  the  localization  of  the  lesion  is  rendered  ofttimes  very  definite  by 
the  limited  and  definite  area  of  destruction.  As  these  lesions  impli- 
cate more  or  less  transversely  the  nervous  paths,  the  degeneration 
travels  in  opposite  directions  away  from  it.  Remaining  always  in  the 
same  system  wherein  it  started,  it  advances  upwards  in  the  sensory 
and  downwards  in  the  motor  paths  if  the  lesion  is  anywhere  between 
the  cerebral  cortex  and  the  posterior  spinal  ganglia.     If  the  lesion  be 


^8  GEXKRAL    (ONSIDERATIOXS    UPOX    XERVOUS   DISEASES 

outside  of  the  posterior  spinal  ganglia  and  include  the  paths  of  both 
the  anterior  and  posterior  roots,  the  degeneration  will  be  downward 
in  lioth  the  motor  and  sensorv  fibers  in  the  nerves  beyond  the  seat  of 
the  lesion.  There  will  be  no  degeneration  on  the  proximal  side  of  the 
lesion.  * 

Secondary  degenerations  being,  due  to  damage  of  the  neurone 
bodies  or  severance  of  the  neuraxones  from  their  nutritive  centers,  they 
are  confined  more  distinctly  and  prominently  to  the  neurones  imme- 
diately involved.  The  next  adjoining  lower  or  higher  neurones  are 
but  slightly  afifected  and  then  only  when  they  are  functionally  subor- 
dinate and  dependent. 

In  this  respect  there  is  a  difference  between  the  primary  degener- 
ations due  to  such  general  influences  as  heredity  and  intoxication,  and 
the  secondary  due  "to  separation  of  a  neurone  or  part  of  it  from  its 
nutritive  center. 

Though  localization  symptoms  may  appear  with  the  primary  de- 
generations and  in  some  particular  cases  be  well-defined,  they  will  be 
most  pronounced  and  therefore  most  valuable  in  the  secondary  degen- 
erations. The  whole  question  of  localizations  will  be  discussed  however 
elsewhere. 

The  constant  characteristic  of  all  those  lesions,  whatever  their 
original  cause  may  have  been,  that  eventuate  in  secondary  degenera- 
tion is  that  they  involve  vascular  tissues  and  sooner  or  later  are  ac- 
companied by  inflammation.  Perhaps  the  only  exception  to  this  rule, 
and  that  is  more  apparent  than  real,  is  the  case  wherein  a  local  area 
of  nerve  substance  undergoes  softening  from  the  shutting  off  of  its 
blood  supply  by  an  embolus  or  a  thrombus.  In  this  case  the  degenera- 
tion is  of  the  primary  type,  though  the  lesion  is  grossly  local  and  vas- 
cular. In  all  other  cases,  vascular  trouble  enters  into  the  lesion  with 
the  appearance  of  more  or  less  inflammation  and  secondary  degenera- 
tion. 

Inflammation,  therefore,  is  a  most  important  feature  in  the  pathol- 
ogy of  the  nervous  system.  The  inflammatory  process  itself  is  iden- 
tically the  same  as  it  is  elsewhere  in  the  body.  There  is  the  same  ini- 
tial hypersemia,  extravasation  of  red  corpuscles,  infiltration  of  leu- 
cocytes, redness,  swelling,  softening  and  oedema.  All  this  of  course 
damages  the  delicate  neurones  lying  in  the  midst  of  it.  They  undergo 
the  degenerative  process  which  usually  terminates  in  complete  func- 
tional and  structural  annihilation. 

The  number  of  neurones  that  may  be  implicated  is  always  a  varia- 
ble one,  depending  upon  the  virulence  of  the  cause  and  the  violence 
of  the  lesion.  Many  neurones  weather  the  storm  and  regain  their  func- 
tional integrity  after  the  inflammation  subsides. 

As  inflammation  is  the  reaction  of  the  organism  to  an  irritant, 
whether  traumatic  or  infective,  it  is  really  a  reparative  process,  an  effort 
of  nature  to  rid  herself  of  noxious  conditions.  It  is  therefore  always 
regressive  rather  than  progressive  and  tends  to  limit  itself  so  soon  as 
it  conquers  the  baleful  cause  which  brought  it  into  existence.  In  the 
warfare  which  it  is  carrying  on  against  the  agents  of  harm,  it  causes 
damage  itself,  some  of  which  remains  as  a  sort  of  a  scar  long  after- 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  39 

wards  in  the  conditions  of  sclerosis,  cavity-formation  and  atrophy. 
Among  the  last  of  course  are  to  be  included  the  secondary  degenera- 
tions. 

Usually  we  recognize  three  types  of  inflammation  in  the  nerv^ous 
system,  just  as  we  do  elsewhere.  They  are  the  simple  exudative,  the 
purulent  and  the  so-called  productive  or  proliferative  inflamrnation. 
The  former  two  are  acute  or  subacute  processes  and  differ  from  each 
other  in  regard  to  the  presence  of  pus.  The  last  is  a  chronic  process ; 
is  characterized  by  little  congestion  and  exudation  but  rather  by  the 
slow  formation  of  connective  tissue. 

The  cause  of  all  these  inflammations  is  not  the  same  of  course, 
some  being  due  to  mechanical,  others  to  chemical,  and  still  others  to 
bacterial  factors. 

It  is  unnecessary  to  discuss  these  further  here  as  they  are  not  at 
all  peculiar. 

Among  the  residua  and  after-effects  of  inflammation  in  the  nerv- 
ous system  there  are  several  of  great  importance.  The  secondary  de- 
generations I  have  alread}'  spoken  of.  There  is  often  local  softening, 
general  destruction  and  necrobiosis  in  the  vicinity,  with  a  mass  of  de- 
bris consisting  of  broken  down  nervous  tissue,  and  blood  elements. 
This  undergoes  absorption  and  leaves  a  scar  or  cyst  in  some  cases.  In 
others,  especially  when  the  inflammatory  process  has  been  chronic, 
sclerosis  takes  place.  By  this  term  is  meant  a  hardening  of  the  tissues 
from  an  overgrowth  of  the  connective  tissue  elements  and  the  replac- 
ing of  the  wasted  true  nerve  cells  and  processes  by  them.  The  neu- 
roglia usually  proliferates  also. 

In  sclerosis  then  we  observe  an  absence  or  diminution  of  the  num- 
ber of  neurones  with  an  increase  of  the  neuroglia  and  connective  tis- 
sue. Whether  the  overgrowth  of  the  sustentacular  tissue  is  first,  caus- 
ing destruction  of  the  neurones  by  compression,  or  whether  the  neu- 
rones degenerate  first  and  the  sustentacular  elements  proliferate  to  fill 
up  the  vacuity,  is  not  alwa3's  easy  to  determine.  It  is  generally  con- 
sidered, however,  that  the  latter  method  occurs  in  the  primary  degen- 
erative diseases,  whereas  the  former  mode  obtains  in  the  inflammatory 
and  secondary  degenerations. 

From  what  has  been  said  under  the  head  of  degeneration,  it  is 
easy  to  infer  that  when  the  neurone-cells  are  destroyed  they  are  never 
regenerated. 

This  is  a  fact  of  common  observation  and  accounts  for  the  perma- 
nency of  many  forms  of  paralysis  and  trophic  disturbance.  A  neu- 
raxone  that  is  destroyed  may,  however,  completely  regenerate.  Just 
how  it  does  so  is  not  minutely  known.  All  evidence  seems  to  point 
out  that  the  neurilemma  and  white  substance  of  Schwann  grow  again 
in  situ,  but  that  the  axis-cylinder  extends  forward  from  the  proximal 
or  cellular  end  into  the  new  nervous  tissue.  The  former  reappear  some- 
how from  the  local  elements,  whereas  the  latter  steadih'  pushes  for- 
ward like  a  branch  growing  from  the  trunk  of  a  tree.  It  grows  of 
course  always  from  the  trophic  center. 

Some  recent  experiments  made  at  the  University  of  Chicago 
demonstrate  in  the  lower  animals  that  neuraxones  can  thus   extend 


40  GENERAL    COXSIDERATIONS    UPON    NERVOUS    DISEASES 

across  lacerations  and  other  forms  of  solntion  of  continuity  in  the  cen- 
tral nervous  svstem. 

An  interesting  pathological  condition  which  belongs  solely  to  the 
nervous  svstem  is  what  is  known  as  gliosis  or  glioniatosis.  It  is  the 
basis  of  a'  certain  form  of  tumor  and  cavity  formation.  It  is  essen- 
tially a  proliferation  of  the  glia  cells  and  neuroglia  tissue.  Being  non- 
vascular and  epiblastic  in  origin  it  undergoes  both  primary  and  sec- 
ondary degeneration.  In  certain  slates  of  embryonic  defectiveness,  it 
proliferates,  breaks  down,  is  reabsorbed  and  leaves  a  cavity.  Syringo- 
myelia is  such  a  case  in  point.  Sometimes  with  or  without  apparent 
cause,  it  spreads  out  and  creates  a  tumor-like  formation.  These  are 
the  well-known  gliomata  of  the  nervous  system.  Finally  it  joins  in  the 
proliferative  process  of  the  cormective-tissue  elements  in  the  production 
of  the  scleroses  of  the  cerebrospinal  axis. 

In  regard  to  the  diseases  of  the  nervous  system  in  which  no  patho- 
logical changes  can  be  discovered  we  can  only  argue,  form  hypotheses, 
and  balance  our  logic.  It  is  a  time-honored  custom  to  call  such  diseases 
functional,  and  to  describe  them  as  depending  upon  change  of  func- 
tion without  change  of  structure.  I  must  confess  that  I  am  incapable 
of  comprehending  such  a  paradoxical  condition.  I  cannot  grasp  the 
idea  that  an  abnormal  manifestation  can  be  the  outgrowth  of  a  normal 
structure.  It  is  argued,  however,  that  malnutrition,  and  possibly 
slight  blood  changes,  are  the  cause  of  the  functional  disturbances. 
When  pushed  to  the  wall,  those  who  argue  thus  say  that  they  presume 
there  may  be  some  temporary  physical  or  physio-chemical  change  in 
the  neurones  as  a  result  of  the  malnutrition  or  reflex  irritation.  That, 
however,  is  included  in  what  I  conceive  of  as  change  of  structure.  It 
is  too  fine  for  our  present  means  of  detection  undoubtedly  but  logic 
can  penetrate  often  where  physical  means  of  research  fail  utterly.  Logic 
seems  to  me  to  affirm  beyond  all  question  that  an  attribute  of  a  thing 
cannot  alter  in  the  slightest  degree  without  some  alteration  in  the 
the  thing  itself.  An  attribute  does  not  exist  apart  from  the  thing.  It 
is  but  another  point  of  view  from  which  w.e  behold  that  thing.  A  func- 
tion is  an  attribute  of  a  functionating  body.  It  has  no  more  real  ex- 
istence apart  from  that  body  than  has  its  color,  consistency  or  shape. 
Not  one  of  the  latter  can  vary  without  some  variation  having  taken 
place  in  the  body.  In  the  same  way,  the  function  cannot  change,  it 
seems  to  me,  without  a  change  having  taken  place  in  the  functionating 
substance.  Of  course  this  has  no  reference  to  what  may  be  called  sec- 
ondary functions  or  functions  resulting  from  the  action  of  one  normal 
structure  upon  another.  Psychosis  is  a  secondary  function,  for  it  is  the 
result  of  the  interplay  of  certain  elementary  impulses.  An  abnormal 
psychosis  may  be  a  functional  trouble  with  a  normal  physical  basis. 
This  is  further  discussed  under  hysteria. 

Therefore,  in  my  opinion,  there  is  a  pathology  for  the  so-called 
neuroses  and  functional  diseases.  Our  knowledge  of  it,  like  our  knowl- 
edge of  a  good  many  other  things,  is  still  wanting.  In  their  last 
analysis,  functional  diseases  are  as  organic  as  any  degenerative  disease 
but  not  to  s'O  great  a  degree  or  so  grossly  as  in  what  are  commonly 
denominated  the  crs'anic  diseases. 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  4I 

As  a  resume  of  the  pathology  of  diseases  of  the  nervous  system 
the  following  schema  may  be  useful : 

A.  Pathological  changes  distinctively  and  primarily  Neural  (in- 
cluding the  Neurones  and  the  Neuroglia). 

a.  Malformations ;  Hereditary  and  Congenital  Defects ;  In- 
complete Development  or  Agenesis  ;  Defective  Development 
or  Dysgenesis. 

b.  Degeneration,  Primary  and  Secondary. 

c.  Gliosis  and  Gliomatosis. 

B.  Pathological  changes,  not  distinctively  nor  primarily  Neural 
(including  the  connective  tissues,  blood-vessels,  Ivmphatics  and  epithe- 
lia). 

a.  Inflammations. 

b.  Hyperemia,  Anaemia,  Hemorrhage,  Qidema,  Arterial  and 
Venous  Diseases  generally. 

c.  Connective  Tissue  Sclerosis. 

d.  Infective  Processes  like  Tuberculosis,  vSyphilis,  etc. 

e.  All  Neoplasms,  Tumors,  Parasitic  Growths,  Cysts,  Ab- 
scesses, etc.   (excepting  Gliomata). 

GENERAL  CONSIDERATIONS    UPON    THE    SYMPTOMAT- 
OLOGY AND  DIAGNOSIS  OF  DISEASES  OF  THE 
NERVOUS  SYSTEM  AND  THE  EXAMINA- 
TION OF  THE  PATIENT. 

It  will  be  most  appropriate  to  discuss  the  general  semeiology  of 
diseases  of  the  brain,  spinal  cord,  nerves  and  sympathetic  system,  at 
the  head  of  the  sections  devoted  to  these  diseases  and  immediately  after 
the  consideration  of  the  anatomy  and  physiology  of  the  respective  parts 
of  the  nervous  system.  In  this  chapter  I  will  take  up,  merely  in  a  gen- 
eral way,  the  symptoms  that  belong  to  the  nervous  system  as  a  whole, 
and  will  attempt  some  practical  suggestions  in  regard  to  the  proper 
method  of  examining  a  patient. 

On  account  of  the  inaccessibility  of  the  nervous  apparatus  to  direct 
examination,  except  in  the  one  little  spot  back  of  the  eye, 
and  on  account  of  the  multiplicity  and  interrelations  of  its 
functional  activities,  the  examination  of  it  is  a  supreme  test  of  the 
physician's  natural  ingenuity,  skill  and  knowledge.  One  must  ap- 
proach it  with  his  mind  completely  unbiased,  alert,  and  flexible.  New 
points  of  view  must  be  taken  when  unexpected  hints  are  thrown  out 
by  the  patient  or  his  guardians.  No  opinions  must  be  formed  until  the 
examination  is  finished,  and  even  then  it  is  sometimes  well  to  with- 
hold them  until  after  two  or  three  future  examinations.  Snap  diagno- 
ses are  especially  dangerous  in  neurology.  There  are  geniuses,  ex- 
ceedingly rare  and  far  between,  however,  who  can  instinctively  grasp 
the  full  situation  after  the  patient  has  uttered  a  few  sentences  and  ex- 
hibited a  few  signs.  Even  they  sometimes  make  outrageous  blunders. 
The  more  experienced  a  man  is  and  the  more  learned  in  regard  to  the 


42  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

nervous  mechanism  of  course  the  more  swiftly  and  accurately  will  he 
arrive  at  his  final  diagnosis.  It  is  the  safest  plan  for  every  one,  how- 
ever, to  be  patient  and  painstaking,  to  omit  no  details  and  to  weigh  and 
test  every  phenomenon  even  to  the  point  of  tediousness. 

A  mere  glance  at  the  anatomy  and  physiology  of  the  nervous  sys- 
tem demonstrates  how  absolutely  necessary  that  every  organ,  tissue  and 
function  must  be  closely  interrogated.  In  this  respect  a  neurological 
examination  differs  pre-eminently  from  every  other  that  the  medical 
man  is  called  upon  to  make.  Only  in  cases  of  the  greatest  emergency 
should  a  hurried  manner  and  a  quick  diagnosis  be  adopted.  It  is  un- 
fortunate, though  necessary  of  course,  that  such  has  to  be  done  even 
then,  for  it  is  sometimes  the  cause  of  some  very  sad  mistakes.  When 
there  is  grave  doubt,  or  not  a  reasonably  clear  symptomatology  under 
these  circumstances,  the  physician  VN'ill  do  well  to  do^  nothing.  Under 
such  conditions  nature  is  less  liable  to  err  than  is  human  blindness. 

When  there  is  no  emergency  or  need  of  special  haste,  the  phy- 
sician should  first  note  carefully  all  of  the  attendant  circumstances  sur- 
rounding the  patient.  If  he  visits  the  latter  at  his  home  he  should  ob- 
serv'e  the  environment  as  closely  as  possible,  for  hints  are  sometimes 
thrown  out  in  this  way  in  regard  to  the  mental  and  social  status,  the 
mode  of  life,  the  joys  and  the  sorrows.  The  relatives  and  companions 
about  him  may  be  highly  suggestive.  Alcoholic  coma  might  not  in- 
appropriately be  thought  of  in  a  saloon ;  hystero-neurasthenia  in  a  girl 
might  justly  be  suspected  if  a  brutal  father  and  a  termagant  mother 
are  present;  trouble  from,  excessive  mental  study  would  hardly  be  ex- 
pected where  there  were  no  signs  of  a  book. 

The  patient's  own  attitude  must  be  quickly  remarked  and  the 
changes  it  undergoes  during  the  examination.  By  the  attitude  I  mean 
both  the  physical  and  the  mental. 

It  is  wise  to  examine  the  patient  alone  and  in  the  presence  of  oth- 
ers. In  hysteria  it  is  sometimes  risky  to  remain  alone  in  the  room 
with  the  patient,  but  the  door  can  be  left  partly  open  while  the  friends 
and  relatives  are  in  a  distant  room.  The  presence  of  one  of  the  latter 
when  distasteful  may  cause  all  sorts  of  irregularities  in  the  symptoms. 
A  temporary  change  of  environment  often  astonishingly  changes  the 
complexion  of  things.  I  remember  a  woman  who  was  sent  to  a  pri- 
vate hospital  several  times  by  me.  It  was  almost  ludicrous  how  reg- 
ularly as  clock-work  she  flew  into  her  hysterical  attacks  at  home  while 
during  weeks  at  the  hospital  she  was  as  docile  and  reasonable  as  any 
creature.  Syphilitics  will  often  admit  to  the  consultant,  who  charges 
them  a  good  fee  and  for  whom  they  have  therefore  perhaps  an  exag- 
gerated reverence,  the  disease  that  they  have  constantly  and  strenu- 
ously denied  to  their  family  doctor. 

Get  the  patient  always,  if  possible,  under  other  conditions  and 
examine  further  before  forming  a  final  opinion. 

Avoid  leading  questions  in  eliciting  the  history  of  the  case.  Neu- 
rotics are  particularly  open  to  suggestion.  I  have  seen  diagnoses  made 
that  were  really  constructed  on  the  semeiology  suggested  by  the  doc- 
tor and  acquiesced  in  by  the  susceptible  patient.  This  is  an  easy  and 
common  pitfall  and  should  be  carefully  guarded  ao-ainst. 


GEXERAL    COXSIDER-\TIOXS    UPOX    XERVOUS   DISEASES  43 

.  Let  the  patient  first  tell  his  own  story,  often  in  his  own  verbose 
^vay,  for  thereby  most  valuable  hints  may  be  dropped  and  leading  lines 
of  examination  suggested.  After  he  has  said  all  he  has  to  say,  then 
let  the  relatives  and  associates  tell  their  story.  Even  let  them  give 
their  opinions.  Ee  most  patient  with  them  for  they  are  reasoning, 
albeit  ignorant  laymen;  and  the  very  picturesqueness  of  their  descrip- 
tion, the  energy  and  interest  with  which  they  tell  of  the  patient's 
strange  exhibitions,  the  biased  yet  unbiased  attitude  of  mind  in  which 
they  are,  may  go  a  long  way  tow-ard  giving  a  complete  clinical  pic- 
ture, whereas  a  too  close  limitation  to  the  mere  scientific  data  may  lead 
to  some  confusion. 

In  the  examination  of  hysterics,  epileptics  and  the  insane  we  have 
to  depend  very  largely  upon  the  accounts  of  the  family  and  of  the 
friends.  We  must,  however,  be  always  guarded  against  letting  their 
views  determine  ours.  A  nice  adjustment  between  the  medical  and 
the  lay  prejudices  will  here  reveal  the  keen  examiner  and  the  skillful 
physician. 

During  the  telling  of  the  history  of  the  case  by  the  relatives  note 
the  trend  of  their  ideas  and  the  degree  of  their  intelligence.  The  pa- 
tient may  have  moved  intellectually  beyond  their  sphere,  and  his  en- 
vironment being  uncongenial  he  may  act  in  a  wa}-  that  seems  queer  to 
them  but  is  not  entirely  illogical.  This  is  the  origin,  in  a  large  meas- 
ure, of  the  popular  conception  of  the  insanity  and  'eccentricity  of 
geniuses  and  of  artists. 

After  acquiring  all  the  information  he  can  from  the  patient  and 
his  friends,  the  physician  takes  up  the  examination  himself  and  while 
allowing  them  to  interject  an  occasional  remark  that  may  add  new  light 
to  some  things,  he  avoids  being  diverted  from  his  owm  course  of  proce- 
dure. He  should  have  a  general  systematic  method  whereby  to  con- 
duct his  examination,  else  he  will  be  certain  to  overlook  many  things. 
Even  though  he  may  not  have  to  go  through  the  whole  form  every 
time  before  arriving  at  a  diagnosis,  it  is  nevertheless  good  to  do  so 
"because  important  m.atters  may  thus  be  brought  out,  time  may  really 
be  saved  in  the  end,  and  the  practice  of  being  systematic  may  develop 
a  desirable  facility  for  examining  future  patients.  A  scheme  some- 
what like  the  following  may  be  adopted,  even  printed  out  in  one's 
case  book : 


44 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES 


Xame Age Sex Nationality Occupation. 

Marriage Temperament Culture Date... 


Family  History: 

Grandparents 

Parents 

Brothers  and  Sisters 

Other  near  Relatives 

Personal  History  : 

Habits  as  to  Diet 

Habits  as  to  Alcohol 

Habits  as  to  Tobacco  and  Drugs . 

Habits  as  to   Venery 

Inherited  and  Acquired  Dis- 
eases : 

Syphilis    

Gonorrhoea    

Other   Infections .  .  . 

Condition  of  the — 

Lungs    

Heart   

Arteries    

Alimentary  Tract    

Genito-Urinarv  Tract   


Traumata   

Deformities   

Pulse 

Temperature 

Respiration    

Urine    

Gait    

Attitude 

Patient's      Account 
Trouble  in   Brief 


of      Present 


Motor  Symptoms 


Sensory   Symptoms 


Reflexes 


Electrical  Phenomena 


\'asomotor  and  Secretor\-  Symp- 
toms     


Trophic  Symptoms 
Eye  and  X'ision.  .  . 
Ear  and  Hearing.  . 
Nose  and  Smell.  . . 
Mouth  and  Taste.  . 
General  Remarks   . 


Diagnosis 


A'oice   

Speech   

Handwriting 

Psychic   Symptoms    

The  diagnosis  of  disease  of  the  nervous  system  depends  upon  both 
etiology  and  symptomatology.  It  must  be  made  from  all  available  phys- 
ical and  mental  data.  Its  end  is  the  determination  of  the  actual  exist- 
ence of  a  nervous  disease,  the  character  of  the  lesion  and  its  loca- 
tion. 

The  real  presence  of  a  nervous  disease  is  decided  almost  wholly  by 
etiological  factors  and  a  few  obser\^able  changes  like  a  choked  disc  or 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  45 

muscular  atrophy.  In  other  words  not  all  motor  and  sensory  and 
psvchic  abnormal  manifestations  represent  actual  disease.  Simulation 
and  malingering  may  be  present.  Suggestibility  may  provoke  mislead- 
ing exhibitions.  Secondary  irritation  from  extraneous  conditions  of 
all  sorts,  both  in  and  out  of  the  body,  may  give  rise  to  the  exaltation 
or  suppression  of  nervous  functions  that  closely  imitate  inherent  nerve 
trouble. 

It  is  sometimes  the  hardest  part  of  the  diagnosis  to  determine 
whether  there  is  an  actual  disease  of  the  nervous  system  present.  No 
fast  rules  can  be  laid  down  for  determining  this.  It  is  all  a  matter 
of  the  logical  ability,  the  shrewdness,  the  skill,  and  the  knowledge  of 
the  diagnostician. 

When  it  is  recognized  that  an  actual  disease  of  the  nervous  sys- 
tem is  present,  the  nature  of  it  must  be  decided  by  a  careful  study  of 
both  its  etiology  and  symptomatology.  The  location  of  the  lesion  is 
inferred  almost  wholly  from  the  symptoms,  though  the  etiology  helps 
in  determining  it  slightly  in  some  cases. 

In  the  preceding  chapter  upon  pathology,  I  have  pointed  out  some 
general  facts  in  regard  to  the  nature  of  the  various  lesions  and  how 
they  may  be  inferred.  Localization  symptoms  Avill  be  taken  up  at  the 
head  of  the  various  sections  devoted  to  the  brain,  the  spinal  cord  and 
the  nerves. 

The  gait  of  the  patient  in  walking  is  a  most  obvious  symptom 
sometimes,  and  to  one  experienced  in  nervous  troubles  will  alone  often 
suggest  the  diagnosis.  The  hemiplegic,  the  tabetic,  the  victim  of  dis- 
turbed equilibrium  of  the  cerebellar  or  other  type,  and  of  spastic  para- 
plegia, can  almost  instantaneously  be  recognized. 

The  attitude,  with  or  without  the  peculiar  gait,  is  frequently  very 
significant.  Who  does  not  recognize  the  characteristic  stoop  and  posi- 
tion of  the  hands  in  paralysis  agitans?  Even  the  laity  notice  the  list- 
less, fixed,  indifferent  position  of  the  victim  of  melancholia.  If  atti- 
tude were  given  more  consideration,  hysteria,  neurasthenia,  many  forms 
of  psychosis  and  not  a  few  organic  troubles  would  almost  be  suspected 
at  once  sometimes.  The  attitudes  of  disease  are  not  infrequently  path- 
ognomonic. 

While  the  patient  is  giving  his  account  of  the  first  appearance  of  his 
present  trouble  and  of  its  course  and  symptoms  up  to  the  present  mo- 
ment, note  carefully  the  character  of  his  voice  and  the  mode  of  his 
speech.  Does  he  speak  loudly  or  softly?  Is  his  voice  rasping  or 
smooth?  Is  there  aphonia  and  does  he  have  to  whisper?  Observe 
whether  he  trips  in  his  speech  or  runs  his  words  together  or  scans 
his  sentences  as  if  he  Avere  scanning  a  line  of  poetry.  Does  he  omit 
or  repeat  words  or  introduce  irrelevant  words  into  his  sentences  ?  Ask 
him  to  read  and  note  if  he  does  the  same  thing  when  reading.  Aphonia, 
dysarthria  and  aphasia  will  all  be  discussed  after  the  consideration  of 
the  physiology  of  the  brain.  They  are  mentioned  here  simply  to  im- 
press the  importance  of  noting  them  carefully  in  the  course  of  the  ex- 
amination. Agraphia,  trembling  and  other  impediments  to  writing  will 
also  be  described  elsewhere. 

Psychic  symptoms  are  hardly  of  less  importance  in  neurology  than 


46  GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES 

they  are  in  psychiatry.  The  niincl  is  the  product  of  cerebral  activity, 
and  cerebral  activity  is  provoked  by  afferent  nervous  impulses.  It 
may  be  interesting  but  hardly  profitable  to  discuss  such  questions  as 
the  immateriality  of  mind  and  the  duality  of  man's  nature.  We  have 
no  proof,  that  can  be  called  scientific,  of  a  consciousness  apart  from 
cerebral  function.  To  say  this  is  not  to  deny  the  mind's  possible  im- 
material existence ;  it  is  merely  affirming  the  scientific  limitations  of 
the  question. 

To  escape  all  such  gross  notions  as  mental  telepathy,  mental  trans- 
ference, mind-reading,  clairvoyance,  spiritism,  etc.,  one  has  but  ta 
recollect  that  psychic  phenomena  are  never  known  to  occur  without 
simultaneous  cerebral  phenomena.  Dead  brains  have  never,  in  all 
the  ages,  given  the  slightest  evidence  of  the  presence  of  mind,  and 
mind  has  never  been  observed  apart  from  living  brains. 

This  interdependence  is  further  shown  in  the  parallelism  that  ob- 
tains between  physical  disease  and  mental  aberration.  In  many  cases- 
actual  gross  changes  are  observed  in  the  brain ;  in  others  the  changes 
are  so  slight  that  our  present  means  of  investigation  cannot  detect 
them.  It  is  not  improbable  that  a  disturbance  of  the  normal  flow  of 
inpouring  sensations,  by  means  of  various  nervous  and  other  diseases,, 
may  underlie  a  large  number  of  the  phenomena  of  psychiatry.  At 
all  events,  as  the  nervous  system  is  the  seat  of  the  mind  pre-eminently,. 
and  as  it  is  the  apparatus  upon  which  it  seems  immediately  to  depend 
both  for  its  own  portrayal,  activity,  and  communication  with  the  outer 
world,  it  is  obvious  that  mental  symptoms  are  of  immense  significance 
in  neurology. 

A  detailed  description  of  these  symptoms  will  be  more  appropri- 
ately considered  along  with  the  physiology  of  the  brain.  It  may  be 
noted  here,  however,  that  chief  among  them  are  the  mental  stigmata 
of  degeneracy,  a,bnormal  emotional  states  with  exaltation  or  depres- 
sion, delirium,  maniacal  violence,  illusions,  hallucinations  and  delusions, 
loss  of  consciousness,  or  coma,  double  consciousness,  amnesia,  aphasia, 
word-deafness,  word-blindness,  agraphia,  etc. 

Motor  and  sensory  symptoms  have  very  dissimilar  diagnostic  valu- 
ation. The  motor  symptoms,  being  objective  and  capable  of  being  ex- 
amined apart  from  the  patient's  consciousness,  are  the  more  definite, 
distinct  and  reliable  to  base  a  diagnosis  upon. 

The  sensory  symptoms  are  almost  wholly  subjective.  To  be  sure 
we  can  infer  a  good  deal  objectively  in  reference  to  them  bv  varving 
ourselves  the  stimuli  that  provoke  them  and  by  testing  them  in  the 
reflex  arcs ;  but  nevertheless  even  here  it  is  practically  impossible  +o- 
eliminate  entirely  the  patient's  consciousness  during  their  examm^ 
tion.  Under  ether  narcosis  they  are  not  in  evidence  even  in  relation 
to  the  reflex  arcs. 

Too  much  stress,  therefore,  should  not  be  laid  upon  sensory  phe- 
nomena except  in  association  with  others.  They  are,  however,  the 
most  important  symptoms  to  the  patient  and  sometimes  the  onlv  ones. 
Their  greatest  value,  after  their  reality  has  been  positively  determined, 
is  in  the  localization  of  the  lesion.  The  psychic  nature  of  hvsteria  is 
all  but  positively  affirmed  by  the  peculiar  distribution  and  prominence 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  4/ 

of  its  sensory  symptoms.  A  moving  myelitis  can  sometimes  be  beau- 
tifully watched  by  the  rise  and  fall  of  the  border-line  of  anaesthesia. 

The  symptomatic  significance  of  the  various  forms  of  sensory  dis- 
turbance will  be  referred  to  again  in  the  introductory  chapters  to  the 
special  diseases.     Only  some  general  features  will  be  noted  here. 

There  are  five  forms  of  sensation,  commonly  spoken  of  as  gen- 
eral and  special  sense.  Biologically  they  are  all  evoluted  out  of  com- 
mon or  simple  touch  sense.  So  far  as  the  nervous  apparatus  itself 
goes  there  are  nothing  but  afferent  impulses.  The  naming  of  these 
impulses,  touch,  pain,  heat  and  cold,  sight,  smell,  taste  and  hearing,  is 
the  result  of  the  special  end-organs  in  connection  with  the  nerves.  A 
nervous  atrophy  that  produces  blindness,  for  instance,  is  no  different 
from  a  nervous  atrophy  that  produces  cutaneous  anaesthesia;  the  form 
of  nervous  lesion  that  causes  auditory  hallucinations  may  be  exactly 
the  same  as  the  form  of  nervous  lesion  that  causes  a  parsesthesia. 

With  all  the  sensory  phenomena,  therefore,  there  should  be  a  most 
careful  determination  as  to  whether  the  lesion  resides  in  the  outer  end- 
organs,  the  receiving  brain  centers,  or  the  intervening  nervous  pathway. 
It  would  be  ludicrous,  if  it  were  not  so  tragical,  to  note  how  frantic- 
ally and  persistently  glasses  are  worn  and  changed,  even  upon  the 
recommendation  of  careless  and  ignorant  opticians,  for  a  fading  eye- 
sight, when  an  examination  of  the  eye-ground  would  reveal  a  progres- 
sing optic  atrophy. 

It  is  a  common  fact  for  the  pains  of  tabes,  a  central  disease,  to 
be  mistaken  for  the  pains  of  rheumatism,  a  peripheral  trouble. 

The  diagnosing  of  the  presence  of  a  sensory  disturbance  is  not 
enough.  It  must  be  determined  why  and  wherefore  the  disturbance  is 
present. 

In  the  skin  are  located  three  forms  of  common  sensation,  namely, 
touch,  pain  and  temperature  sense. 

In  the  muscles,  tendons,  fascia,  joints  and  contiguous  structures 
there  is  what  is  called  a  muscular  sense,  a  sense  which  gives  us  some- 
what an  idea  of  the  location  of  the  limbs. 

The  nature  of  the  latter  sense  is  not  clearly  established  yet  and 
some  authorities  even  doubt  its  existence  as  a  special  sense. 

The  cutaneous  and  muscular  senses  are  as  much  dependent  upon 
special  end-organs  for  their  differentiation  as  are  the  so-called  special 
senses  of  hearing,  smell,  taste  and  sight. 

When  a  sensation  is  excessively  or  abnormally  acute  we  speak 
of  the  condition  as  hypercesthesia.  When  it  is  abnormally  dull  we  re- 
fer to  it  as  hypcesthesia.  If  it  is  absent  entirely  it  is  armsthesia.  Per- 
verted sensations  such  as  numbness,  "pins-and-needles"  feeling,  formi- 
cation or  the  sensation  as  of  ants  crawling  over  the  skin,  are  known  as 
parcesthesia. 

These  terms  have  been  so  universally  applied  to  the  tactile  sense 
alone  that,  I  am  satisfied,  it  has  had  a  good  deal  to  do  with  keeping 
alive  the  common  notion  that  special  sense  is  in  some  way  something 
extraordinarily  different  from  the  sense  of  touch.  Nerve  blindness  is 
nothing  but  optic  anaesthesia ;  visual  hallucinations,  like  flashes  of  light, 
fortification  figures,  are  really,  when  of  nervous  origin,  only  instances 


48  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

of  Optic  parjesthesia.  This  should  never  be  forgotten  as  it  will  save 
one  from  propounding  such  absurd  questions  as,  Why  should  blind- 
ness occur  in  hysteria  along  with  cutaneous  anaesthesia,  as  a  notable 
symptom?  A  proper  knowledge  of  the  basic  character  of  all  sensa- 
tion would  cause  the  question  to  be  asked,  Why  shouldn't  it  occur? 

Disease,  it  must  be  remembered,  may  attack  the  end-organs  and 
produce  hypersesthesia,  anesthesia  or  parsesthesia ;  a  cataract  produces 
blindness ;'  a  scar  in  the  skin  causes  local  loss  of  sensation ;  the  loca- 
tion and  lesion  are  unlike  but  the  manfestations  are  the  same,  anaes- 
thesia, but  not  pure  neural  anaesthesia.  Atrophy  of  the  optic  nerve  and 
atrophy  of  the  spinal  sensory  nerves  cause  respectively  loss  of  vision 
-and  loss  of  the  sense  of  touch ;  the  lesion  is  the  same  but  the  location 
merely  is  different.  That  is  pure  neural  anaesthesia.  Destruction  of 
the  visual  centers  in  the  occipital  cortex  and  destruction  of  the  sen- 
sory centers  in  the  parietal  cortex  alike  cause  sensory  anaesthesia. 

The  universality  of  irritability  in  the  nervous  system  is  a  most  im- 
portant fact  for  it  helps  to  give  valuation  to  these  phenomena  as  a 
means  of  localization,  since  it  is  thus  varied  merely  by  reason  of  the 
connections  which  the  nervous  apparatus  makes.  In  this  respect  the 
sensory  apparatus  is  the  same  as  the  motor  M^herein  we  localize  lesions 
chief! V  bv  the  particular  muscles  with  which  it  is  connected. 

For  the  alterations  in  the  pain  sense  we  use  the  terms  hyperalgesia 
and  analgesia.  Sometimes  pain  arises  spontaneously  in  an  analgesic 
area.    This  is  known  as  analgesia  dolorosa. 

Therman<zsthesia  is  of  course  a  loss  of  the  temperature  sense ;  hot 
and  cold  are  not  felt  at  all,  only  the  touch  of  the  heated  or  frozen  ob- 
ject.    In  syringomyelia. this  is  a  remarkable  and  troublesome  symptom. 

A  localized  pain  without  a  known  cause  is  a  topoalgia. 

Causalgia  is  a  pain  like  that  of  burning. 

Polycesthesia-  refers  to  successive  repetitions  of  a  sensation  after 
one  stimulation. 

In  macrocBSthesia  objects  feel  larger  than  they  actually  are. 

A  sensation  may  be  quite  normal  in  all  respects  except  in  being 
delayed.  This  is  not  an  uncommon  phenomenon  and  must  always  be 
looked  for. 

Transference  of  a  sensation  is  a  curious  exhibition  sometimes 
called  allochciria.  A  stimulation  on  one  side  of  the  body  is  referred 
to  a  similar  spot  on  the  other. 

Ataxia  or  incoordination  of  movement,  astereognosis  or  loss  of  the 
sense  of  the  shape  of  objects  when  held  in  the  hand,  and  loss  of  reflex, 
are  some  of  the  sequelae  of  disturbed  sensation  that  will  be  discussed 
more  in  detail  elsewhere. 

A  knowledge  of  the  sensory  innervation  of  the  skin  is  necessary 
for  localization  purposes. 

To  test  the  sensations  demands  but  a  little  ingenuity.  Touch  can 
be  examined  by  passing  lightly  over  the  skin,  with  the  patient  blind- 
folded, a  camel's  hair  brush,  a  piece  of  raw  cotton  or  other  light,  soft 
object.  Note  the  quickness  of  the  response,  the  accuracy  of  the  local- 
ization and  how  it  feels  to  the  patient. 


GENERAL    CONSIDERATIONS    UPON 'NERVOUS   DISEASES 


49 


The  temperature  sense  is  proved  by  the  apphcation  to  the  skin 
of  a  piece  of  ice  or  a  test-tube  filled  with  hot  water. 

The  use  of  excessive  heat,  pricking  with  a  pin,  or  pinching  will 
tell  whether  the  pain  sense  is  lost  or  not. 

The  muscular  sense  is  noted  b}^  placing  the  limbs  in  different 
positions,  while  the  patient  is  l3^ing  in  bed,  and  asking  where  they 
are  without  his  looking  at  them.  Place  various  weights  in  his  hands 
and  note  whether  he  remarks  the  difference.  This  tests  the  pressure 
sense.  Any  small  object  like  a  watch,  a  key,  a  match-box,  placed  in 
the  hand  will  aid  in  the  detection  of  astereognosis.  The  patient  gives 
an  erroneous  description  of  its  shape  or  says  he  cannot  describe  it  at  all. 

The  (esthesiometer  is  a  compass-like  apparatus  with  a  graduated 
scale  on  it  for  the  accurate  measurement  of  the  tactile  discrimination 
in  the  skin.  The  two  points  of  a  hairpin  or  pair  of  sharp  scissors  may 
even  be  conveniently  employed.  The  tongue,  tips  of  the  fingers  and 
lips  are  the  most  sensitive  parts  of  the  body  and  serve  well  for  tests 
with  the  sesthesiometer.  Iij  order  to  have  a  normal  standard  ready 
at  hand  for  purposes  of  comparison,  the  following  table  from  Weber, 
indicating  the  shortest  distances  and  the  parts  of  the  body  on  which  two 
points  can  be  recognized,  is  presented. 

Tip  of  tongue 

Palmar  surface  of  third  phalanx  of  forefinger. .  . 
Palmiar  surface  of  second  phalanges  of  fingers.  . 

Red  surface  of  underlip   

Tip  of  nose 

Middle  of  dorsum  of  tongue 

Palm  of  hand 

Center  of  hard  palate 

Dorsal  surface  of  first  phalanges  of  fingers 

IBack  of  hand   

Dorsum  of  foot,  near  toes i 

•Gluteal   region    i 

Sacral  region    i 

Upper  and  lower  parts  of  forearm i 

Back  of  neck  near  occiput   2 

Upper  dorsal  and  mid-lumbar  regions 2 

Middle  part  of  forearm   2 

Middle  of  thigh  2 

Mid-cervical  region   2 

Mid-dorsal  region    2 

Such  wide  variations  of  judgment  occur  among  normal  individuals 
that  not  much  reliance  can  be  placed  on  the  sesthesiometer  findings  un- 
less they  are  very  gross  and  constant.  In  general  it  may  be  consid- 
ered abnormal  if  the  points  have  to  be  separated  double  the  above  dis- 
tances before  they  are  able  to  be  distinguished  apart. 

The  pain  sense  may  be  approximately  measured  and  the  differences 
•observed  by  the  employment  of  different  strengths  of  the  faradic  cur- 
rent. Of  course  here  as  in  all  tests  for  sensation  the  eyes  must  be 
■covered,  normal  parts  of  the  body  must  be  compared  with  abnormal, 


1-24 

inch. 

I   Mm 

1-24 

inch. 

I   Mm 

I-I2 

inch. 

2  Mm 

1-6 

inch. 

4  Mm 

1-6 

mch. 

4  Mm. 

1-4 

inch. 

6  Mm 

1-3 

inch. 

8  Mm 

S-12 

inch. 

10  Mm 

1-2 

inch. 

12  Mm 

7-12 

inch. 

14  Mm 

1-6 

inch. 

25  Mm 

1-2 

inch. 

37  Mm 

1-2 

inch. 

37  Mm 

1-2 

inch. 

37  Mm 

inch. 

50  Mm 

inch. 

SO  Mm 

1-2 

mch. 

62  Mm 

1-2 

inch. 

62  Mm 

1-2 

inch. 

62  Mm 

1-2 

inch. 

62  Mm 

50  GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES 

repetitions  of  the  test  must  be  made  at  difterent  times  and  false  touches 
and  deceptions  must  be  practiced  to  riote  the  amount  or  presence  of  sug- 
gestibility. It  is  well  to  outline  an  anaesthetic  area  sometimes  with  a 
blue  pencil  or  iodine  brush  and  note  the  changes  from  time  to  time. 
Blanks  with  printed  outlines  of  the  body  upon  them  are  useful  for  keep- 
ing a  record  of  such  data. 

The  special  senses  have  their  own  particular  ways  of  being  exam- 
ined which  will  be  noted  under  the  heads  of  the  respective  cranial 
nerves. 

Motor  phenomena  usually  owe  their  initiation  to  some  form  of 
efferent  nervous  impulse.  Nerves  and  muscles  make  up  a  very  compact 
and  closely  united  neuromuscular  apparatus.  The  nervous  tissue  in- 
cites the  movement,  the  muscle  executes  it.  Only  under  exceptional 
circumstances  do  muscles  contract  from  other  than  neural  stimulation. 
Direct  irritation  by  blows  or  other  means  may  in  some  instances  cause 
the  muscular  fibrillse  to  coiiitract,  and  undoubtedly  muscular  paresis  re- 
sults from  inherent  muscular  disease.  Nevertheless  it  is  so  true  that 
the  vast  majority  of  muscular  contractions  are  due  to  nervous  stimu- 
lation, that  it  may  be  generally  affirmed  that  disturbance  of  the  former 
is  indicative  of  disease  of  the  latter.  The  impulse  that  provokes  a  mus- 
cle into  activity  usually  has  its  origin  in  a  nerve  cell  or  neurone-body. 
It  is  not  probable  that  direct  irritation  to  the  neuraxones  of  the  motor 
neCtrones  awaken  muscular  phenomena.  In  the  cases  in  which  irritation 
of  the  peripheral  nerves  provokes  spasms,  the  sensory  neuraxones  are 
in  all  likelihood  irritated  and  in  a  reflex  way  the  motor  side  of  the  arc  is 
put  into  functional  activity.  Motor  impulses  therefore  always  start 
from  the  cell-bodies  of  the  motor  neurones.  Tliey  may  arise  de  novo 
there  or  they  may  be  the  result  of  stimulation  by  the  related  sensory 
neurones. 

In  all  forms  of  motor  activity,  therefore,  normal  or  exalted,  the 
cell-bodies  of  the  related  motor  neurones,  are  more  or  less  implicated. 
If  the  activity  is  diminished  or  annihilated  the  trouble  may  be  anywhere 
in  the  motor  neurones,  their  cell-bodies  or  their  processes.  Hence  mus- 
cular over-activity  has  a  much  wider  origin  than  has  under-activity. 
This  is  an  important  distinction  when  it  comes  to  a  question  of  diag- 
nosis.   Spasms  are  due  to  far  more  numerous  causes  than  are  paralyses. 

Beyond  the  mere  statement  that  stimulation  is  present,  we  can 
offer  no  explanation  as  to  how  nerve  force  passes  over  into  muscular 
force,  how  excitement  merely  provokes  contraction.  Much  more  im- 
portant is  it  to  know  that  all  muscular  movements  of  neural  origin  are 
due  to  impulses  from  two  sets  of  neurones,  the  upper  and  the  lower. 
An  examination  of  the  neuronic  architecture  of  the  nervous  system  re- 
veals the  fact  that  the  muscles  are  under  the  direct  and  immediate  con- 
trol of  the  neurones  whose  cell-bodies  are  in  the  gray  matter  of  the 
cord  and  its  homologue  the  cranial  nuclei,  and  that  they  are  under  the 
indirect  or  mediate  control  of  the  neurones  whose  cell-bodies  are  in  the 
cerebral  cortex.  Individual  muscles  therefore  are  the  executive  agents 
of  the  lower  neurones ;  generalized  movements,  inhibition,  and  control 
of  the  lower  neurones  constitute  the  primary  purpose  of  the  activity  of 
the  upper  neurones. 


GENERAL    COXSIDEKATIOXS    UPOX    XERVOUS    DISEASES  5I 

So  far  as  we  know,  the  essential  nature  of  nerve  activity,  the  ex- 
pression of  neurihty,  is  identically  the  same  in  both  sets  of  neurones. 
They  differ  in  function  solely  on  account  of  their  respective  end  rela- 
tionships. Thus,  as  will  be  described  more  in  detail  in  other  sections 
of  this  book,  they  lend  themselves  by  reason  of  the  difference  of  func- 
tion to  focal  diagnosis.  Individual  muscle  disturbances  will  point  to 
the  location  in  the  cord  or  cranial  nuclei. 

The  disturbance  of  bodily  movements  will  indicate  quite  as  sharply 
just  where  the  trouble  is  located  in  the  cerebral  cortex  or  its  subsidiary 
structures. 

The  symptoms  upon  which  this  localization  diagnosis  is  to  be  made 
will  be  discussed  at  the  head  of  brain  and  cord  diseases. 

The  character  of  the  motor  disturbance  is  indicative  of  both  the 
location  and  nature  of  the  lesion.  As  the  cerebral  set  of  neurones  ex- 
ercise normally  an  inhibitory  control  over  the  spinal,  when  they  are 
diseased  that  control  is  relaxed  and  the  resulting  motor  disturbance  is 
rigid  and  spastic  in  character.  Where  the  disease  involves  only  or  pri- 
marily the  spinal  neurones,  the  disturbance  is  flaccid  and  limp  in  char- 
acter. In  either  upper  or  lower  neurone  disease,  the  lesion  may  be  only 
such  as  to  irritate  and  cause  overaction  or  irregular  action  in  the  mus- 
cles.. The  irritative  influence  usually  has  its  origin  entirely  outside 
of  the  neurone,  either  from^  disease  in  the  sensory  apparatus  or  in 
gross  forms  of  trouble  in  the  mesoblastic  tissues.  Lesions  that  are  de- 
structive of  the  motor  neurones  are  therefore  usually  inherent  lesions 
and  directly  abolish  the  function  cif  the  neurones.  Lesions  that  are 
merely  irritative  are  more  generally  extraneous,  affect  the  motor  neu- 
rones secondarily,  and  exaggerate  or  otherwise  disarrange  their  func- 
tion. 

The  common  evidence  of  destructive  lesions  is  therefore  paralysis, 
of  irritative  lesions  spasm  and  inco-ordination. 

It  is  extremely  important  that  the  term  paralysis  or  akinesis  should 
be  limited  to  the  abolition  of  muscular  movements  from  neural  lesions 
alone. 

As  I  have  already  intimated,  immobility  may  be  due  to  many  other 
causes,  as  for  example  ankylosis,  muscular  disease,  rheumatism,  frac- 
tures and  dislocations. 

Both  the  voluntary  and  involuntary  sets  of  muscles  may  be  par- 
alyzed. 

There  are  degrees  of  paralysis  so  that  we  speak  of  complete  and 
incomplete  paralysis.  The  term  paresis  is  sometimes  used  for  the  lat- 
ter. Individual  muscles  may  be  paralyzed  or  physiological  grotrps  of 
muscles  concerned  in  particular  forms  of  movement.  A  flaccid  paralysis 
is  one  in  which  the  part  hangs  dead,  limp,  immobile ;  a  spastic  paraly- 
sis, one  in  which  there  is  stiffness,  rigidity  and  tension  in  the  part. 

A  paralysis  may  have  its  origin  in  the  higher  psychic  centers  even. 
This  is  commonly  spoken  of  as  pseudoparalysis. 

The  distribution  of  the  paralysis  is  indicated  by  the  use  of  snch. 
terms  as  monoplegia,  hemiplegia,  paraplegia  and  crossed  paralysis.  As 
these  belong  to  localizing  signs,  they  will  be  referred  to  again. 

In  testing  a  paralysis  the  patient  should  relax  himself  as  completely 


52  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

as  possible  and  should  be  examined  in  various  positions,  in  and  out  of 
bed.  The  normal  physiological  movements  should  be  well  known  and 
the  diseased  side  should  be  carefully  compared  with  the  well.  First 
let  the  patient  show  what  he  himself  can  or  cannot  do.  If  the  paralysis 
is  only  partial,  take  hold  of  the  part  and  note  the  force  of  resistance 
exerted  by  the  patient. 

The  dxnamometer  is  a  graduated  oval  spring  which  can  be  used, 
by  pressing  it,  to  measure  the  comparative  power  of  resistance.  Its  use 
is  limited,  however.  Remember  that  the  left  side  is  normally  weaker 
than  the  right.  Paralysis  of  individual  muscles  can  be  sometimes  tested 
thus,  though  in  most  cases  it  has  to  be  noted  by  the  attitude  of  the  part 
and  by  the  electrical  tests  and  associated  atrophy. 

Tests  for  paralysis  should  be  made  repeatedly  and  varied  in  every 
possible  way.     It  should  be  noted  whether  there  is  the  slightest  shade 

FIGURE    I. 


Dynamometer. 

of  associated  movement  in  the  paralyzed  member  when  the  well  one  is 
stretched  out. 

A  little  ingenuity  and  a  perfect  familiarity  with  the  normal  func- 
tions of  the  muscles  are  all  that  is  needed  for  testing  paralysis.  Various 
instruments  have  been  devised  but  immediate  examination  without  in- 
struments of  any  sort  will  give  a  careful,  skillful  and  experienced  ex- 
aminer more  and  better  information  than  am-  form  of  mediate  test. 

Spasm  or  hyperkinesis  is  an  exaggeration  of  motilit}".  Its  real  na- 
ture is  hidden  somewhat  in  obscurity,  though  it  is  probably  due  to  exag- 
gerated or  incessant  nerve  stimulation.  It  is  not  necessarily  due  to 
disease  in  the  motor  Tieurones.  In  fact,  it  is  usually  the  result  of  irri- 
tation of  these  neurones  by  disease  outside  of  them.  The  latter  may 
be  of  a  vascular  or  connective-tissue  type,  of  a  toxemic  nature,  or  a  le- 
sion involving  the  sensor}-  neurones.  Muscular  spasm  is  very  often  a 
mere  reflex  phenomenon  and  so  far  as  the  nervous  system  is  concerned 
may  not  be  the  expression  of  disease  at  all. 

We  do  not  know  that  there  is  any  essential  difference  between 
tonk  and  clonic  spasms  except  that  the  stimulating  impulses  in  the 
former  are  so  short  and  rapid  in  succession  that  the  muscle  fibres  have 
no  chance  to  relax  and  the  whole  muscle  remains  in  prolonged  and 
constant  contraction.  In  clonic  spasms  there  is  an  alternation  of  con- 
traction and  relaxation  so  gross  as  to  be  easily  observed. 

A  cramp  is  nothing  but  a  painful  spasm. 

A  convulsion  is  a  spasm  that  involves  the  entire  musculature  of  the 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  53 

body  or  parts  of  the  body.  Convulsions  may  be  tonic  or  clonic,  co-ordi- 
nate or  inco-ordinate.  Unconsciousness  usually  accompanies  a  con- 
vulsion. 

Choreiform  movements  are  spasmodic  jerkmgs,  in  certain  groups 
of  muscles,  irregular,  inco-ordinate  and  more  or  less  violent  and  par- 
tially under  the  control  of  the  will. 

What  is  called  convulsive  tic  is  a  very  localized  form  of  choreiform 
spasm,  possibly  even  in  one  muscle,  but  more  generally  in  a  group  of 
muscles  that  perform  a  certain  physiological  act. 

Athetoid  movements,  athetosis,  consist  of  slow,  ceaseless,  waxy- 
like  flexion  and  extension  of  the  hands  and  feet  and  their  various  parts. 

Other  forms  of  muscular  spasm  are  the  excessive  muscular  tension 
and  contracture  seen  in  some  diseases.  These  are  more  or  less  perma- 
nent or  at  least  chronic  conditions  and  are  consequently  accompanied 
by  a  certain  degree  of  organic  change.  If  either  one  should  disappear 
during  sleep  or  under  etherization,  it  would  show  that  it  was  merely  a 
functional  trouble,  probably  hysterical. 

A  forced,  movement  is  a  sort  of  convulsion  in  which  a  patient  in- 
voluntarily turns  and  moves  in  various  peculiar  but  not  altogether  un- 
natural ways.  He  may  wdiirl  aboiit  suddenly  or  start  off  in  a  particular 
direction. 

Associated  movements  are  another  sort  of  curious,  spasmodic  phe- 
nomena. A  limb  lying  at  rest  involuntarily  performs  the  same  or  simi- 
lar movement  that  is  voluntarily  performed  in  the  other  limb.  Hemi- 
plegic  lim.bs  sometimes  thus  move  in  more  or  less  imperfect  unison  with 
the  movements  in  the  sound  limb. 

As  with  paralysis  so  in  cases  of  hyperkinesis,  the  localization  of 
the  lesion  can  be  partly  inferred  from  the  distribution  of  the  phenom- 
ena. We  speak  therefore  of  monospasms,  hemispasms  and  other  types. 
The  symptom  is  so  obvious  that  it  requires  no  special  skill  to  distin- 
guish it. 

Tremor  is  a  fine  clonic  spasm,  rhythmical,  constant,  independent  of 
the  will  and  due  to  faulty  innervation.  There  is  an  ataxic  form  of  it 
revealed  upon  volitional  movement.  The  parts  affected  are  kept  con- 
stantly oscillating,  usually  without  pain  or  marked  exhaustion.  The 
oscillations  vary  from  3  to  12  per  second.  When  they  are  from  3  to  5 
per  second  the  tremor  is  coarse,  when  from:  8  to  12  it  is  fine.  Weak- 
ness is  usually  associated  with  it.  The  ataxic  tremor  is  badly  named 
intentional  tremor. 

Fibrillary  tremor  is  one  in  which  the  phenomenon  seems  to  be  lim- 
ited to  particular  fascicuH  in  bundles  of  muscular  fibres.  It  is  often- 
times so  delicate  that  it  can  only  be  detected  by  resting  the  finger  on  the 
part  affected  and  feeling  it. 

Tremor  is  often  increased  by  voluntary  effort,  as  witness  the  tremor 
of  dementia  paralytica  when  the  patient  attempts  to  speak  or  write. 

Incoordination  of  movement,  or  dyskinesis  is  a  most  important  neu- 
rological symptom.  We  have  already  seen  that  incoordination  of  move- 
ment may  be  due  to  sensory  disturJDance.  Such  is  the  cause  of  it  in 
locomotor  ataxia  for  instance.  The  various  attitudes  assumed  by  our 
bodies,  the  gait  adopted  in  our  walking,  the  physiological  movements  of 


54  GENERAL    COXSIDERATIOXS    UPON    NERVOUS    DISEASES 

all  sorts,  are  the  result  of  the  harmonious  combined  action  of  a  number 
of  muscles.  There  is  normally  a  nice  adjustment  between  antagonistic 
or  opposing  sets  of  muscles  so  that  action  and  counteraction  are  never 
allowed  to  pass  beyond  the  point  necessary  to  accomplish  a  given  move- 
ment. Flexion  is  always  nicely  opposed  to  extension,  pronation  to  su- 
pination, dilatation  to  contraction.  This  is  an  unconscious  adjustment, 
though  it  is  obviously  submissive  to  the  will.  We  can  overflex  the  arm 
but  we  cannot  release  the  extensors  from  their  entire  control  of  the  ac- 
tion at  the  same  time.  We  can  close  the  orbicularis  oris  but  we  cannot 
prevent  the  other  facial  muscles  from  taking  part  in  the  performance. 
In  some  of  the  sphincters  the  will  is  entirely  inoperative,  and  yet  the 
sphincter  functionates  under  an  opposing  inhibition.  Whenever  this 
adjustment  is  broken,  the  movements  become  most  indefinite,  irregular, 
ludicrous  and  bizarre.  The  volition  starts  the  muscles  to  contract,  but 
what  they  will  do  not  even  the  patient  himself  can  imagine.  Anarchy 
seems  to  rule  among  them  and  most  surprising  exhibitions  are  pre- 
sented. 

Such  is  nicoordiiiation  or  ataxia.  It  is  from  its  very  nature  not  a 
disease  of  one  anatomical  structure,  though  it  is  the  product  many 
times  of  a  more  or  less  anatomically  limited  lesion. 

We  have  said  that  movements  are  the  results  of  activity  in  the  cell 
bodies  of  the  motor  neurones  and  that  this  activity  may  arise  dc  novo, 
or  as  the  result  of  sensory  stimulation.  When  sensation  is  disturbed, 
one  important  cause  of  muscular  action  is  at  fault  and  as  a  result  that 
muscular  action  itself  is  confused. 

Again,  for  most  of  the  automatic  and  involuntary  movements,  such 
as  walking  and  the  contractions  of  the  uterus  in  parturition,  there  is 
somewhere  in  the  central  nervous  system  an  arrangement  of  neurones 
for  the  adjustment  of  the  various  muscular  activities  that  go  to  make 
up  the  completed  movements. 

And  finally  in  all  voluntary  movement  the  adjustment  is  uncon- 
sciously managed  so  that  all  muscles  work  harmoniously  together,  for 
the  accomplishment  of  the  particular  end  in  view. 

Ataxia  therefore  may  result  from  a  disturbance  of  afferent  im- 
pulses, from  disease  in  the  central  coordinating  apparatuses,  or  from 
the  upsetting  of  normal  mentalization.  In  all  of  this  there  may  be  no 
essential  motor  disturbances,  no  paralysis,  no  spasm,  but  merelv  sen- 
sory and  reflex  and  mental  trouble.  The  movements  are  bizarre  because 
their  sources  of  stimulation  are  in  an  abnormal  state.  There  may,  how- 
ever, be  a  purely  motor  incoordmation.  One  set  of  opposing  muscles 
may  be  functionally  disturbed,  wherebv  the  normal  balance  of  power 
between  the  two  sets  is  broken.  Indeed  the  dillerent  parts  of  the  same 
muscle,  and  even  different  sets  of  fibrils^,  may  be  so  affected  that  an 
intramuscular  incoordination  obtams.  This  doubtless  is  the  underlying 
cause  of  many  forms  of  coarse  and  fine  tremor  of  irregular  character. 

As  I  have  intimated  ataxia  is  the  typical  form  of  incoordination.  It 
may  be  sensory  or  motor,  usually  sensory,  in  origin  or  due  to  trouble 
in  the  central  organs  that  subserv^e  the  maintenance  of  coordination  and 
equilibrium.     In  ataxia  the  disturbance  of  the  certainty  of  purposive 


GENERAL    COXSIDERATIOXS    UPON    NERVOUS   DISEASES  55 

movements  is  most  obvious  or  with  a  little  ingenuity  can  be  easilv 
elicited. 

Sensory  ataxia  is  beatttif  ally  seen  in  tabes ;  sensory  and  motor 
ataxia  is  probably  observed  in  multiple  neuritis  and  disseminated 
sclerosis. 

Cerebellar  ataxia,  in  which  the  reeling  gait  of  acute  alcoholism  is 
most  accurately  imitated,  is  due  to  trouble  in  the  central  coordinating 
apparatus. 

Vertigo  is  a  form  of  central  ataxia,  so  also  is  the  confusion  some- 
times observed  in  the  ps\chosesof  mild  and  severe  degree  wherein  the 
ideas  of  movement  are  concerned. 

It  requires  a  harmonious  action  between  muscles  to  maintain  an 
attitude  as  well  as  to  perform  a  movement ;  hence  there  is  static  as  well 
as  motor  ataxia.  All  the  senses  help  in  the  maintenance  of  equilibrium, 
therefore  shutting  off  the  visual  sense  by  closing  the  eyes  causes  a 
static  or  motor  ataxia  to  be  increased. 

All  one  has  to  do  to  test  for  ataxia  is  to  ask  the  patient  to  per- 
form some  complicated  movement — walk  a  chalk  line  on  the  floor,  touch 
the  end  of  his  nose  with  his  finger  while  his  eyes  are  shut. 

Speech  may  be  ataxic  in  character  and  it  may  be  of  motor  or 
psychic  origin.  This  will  be  referred  to  again  in  the  section  on  the 
brain. 

A  most  important  nervous  manifestation  is  that  of  reflex  action. 
In  fact,  reflex  action,  which  m.eans  in  its  last  analysis  nothing  more  nor 
less  than  stimulation  and  return  response,  is  the  fundamental  raison 
d'etre  of  the  nervous  system.  To  be  cognizant  of  external  irritants 
and  to  send  back  appropriate  counter  effects  to  the  part  or  parts 
related  to  the  source  of  irritation,  is  what  nervous  tissue  was  biologically 
evolved  for. 

There  is  thus  an  ingo  and  an  outgo  as  the  fundamental  fact  in 
all  primary  nervous  manifestations.  Every  move  in  life,  even  thought 
itself,  is  but  a  reflex  or  a  modification  of  a  reflex. 

Impulses  in  some  low  forms  of  animal  life  may  travel  in  and  out 
over  the  same  pathways.  In  the  higher  forms  the  afferent  are  diflr'erent 
from  the  efferent  pathways.  Between  the  two,  at  their  central  ap- 
proximation, there  may  be  interjected  special  cells  or  neurones  to 
modify  the  impulse  in  its  round  from  afferent  to  efferent  path. 

A  reflex  action  therefore  is  seen  to  involve  a  more  or  less  compli- 
cated arc  consisting  of  afferent,  central,  and  efferent  elements.  The 
first  originates  in  the  skin  or  other  special  end-organ  of  sense  and 
terminates  in  some  central  gray  matter.  This  gray  matter  contains  the 
modifying  intervening  neurones  and  is  usually  under  the  inhibitory 
control,  to  a  certain  extent,  of  the  higher  or  cortical  neurones.  The 
efferent  pathway  starts  in  the  central  gray  matter  and  terminates  in 
the  muscle,  gland  or  secretory  organ.  An  irritation  in  the  skin  there- 
fore sends  an  impulse  imvard  and  around  the  arc  until  it  expends  itself 
finally  in  muscular  action  or  altered  secretion.  In  its  course  this  im- 
pulse, under  certain  circumstances,  may  be  halted  by  a  central  im- 
pulse sent  down  from  the  brain  or  it  may  send  an  impulse  itself  up  to 
the  brain. 


56  GENERAL    CONSIDERATIONS    UPON    NerVOUS    DISEASES 

That  is  in  brief  the  whole  picture  of  a  reflex  action. 

It  is  clear  that  a  lesion  anywhere  in  the  arc,  in  the  afferent,  the 
central  or  the  eft'erent  tract,  may  put  an  end  to  the  reflex.  Moreover, 
disease  in  the  controlling  inhibitory  path  reaching  down  from  above 
will  undoubtedly  modify  the  activity  of  the  reflex  arc.  If  the_  inhibitory 
control  is  destroyed,  the  reflex  will  of  course  be  released :  if  it  is  in- 
creased the  reflex  may  be  completely  throttled.  According  to  the  loca- 
tion of  the  center  of  the  reflex  arc,  and  according  to  the  terminations 
of  either  end  of  it,  will  the  localization  manifestations  be  in  connection 
with  it.  Therefore  the  detailed  description  of  the  individual  reflexes 
will  be  postponed  until  the  discussion  of  the  special  parts  of  the  ner- 
vous system  is  taken  up. 

It  may  be  well  to  state  here,  however,  that  there  are  recognized 
in  neurological  symptomatology,  four  kinds  of  reflexes,  the  skin,  or  su- 
perficial, reflexes';  the  tendonous,  or  deep,  reflexes;  the  idiopathic  mus- 
cle reflexes,  and  the  visceral  reflexes. 

Reflexes  may  be  absent,  or  they  may  be  merely  exaggerated  or 
diminuished. 

Reflex  phenomena  occur  wherever  there  is  a  neuro-muscular  ap- 
paratus, hence  these  phenomena  are  observed  in  connection  with  the 
sympathetic  as  well  as  the  cerebrospinal  system:  in  the  organs,  and 
the  vasomotor  apparatus  of  the  body. 

The  supeiijcial  or  skin  reflexes  are  best  elicited  by  a  slight  touch, 
a  gentle  pinch,  a  pin  prick,  a  tickling  or  a  momentary  application  of 
cold  or  heat  to  the  skin.  The  value  of  these  reflexes  as  localization 
symptoms  is  variable,  as  will  be  pointed  out  elsewhere.  The  more  im- 
portant of  them  and  the  method  of  provoking  them  are  as  follows. 

About  the  head  many  are  obvious  and  are  seen  in  the  winking  and 
the  twitching  of  the  facial  muscles,  and  in  animals  in  the  shaking  of 
the  ears  to  remove  insects  and  irritating  objects.  The  scratching  of 
the  skin  of  the  face  or  chin  causes  the  pupil  to  dilate.  Irritating  the  skin 
over  the  back  muscles,  as  for  example  over  the  erector  spinse  and  scap- 
ular muscles,  causes  the  latter  to  contract.  The  same  is  true  of  the 
muscles  of  the  abdomen  and  thorax;  cutaneous  irritation  at  the  sides 
causes  them  to  contract,  especially  the  rectus  abdominis. 

The  cremasteric  reflex  consists  of  the  drawing  up  of  the  testicle 
when  the  skin  of  the  inner  thigh  of  the  same  side  is  pinched  and 
tickled.  The  scrotum  alone  is  not  affected.  The  palmar  reflex  is  of 
very  little  importance,  but  in  sleep  some  people  move  the  fingers  when 
the  palm  of  the  hand  is  touched.  The  plantar  reflex  is  usually  well 
marked  and  in  fact  enters  into  the  Babinski  sign.  This  observer  noted 
that  when  the  sole  of  the  foot  is  stroked,  there  is  a  dift'erence  between 
the  movement  of  the  foot  and  of  the  toes.  Normally  when  tlie  plantar 
skin  is  slightly  irritated,  the  foot  is  thrown  into  dorsal  flexion  and  the 
toes  into  plantar  flexion.  That  is  the  ordinary,  long-recognized,  fa- 
miliar plantar  reflex.  Babinski  noticed  that  in  disease,  when  the  sole 
is  tickled,  dorsal  flexion  of  the  foot  takes  place,  but  the  toes,  especially 
the  great  toe,  undergo  dorsal  reflexion  also,  or  what  is  the  same  thing, 
extreme  extension.  This  is  a  most  important  criterion  of  disease, 
though  its  fullest  significance  we  have  yet  to  learn. 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  57 

Oppenheim's  reflex  is  close  to  that  of  Babinski's.  It  consists  of  a 
dorsal  flexion  of  the  toes  and  foot  when  the  inner. surface  of  the  leg 
is  stroked  from  above  downward. 

The  comparative  importance  of  the  plantar  over  the  palmar  reflexes 
illustrates  a  cardinal  law  that  is  true  of  all  the  spinal  reflexes  appar- 
ently, namely,  that  the  nearer  they  are  to  the  brain,  the  less  active 
they  are. 

The  presence  of  these  skin  reflexes  leads  to  the  inference,  of 
course,  that  their  arc  through  the  cord  is  normal.  Their  absence,  how- 
ever, does  not  signify  very  much,  because  the  mind  of  the  patient  is 

FIGURE  2. 


Method  of  testing  the  patella   reflex. 

so  intimately  implicated  in  them,  that  it  is  always  a  matter  of  uncer- 
tainty as  to  the  physical  or  psychical  cause  for  their  non-appearance. 

Among  the  most  valuable  symptoms  in  neurology  are  the  deep, 
tendon  reflexes.  It  is  not  necessary  to  discuss  here  the  many  views  in 
regard  to  their  essential  nature.  Investigators  of  equal  reliability 
hold  that  they  are  true  reflex  phenomena  on  the  one  hand,  or  mere  ex- 
pressions of  muscle  tonus,  itself  a  reflex  phenomenon,  on  the  other. 
For  the  clinician  it  is  enough  that  they  are  regularly  modified  in  dis- 
ease and  that  they  represent  a  reflex  impulse. 

The  muscular  contraction  is  provoked  by  a  stroke  upon  the  muscle 
or  its  tendon.  The  examiner's  ingenuity  will  suggest  the  best  attitude 
of  the  patient  for  placing  the  muscle-tendon  in  a  condition  of  slight 


58 


GEXERAL    COXSIDERATIOXS    UPON    NERVOUS   DISEASES 


tension  withcut  being  pressed,  stretched  or  otherwise  prevented  from 
acting.  A  shght  blow  with  the  percussion-hammer,  or  edge  of  the 
hand,  will  then  cause  the  muscle  to  suddenly  contract  and  throw  out 
the  limb. 

There  are  many  conditions  that  might  interfere  with  the  demon- 
stration of  this  phenomenon  and  of  course  they  must  be  removed  or 
given  due  consideration.  The  patient's  mind  may  interfere.  This  is 
particularly  the  case  in  children.  Hence  distract  their  attention  in  some 
way  or  keep  repeating  Lhe  test  while  talking  to  them  and  in  a  moment 

FIGURE  3- 


Method  of  testing  the  patella  reflex. 

of  distraction  it  will  suddenly  appear.  Disease  states,  in  and  about  the 
related  joint,  in  the  muscles,  and  many  other  conditions,  mav  interfere. 

As  a  general  rule  it  may  be  stated  that  diminution  or  loss  of  the 
reflex  means  disease  in  the  lower  or  peripheral  motor  neurones ;  in- 
crease of  it  means  disease  in  the  upper  or  central  neurones.  In  this 
way  the  deep  reflexes  become  invaluable  as  localizing  signs. 

In  accordance  with  the  muscle  involved  the  symptom  also  helps 
us  to  localize  the  lesion  in  the  segmental  levels  of  the  cord. 

The  most  important  of  the  deep  reflexes  is  that  of  the  patella.     A 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  59 

child  to  be  examined  is  placed  on  the  edge  of  a  chair ;  an  adult  may  sit 
upon  a  table.  The  legs  are  allowed  to  hang  down  at  a  right  angle  to  the 
thigh.  The  examiner  passes  his  arm  under  the  knee  of  one  leg  and 
Tests  his  hand  upon  the  knee  of  the  other.  The  patient  is  told  to  relax 
his  muscles  and  to  let  his  leg  hang  dead,  as  it  were,  and  with  full 
weight  on  the  examiner's  arm.  I  prefer  this  method  to  the  common  one 
of  crossing  one  knee  over  the  other  in  the  ordinary  sitting  position. 
By  the  latter  method  there  is  sometimes  considerable  interference  with 
the  movement  of  the  limb  on  account  of  the  stoutness  of  the  patient,  the 
excessive  tension  put  upon  the  tendon,  or  the  occasional  general  incon- 
venience of  the  attitude.     In  the  former  method  the  patient  can  relax 

FIGURE  4. 


Method  of  testing  the  patella  reflex  with   reinforcement. 

his  muscles  better,  his  mind  is  not  centered  upon  the  performance  by 
the  discomfort  and  the  examiner  can  vary  the  tension  of  the  tendon 
by  slightly  raising  or  lowering  his  arm. 

The  tendon  just  below  the  front  of  the  knee  or  just  above  it 
should  be  given  a  quick,  sharp  tap  with  the  hammer  or  edge  of  the 
"hand.  The  quadriceps  femoris  will  then  undergo  a  short,  vigorous 
contraction  and  throw  the  foot  out.  If  the  patient  flexes  and  grips  to- 
gether the  fingers  of  his  two  hands,  and  then  keeps  trying  to  pull  them 
apart,  or  if  a  child  is  given  a  small  object  to  squeeze  in  either  hand,  the 
reflex  response  will  be  rendered  considerably  more  distinct.  This  is 
what  is  known  as  reinforceuient. 


6o 


GEXKKAL    COXSini-.RATIOXS    UPOX    XF.RVOUS   DISEASES 


Apparatuses  have  been  devised  to  measure  the  force  of  this  reflex 
but  they  are  too  compHcated  for  ordinary  use  and  do  not  add  much  to 
the  information  when  employed. 

The  explanation  of  the  phenomenon  is  that  a  genuine  spinal  reflex 
is  present.  The  muscle — not  the  tendon  and  hence  the  error  in  the 
term  tendon-reflex — is  by  the  blow  put  into  a  state  of  sudden  tension,. 

FIGURE  s. 


Method  of  testing  the  ankle  reflex. 


myotatic  irritability.  An  impulse  rushes  to  and  from  the  cord  causing^ 
the  muscle  to  undergo  the  sharp,  quick  contraction.  Disease  anywhere 
m  the  reflex  arc  therefore  is  indicated  by  diminution  or  loss  of  the 
jerk.  I  have  once  seen  it  absent  in  a  woman  who  was  apparently  in 
perfect  health  and  by  reason  of  her  early  outdoor  life  enjoved  a  vigor  of 
physique  above  that  of  the  average.  Oppenheim  savs  he  has  known 
two  or  three  such  individuals.  In  a  neuropath  with  various  anomalies 
of  development,  he  assumed  that  the  absence  of  the  knee-jerk  was  a 


GENERAL    COXSIDERATIOXS    UPON    NERVOUS    DISEASES  6l 

liereditary  stigma  degenerationis.  These  exceptional  cases  only  prove 
the  rule,  that  loss  of  the  knee-jerk  means  disease. 

Next  in  importance  among  the  deep  reflexes  is  the  ankle  reflex 
and  ankle  clonus  as  it  is  called.  The  heel-phenomenon  or  Achilles  ten- 
don reflex  is  constant  in  health  and  is  well  elicited  by  asking  the  pa- 
tient to  kneel  easily  on  a  chair  and  then  tapping  the  tendo  Achilles.  The 
-calf  muscles  contract  and  the  foot  is  suddenly  extended.  This  ankle 
reflex  is  much  like  the  knee-jerk  and  is  subject  to  the  same  general 
exceptions. 

The  ankle  clonus  is  a  symptom  of  disease  and  never  occurs   in 

FIGURE  6. 


^lode  of  eliciting  an  ankle   clonus. 

liealth.  It  can  be  elicited  by  suddenly  or  gradually  putting  the  calf 
muscles  under  excessive  tension.  The  patient  sits  down  and  extends 
his  leg.  The  examiner  grasps  the  foot  and  forcibly  fl.exes  it  upon  the 
leg.  If  clonus  is  present,  it  immediately  begins  to  oscillate  with  rapid 
and  regular  and  rather  wide  excursions.  These  oscillations  usually 
number  about  eight  or  ten  a  second.  They  cease  when  the  examiner 
lets  go  of  the  foot  and  the  muscles  are  relaxed  again. 

Though  most  of  the  authorities  say  that  this  is  a  phenomenon  of 
the  calf  muscles,  some  recent  investigations  seem  to  point  out  quite 
definitely  that  it  belongs  only  to  the  soleus  and  not  to  the  gastrocnemius. 
This  is  in  line  with  the  fact  long  ago  pointed  out  by  Duchenne  that  in 
spite  of  their  common  insertion,  these  two  muscles  have  distinct  pur- 
poses. 

In  hysteria  and  neurasthenia  there  is  occasionally  seen  a  slighl, 
brief  pseudoclonus. 


62  GKXKKAL    COXSIDKKATIONS    UPON    iNERVOUS   DISEASES 

A  icrist  rcfhw  is  obtained  by  stroking  tbe  tendons  of  the  wrist 
when  the  hand  of  the  patient  is  placed  supine  on  the  hand  of  the  ex- 
aminer. A  t^p  on  the  styloid  process  of  either  the  radius  or  ulna  pro- 
duces the  rad'al  or  nhiar  periosteal  reflex. 

Much  more  important  than  any  of  these  among  the  arm  reflexes- 
is  that  of  the  triceps,  which  is  elicited  by  letting  the  patient  hang  his 
forearm,  while  at  right  angles  to  his  arm,  loosely  over  the  fingers  of 

FIGURE  7- 


Method  of  testing  the  triceps  reflex. 

the  examiner  and  by  tapping  the  tendon  sharply  just  above  the  ole- 
cranon process. 

Bechterew  has  described  a  scapiilo-Jniineral  reflex.  With  the  per- 
cussion-hammer taps  are  made  along  the  entire  inner  edge  of  the 
shoulder-blade,  and  beneath  the  inner  angle  of  the  same.  Especially 
marked  is  the  response  when  the  stroke  falls  on  the  inner  edge  of  the 
scapula  near  the  inferior  angle.  Tliere  is  adduction  and  slight  outward 
lotatjon  of  the  corresponding  humerus. 

J-jOth  a  jazv  reflex  and  a  jazv  clonus  are  observed.  With  the  mouth 
held  loosely  open,  the  muscles  relaxed  as  much  as  possible,  a  pencil^ 
small  ruler,  or  paper  cutter  is  placed  transversely  on  the  lower  teeth 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  63 

and  smartly  tapped.  The  muscles  of  mastication  contract,  especially 
the  masseters ;  the  jaw  leaps  upward.  In  disease  when  forcibly  de- 
pressed a  clonus  or  rhythmical  up-and-down  movement  takes  place 
in  it. 

Among  these  deep  reflexes  must  be  included  the  pupillary  and  ac- 
commodation reflexes  of  the  eye.  A  bright  light  focused  into  the  eye 
causes  the  pupil  to  contract.  If  the  patient  is  asked  to  gaze  at  some 
distant  object  and  then  at  another  object  brought  to  his  usual  reading 

FIGURE  8. 


Method  of  testing  the  scapulo-humeral  reflex. 

distance,  or  if  he  is  asked  to  keep  his  gaze  fixed  on  the  examiner's 
finger  as  the  latter  is  gradually  carried  towards  his  nose,  the  pupils 
will  be  seen  to  contract.  Where  the  former  or  light  reflex  is  lost,  while 
the  latter  or  accommodation  reflex  is  retained,  the  pupil  is  referred 
to  as  that  of  the  Argyll-Robertson  type. 

The  various  visceral  reflexes  are  of  such  familiarity  that  scarcely  a 
word  need  be  said  of  them  here.  The  vasomotor  and  secretory  reflexes 
are  visceral  in  a  sense.  Nausea  and  vomiting  caused  by  rapidly  re- 
volving objects  before  the  eyes  are  of  the  same  nature.  The  heart,  the 
stomach,  the  liver,  the  kidneys,  the  rectum  and  bladder  may  all  be 
affected  by  some  form  of  remote  sensory  disturbance.  We  do  not  make 
use  of  these  reflexes  to  any  extent  in  diagnosis. 

Idiopathic  reflex  irritability  of  the  muscles  is  seen  in  neurasthenic 


64 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 


and  many  other  states.  Diminution  and  increase  of  irritability  are 
both  observed.  Percussion  of  the  muscle  awakens  contractions  that 
are  lively  and  enduring,  for  a  time.  The  same  is  observed  when  elec- 
tricity is  the  stimulant.  In  degenerative  states  both  the  mechanical 
and  electrical  irritability  are  usually  reduced. 

When  a  muscle  is  suddenly  relaxed  and  undergoes  a  slow  tonic 
contraction,  Westphal  spoke  of  the  condition  as  a  paradoxical  muscular 

FIGURE  9. 


Showing  the  mode  of  testing  the  jaw  reflex 

contraction.  It  is  best  observed  in  the  tibialis  anticus  when  the  foot 
is  suddenly  flexed  on  the  leg.  The  mechanism  is  not  known,  nor  are 
we  acquainted  with  its  full  significance.  It  is  a  rare  phenomenon  and 
never  occurs  in  health.  A  somewhat  similar  exhibition  has  been  seen 
in  hysteria 

Electro-diagnosis  in  neurology  is  much  more  satisfactory  than 
electro-therapy,  in  the  fact  that  it  is  much  more  definite  and  accurate. 
And  yet  it  is  less  resorted  to  than  it  should  be,  partly  I  suspect  from  the 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  65 

fright  produced  in  the  minds  of  some  by  the  vast  array  of  symbols  and 
formulae  presented  in  certain  works  upon  the  subject.  Neither  the 
apparatus  nor  the  principles  upon  which  electro-diagnosis  depends,  are 
at  all  complicated. 

All  that  is  needed  in  the  way  of  proper  paraphernalia  are  a  good 
faradic  battery,  a  good  galvanic  battery  capable  of  furnishing  a  current 
of  thirty  or  more  milliamperes,  a  galvanometer  for  accurate  measure- 
ments, though  for  general  examinations  even  this  is  not  necessary, 
good  conduction  cords,  a  rheostat  and  a  number  of  electrodes  of  vari- 
ous sizes,  in  the  handle  of  one  of  which  is  conveniently  arranged  a  cur- 
rent interrupter. 

As  time  and  space  will  be  saved  by  the  use  of  symbols,  the  follow- 
ing definitioms  are  in  order  here.  An  will  be  used  for  the  anode,  or 
positive  pole  of  the  battery ;  Ca  will  be  made  to  stand  for  the  cathode ; 
C  is  employed  to  denote  a  contraction  of  the  muscle. 

CaCC  in  electro-diagnostic  parlance  mieans  cathodal  closing  con- 
traction, which  interpreted  further  means  that,  the  anode  being  on  some 
indifferent  part  of  the  body,  when  the  negative  pole  is  placed  over  the 
nerve  or  muscle  to  be  examined  there  is  a  muscular  contraction. 

In  a  similar  manner  CaOC  is  the  formula  for  the  contraction  that 
would  take  place  upon  ihe  opening  of  the  current  by  removal  of  the 
negative  electrode. 

AnCC  stands  for  anodal  closure  contraction  and  AnOC  for  anodal 
opening  contraction.  To  still  further  facilitate  matters  T  is  used  to 
represent  a  strong  continuous  or  tenatic  contraction  in  the  muscle, 
DeR  the  reaction  of  degeneration,  and  D  the  closed  circuit  or  flowing 
current.  Every  examination  for  abnormality  presupposes  a  knowledge 
of  the  normal.  The  same  is  true  in  electro-diagnosis.  The  normal 
polar  formulae  read  thus : 


1.  CaCC;  2-    |  AnOC;  ^-  ^^^C" 


These  are  varied  and  even  reversed  in  disease. 

Moreover  certain  conditions  must  be  observed  and  certain  sources 
of  error  must  be  carefully  avoided. 

Adults  are  more  easily  examined  than  children.  In  very  early 
life,  especially  in  the  newborn,  the  skin,  which  is  always  highly  resist- 
■ent  to  the  current  is  particularly  so,  and  the  peripheral  nerves  and 
muscles  are  incompletely  developed.  Adult  results  in  electrical  exami- 
nation are  not  observed  in  children  until  they  are  well  along  toward 
their  fifth  year. 

The  resistance  of  the  skin  is  overcome  by  moistening  it  and  the 
•electrodes  freely  with  water  in  which  a  modicum  of  salt  has  been  dis- 
solved. The  passage  of  the  current  itself  by  stimulating  the  glands  and 
increasing  the  moisture  of  the  skin  in  a  few  minutes  increases  the 
latter's  conductibility. 

If  one  side  of  the  body  is  diseased  and  to  be  examined,  the  other 
side  should  be  simultaneously  tested  as  a  control.  When  both  sides 
are  affected  resort  must  be  had,  unsatisfactory  as  it  is,  to  a  third  per- 
son for  the  control  tests. 


66 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 


111  adults,  and  especially  in  children,  great  care  must  be  exercised 
net  to  confound  voluntary  and  reflex  movements  with -those  produced 
by  the  electric  current.  The  distinction  can  be  detected  by  close 
watchfulness  and  frequent  repetition  of  the  tests.  Allowances  must  be 
made  for  variations  in  the  size  of  the  electrodes  used,  the  current 
being  dense  in  direct  proportion  to  its  strength  and  in  inverse  propor- 

FIGURE  10. 

(After  Erb.) 


U.  frontalis 
Oberer  FaculUaut 
U.  cortng.  aopercil. 

M.  orbic  palpebr. 
Nasenma2keln{ 

U.  xygomatici 

M.  orbicul.  ori3 

Uittler.  Facialissst 

M.  masseter 

V.  lerator  tneQti 

U.  (^aadr.  meuti 

U.  triang.  menti 

Kerv.  hypoglosa- 

DDter    Kacialisast 

M.platysma  myoid. 

ZQDgeabei 

mu3kelD 

U.  omobyoLdeus 


a .  tboracio.  anUr. 
(M.  pecUir.) 


U.  pli 


Sopraclavicular- 
paokt-  (blrb'schei 
Ponlit.  U.  deltoid, 
bic«ps.  bracbial.  in- 

lero.  Q    BopinaU 

lODg) 


Oegend  dsr 
CeotralwindaagcD 


Gegcnd  d  3.  Slirn- 
w.nduDgD.  Insel 
(Spracbcenttuai) 

U.  temporalis 
Facialis 


vor  de 


Ohr 


N.  facialis    SUimm) 
N.  auricul.  post 
Mitll    Facialisast 
Unter.  Facialisast 
U.  splenms 

U.  slernocleido- 

mastoideus 

N.  accessorioa 

M.  levator  auguU' 

scapul 

calaris 

N.  dora  scapulae 


N.  tboracio.  long. 

(U.  aerratas  aotic. 

maj) 


tion  to  the  diameter  of  the  electrode,  and  for  such  natural  conditions 
as  over-development  of  fat,  etc. 

The  limb  to  be  examined  should  always  be  so  placed  that  the 
effect  of  the  stimulation  can  be  easily  manifested.  A  large  electrode  is 
thoroughly  moistened  and  placed  firmly  against  the  lower  part  of  the 
sternum.  It  is  not  to  be  moved  during  the  entire  examination.  The 
other  electrode,  the  small  one  with  the  interrupting  attachment,  is 
pressed  firmly  down,  after  having  also  been  thoroughly  moistened,  on 
the  nerve  or  muscle  to  be  tested. 

The  accompanying  illustrations  indicate  the  most  favorable  points 
at  which  to  place  this  electrode  to  obtain  the  clearest  responses  from 
the  respective  nerves  and  muscles  under  examination. 

A  weak  current  is  employed  first  and  then  made  stronger  until 
There  is  a  beginning  twitch  in  the  muscle.    That  indicates  that  the  re- 


GEiVERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 


67 


quired  strength  of  current  has  been  attained.  Each  nerve  of  the  hmb 
should  be  examined  above  and  below,  using  the  points  in  the  illustra- 
tions as  guides. 

The  first  great  fact  to  note  in  regard  to  the  use  of  electricity  for 
diagnosis  is  that  it  applies  only  to  the  lower  or  peripheral  neurones. 
We  can  get  no  information  of  the  condition  of  the  upper  or  central 
neurones  by  the  aid  of  electricity.     Moreover,  in  regard  tO'  sensation  it 


FIGURE  II. 

(After  Erl). 


U.  tric«^  t^BpntlongiHD) 


H,  thcepB  (caput  intern 


M.  flezoi  carpi  olnaris 


U.  flox.  digitor.  comm 
profand. 


U.  flex,  diritor   0obli 


11  fiez.  <Jiglus«bl  idjgil. 
indtcis  ek  minimij 


M    p^tmaris  brev 

U.  abdocLor  digiti  inin 

M.  flexor  digit,  min 

U.  opponens   digit,  min 


Hia.  lumbricalea. 


M.  fle:^.  dtgitor.  sublim. 

M.  flex.  polliclB  longnB 
Iferv.  mtdianus 

M.  abdoctor  pollic.  brer* 
M.  opponens  poUicU 

M.  flex.  polL  brer. 

XL  addactoc  pollio. 


can  afford  us  but  very  little  knowledge  that  is  at  all  definite  enough 
to  be  of  service.  Therefore,  electro-diagnosis  is  pre-eminently  con- 
cerned with  giving  us  information  as  to  the  condition  of  the  lower 
motor  neurones.  In  all  diseases  of  the  cord,  the  roots,  and  the  nerves 
in  which  these  neurones  are  implicated,  electricity  furnishes  most  valu- 
able diagnostic  criteria. 

Let  us  now  consider  what  are  the  normal  and  abnormal  exhibi- 


68 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 


tions.     We  have  many  distinct  points  of  view  from  which  to  conduct 
the  examination  and  mark  the  dift'erences  in  the  results. 

In  the  first  place  it  should  be  noted  whether  the  responses  to  any 
form  of  current  are  greater  or  less  than  nornic;!.  This  is  what  is  called 
the  quantitative  test.  It  is  easily  made  and  not  of  very  great  value 
in  diagnosis.  Mere  increase  or  diminution  of  nervous  irritability  and 
muscular  excitability,  as  we  have  already  seen  under  the  head  of  the, 
reflexes,  can  be  determined  by  mechanical  means  almost  as  well  as  by 
electrical  stimulation.     However,  it  is  always  wise  to  make  the  quan- 

FIGURE  12. 

(After  Erb. ) 


U.  delloUeos  (hlntert^ 


S.  radiaht 
II    brachial,  iatent. 

M.  SDpinator  long. 
il  radial,  ext.  loog. 

U.  radiaL  eit.  biet. 
il.  eiUnsor  digit. 


M.  exUDsor  isd 

U  abductor  pollic   loon. 
U.  eiteotor  poUic  btet. 


Id.leUron.donol.  iKtll 


M.  tilcep9(capit  loDgum) 


U.  triceps  Icapnt  ntern.) 


U.  oloar.  eitero. 
M-  sopinat.  brer. 


M.  exteci}.  digiti  minim, 
M.  ext«n8.  indicia 


M.  extena.  poll,  los;. 


H.  aMset.  digiL  -mit. 


titative  tests  and  to  record  them  with  the  galvanometer  readings.  Of 
course  care  must  be  observed  to  use  always  the  same  sized  electrode, 
usually  a  small  one,  and  to  remember  that  normally  different  nerves 
and  muscles  differ  in  their  quantitative  responses.  Stintzing  used  an 
electrode  with  an  area  of  3  sq.  cm.  Neglecting  the  muscle  averages 
as  of  less  importance,  he  found  that  for  the  nen^es  the  averages  were 
as  follows,  the  galvanic  being  given  in  milliamperes  and  the  faradic  in 
centimeters  on  the  scale  attached  to  the  sliding  coil  of  his  battery : 


GENERAL    COXSIDERATIOXS    UPON    NERVOUS    DISEASES 


69 


Galvanic. 
Ma. 

Facial  nerve  ....". i-75 

Frontal  branch    i-45 

Mental  branch 0.95 

Accessor}-  nerve    0.27 

Median  nerve   (in  arm) 0.9 

Ulnar  nerve  0-55 

Musculospiral  nerve i-8 

Crural  nerve   i-05 

Peroneal  nerve  i-i 

FIGURE   13. 

(After  Erb.) 


M.  tensor  fuetet  lirtM 


U.  adductor  nupnas 
H.  addsct  longoi 


U.  qaidricftps  femori» 
(gemeiascbaftl.  FanUI 

U    rectus  femona 


U.  rutus  extersat 


IdL  Tutoj  iatemoj 


Faradic. 

Cm. 

121 

128 

132 

137 
122 

130 

105 
III 

115 


^luscles  vary  more  widely  even  than  do  the  nerves.  Even  if  we 
were  to  duplicate  Stintzing's  apparatus  and  methods  in  every  particular, 
there  are  so  many  sources  of  error  in  the  conditions  of  the  skin,  etc.,^  in 
different  people,  that  only  wide  variations  from  the  above  comparative 
figures  can  be  taken  as  evidence  of  a  pathological  condition. 

Diminution  in  quantitative  excitability  is  much  more  common, 
definite  and  available  for  purposes  of  diagnosis  than  is  increase.  In 
only  one  disease,  tetany,  does  increase  of  excitability  to  the  galvanic 
current  figure  prominently  as  a  symptom. 

Much  more  definite  and  reliable  are  the  qualitative  changes 
that  occur  in  the  electrical  responses  as  the  result  of  disease.  Here  we 
have  to  consider  the  nature  of  the  current,  faradic  or  galvanic,  _  em- 
ployed in  the  examination ;  the  strength  of  the  current ;  and  the  tissue 
undergoing  the  test,  whether  it  is  nervous  or  muscular. 

When  for  anv  reason  a  muscle  or  its  nerve  is  severed  from  its 


70 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 


nutrient' center  in  the  cell  embedded  in  the  anterior  horn  of  the  cord  or 
cranial  nucleus,  it  undergoes  degeneration.  This  causes  a  change  in 
the  electrical  responses.  The  result  is  spoken  of  as  the  reaction  of  de- 
generation and  symbolized  by  ReD,  It  is  obvious,  therefore,  that  re- 
action of  degeneration  appears  as  a  symptom  in  a  great  variety  of 
diseases  affecting  the  cells  in  the  anterior  horns  of  the  cord  and  nuclei 
of  the  cranial  nerves,  the  neuraxones  belonging  to  those  cells,  and  the 
muscles  to  which  the  neuraxones  are  attached.     In  such  affections  as 

FIGURE  14. 

(After  Erb.) 


M.  tibial,  antic 
ttcit«D3.  digit   comra. 
long- 


H.  peronaens  brarlj 


U   exteiuor  tullnelB 
long. 


dp.  Uit«rWMi  dorults  I 


M    gastrocnam.  titars. 
M.  peronteae  Un^u* 


HL  floor  hilluta  long. 


H   Elidaetor  dlglti  nin. 


poliomyelitis,  the  progressive  atrophies  of  spinal  origin,  other  diseases 
that  damage  the  anterior  cornual  cells,  bulbar  nuclear  paralyses,  dis- 
eases that  by  compression  or  otherwise  mjure  the  anterior  spinal  roots, 
and  all  severe  degenerative  diseases  of  the  peripheral  nerves  like  the 
infectious  and  toxic  polyneuritides,  ReD  is  a  most  important  symptom. 
It  never  occurs  as  a  sign  of  any  aft'ection  that  remains  limited  to  the 
cerebral,  upper  or  central  motor  neurones.  In  differentiating  the  two 
sets  of  paralyses  therefore  its  value  is  obvious. 

There  are  various  degrees  of  degeneration  and  the  value  of  the 
symptom  is  furthermore  emphasized  in  the  remarkable  fact  that  there 
is  a  direct  parallelism  between  it  and  the  degree  of  neuro-muscular 
degeneration.  As  the  latter  doesn't  occur  until  about  a  week  after  the 
damage  is  first  done,  the  electrical  symptom  will  not  be  elicited  be- 
fore that  time. 

The  immediate  cause  of  the  reaction  of  degeneration  is  the  fact 
that  the  degenerated  nerve  terminals  in  among  the  muscle  fibres  re- 
quire a  stronger  and  longer  current  than  normal  to  excite  them. 


GENERAL    COXSIDERATIOXS    UPOX    NERVOUS    DISEASES 


71 


As  a  very  late  phenomenon  the  same  electrical  manifestations  may 
obtain  in  pure  muscular  affections  wherein  the  muscular  fibres  are 
wasted. 

The  reaction  of  degeneration  reveals  itself  in  two  ways.  There 
is  a  gradual  loss  of  contractility  to  stimulation,  and  there  is  an  actual 
change  or  reversal  of  the  polar  responses  to  galvanic  stimulation.  If 
the  faradic  ctirrent  is  employed,  and  first  the  nerve  and  then  the  mus- 
cle tested,  it  will  be  noticed  that  there  is  a  gradual  diminution  of  the 
rapiditv  and  force  of  the  contraction.     In  other  words  a  stronger  cur- 

FIGURE  15. 

(After  Erb.) 


Sen  itckiadiatt 
U.  bicep»  fern.  (cap.  long.) 
K.  biceps  ftm.  (cap.  br«T.) 


M.  flexor 'tuUicU  loii£;v      «. 


(   hL  glutaacs  miximas 


v..  addactor  m&gnu 
!if    aemiUadiDosas 
U.  »emImembra.no8U 


M..  g&atrocnem    (cap.  laL.} 


^  fiezot  digit-oi.  tomo. 


rent  of  electricity  will  have  to  be  employed  to  get  a  contraction  anything 
near  like  that  of  the  normal.  Finally  as  the  degeneration  advances,  no 
contraction  whatever  can  be  obtamed,  no  m.atter  what  be  the  strength 
of  the  current  that  is  tolerable.  If  regeneration  occurs  there  is  a  re- 
turn of  the  faradic  response  in  both  the  nerve  and  the  muscle  in  the 
reversed  order  in  which  it  disappeared. 

When  the  galvanic  current  is  used  and -the  nerve  is  tested  the 
phenomena  are  about  the  same  as  they  are  with  the  faradic  stimula- 
tion. In  other  words  the  galvanic  excitability  of  the  nerve  is  lost.  If 
now  the  muscle  be  tested  with  the  galvanic  current,  there  is  for  a  time 
a  remarkable  increase  in  the  contractions  or  what  is  the  same  thing 
a  weaker  current  is  merelv  needed  to  awaken  the  normal  contraction. 


y2  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

As  the  degeneration  advances,  tinally  the  galvanic  current  loses  its 
power  of  stimulation  and  then  differs  in  no  respect  from  the  faradic. 
In  regeneration  of  the  nerve  exactly  the  reverse  order  of  events  takes 
place  until  the  normal  status  is  reached  upon  the  complete  restoration 
to  health. 

The  following  diagram  will  perhaps  illustrate  the  characteristic 
features  of  the  reaction  of  degeneration  better  than  the  above  detailed 
description.  It  is  taken  from  Erb  to  whom  we  owe  much  of  our 
knowjedge  along  this  line. 

Tliere  is  a  change  in  the  character  of  the  polar  responses  also  to 
galvanic  stimulation  of  the  muscles  in  the  reaction  of  degeneration. 
The  contractions  are  slow  and  worm-like  instead  of  being  sharp  and 
lightning-like  upon  the  closing  and  opening  of  the  circuit.  Moreover 
the  normal  superiority  of  the  cathodal  closing  response  over  that  of 
the  anodal  closing  is  reversed  and  the  formula  reads  AnCC>CaCC. 
Even  the  cathodal  opening  contraction  undergoes  a  greater  in- 
crease than,  and  in  very  exceptional  instances  may  even  become  equal 
to  or  stronger  than,  the  anodal  opening  contraction.  That  these  polar 
alterations  are  not  as  important  reactionary  signs  of  degeneration  as 
are  the  differential  phenomena  between  the  faradic  and  galvanic  re- 
sponses described  above,  is  shown  by  the  fact  that  we  can  even  speak 
of  the  condition  as  a  reaction  of  degeneration  when  the  CaCC  is 
equal  to  or  exceeds  still  the  AnCC  provided  the  contraction  is  slug- 
gish in  character.  In  some  cases  of  partial  reaction  of  degeneration 
there  is  a  decrease  of  nerve  and  muscle  irritability  to  both  currents, 
whereas  with  direct  stimulation  of  the  muscle  with  the  galvanic  current, 
a  slow  contraction  and  reversal  of  the  polar  responses  still  obtain. 

The  phenomena  of  the  reaction  of  degeneration  may  be  conve- 
niently summed  up  thus : 

1.  Loss  of  nerve  irritability  to  the  faradic  current. 

2.  Loss  of  muscle  irritability  to  the  faradic  current. 

3.  Loss  of  nerve  irritability  to  the  galvanic  current. 

4.  (a)  Early  increase  of  muscle  irritability  to  the  galvanic  cur- 
rent with  later  decrease,  (b)  Modification  of  the  polar  responses, 
even  to  the  degree  of  complete  reversal  from  those  of  the  normal,  the 
formula  becoming  x\nCC  equal  to  or  greater  than  CaCC,  with  slug- 
gishness of  the  contraction  as  the  most  important  feature  of  all. 

It  may  be  mentioned  that  electricity  is  one  of  our  best  aids  in 
detecting  the  feigning  of  disease,  whether  sensory  or  motor  in  type,  and 
by  it  we  can  distinguish  hysterical  or  pseudo-paralysis  from  the  lower 
neurone  types  of  organic  paralysis.  Consult  the  accompanying  diagram 
for  the  best  points  to  apply  the  poles. 

The  vasomotor,  secretory  and  trophic  symptoms  of  nervous  dis- 
eases call  for  but  the  briefest  notice  here  as  they  are  so  generally  local- 
ized in  character  that  they  can  be  better  treated  of  under  the  head  of 
brain  and  cord  manifestations. 

The  vasomotor  and  secretory  phenomena  are  very  closely  inter- 
related and  are  supposed  to  be  largely  under  the  control  of  the  sympa- 
thetic system. 

Flushing  and  pallor  of  the  skin  and  mucous  membranes,  local  and 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 


73 


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74  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

general,  may  be  frequently  observed.  Sometimes  they  can  be  elicited 
by  causing  a  mental  shock  to  the  patient  or  by  irritating  the  skin. 
Dermographia  is  where  one  can  write  with  the  back  of  his  nail  on 
the  patient's  skin  and  the  tracing  remains  a  long  time.  The  tdche 
hlcnatrc  of  the  French  authors  is  an  unimportant  vasomotor  manifes- 
tation in  the  skin. 

Anv  of  the  secretions  may  be  increased  or  diminished.  This  is 
usually  due  to  associated  vasomotor  trouble.  Special  names  are  em- 
ploved  for  the  various  forms  and  localizations  of  the  secretory  exhibi- 
tions. They  are  such  as  hyperidrosis  and  anidrosis  for  disturbances 
of  the  perspiration ;  salivation  for  increase  of  the  saliva ;  diuresis  for 
excessive  flow  of  urine. 

The  trophic  symptoms  are  usualh  due  to  spinal  disease  and  will 
be  described  at  the  head  of  those  troubles.  True  atrophies  must  be 
carefullv  distinguished  from  pseudo-atrophies  due  to  non-use.  True 
hypertrophies  and  pseudo-hypertrophies  must  be  carefully  differen- 
tiated. The  former  must  not  be  confounded  with  enlargements  from 
other  adventitious  causes  of  enlargement.  A  hypertrophic  joint  for 
instance  is  not  the  same  as  a  swollen  and  oedematous  joint. 

Trophic  disturbances  can  be  observed  in  any  or  all  of  the  tis- 
sues of  the  body  but  they  are  extremely  obvious  at  times  in  the  epi- 
blastic  elements  such  as  the  skin,  the  hair,  the  nails,  etc. 

Ulcerations,  pigmentations  and  many  other  changes  are  observed 
in  the  skin  as  a  result  of  its  diseased  innervation.  It  is  beginning  to  be 
recognized  that  many  skin  affections  are  really  nervous  troubles. 
Herpes,  urticaria,  scleroderma,  pemphigus  are  neurotic  in  origin. 
General  trophic  diseases  like  arthritis  deformans  are,  in  some 
cases  at  least,  of  the  nature  of  trophoneuroses.  Just  how  the  nervous 
centers  preside  over  the  nutrition  of  the  body  we  do  not  clearly  know ; 
whether  their  influence  is  direct  or  indirect,  whether  it  is  physical  or 
chemical.  A\'e  do  know,  however,  that  most  important  trophic  centers 
are  located  in  the  gray  matter  of  the  spinal  cord  and  that  they  oper- 
ate upon  the  tissues  largely  through  the  sympathetic  and  spinal  nerves, 
together  or  separately. 

Trophic  symptoms  need  no  tests  as  the}'  are  wholly  a  matter  of 
observation.  The  trophic  changes  in  the  muscles  are  accompanied  by 
the  peculiar  phenomena  described  under  the  reaction  of  degeneration 
in  the  paragraphs  devoted  to  electro-diagnosis.  Trophic  skin  changes 
are  less  responsive  to  local  medication  than  are  those  due  to  inflam- 
matory troubles,  and  this  sometimes  aids  in  their  diagnosis. 

The  visceral  symptoms  of  neurology  are  motor,  sensory,  secretorv 
or  trophic  in  character  and  may  therefore  be  passed  here.  They  are 
important,  however,  and  should  always  be  carefully  noted  in  the  ex- 
amination of  every  case. 

Local  thermometry  is  sometimes  a  valuable  assistant  in  diagnosis. 
The  vasomotor  condition,  inflammatory  or  spasmodic,  usually  under- 
lies it.  Thermometers  of  various  types  have  been  devised  for  resting 
against  the  head  and  elsewhere.  Tumors  and  abscesses  of  the  brain 
and  focal  inflammations  have  sometimes  revealed  spots  of  slightly 
altered  temperature  in  the  scalp.     The  same  has  been  less  frequently 


GEXERAL    COXSIDERATIOXS    UPON    XERVOUS    DISEASES  75 

observed  in  severe,  focal  cord  troubles.  The  findings,  however,  are 
not  sufficiently  uniform  or  definite  to  make  them  very  satisfactory  as 
diagnostic  criteria. 

General  thermometry  is  the  same  in  nervous  as  in  other  forms  of 
infection  and  inflammation. 

The  pulse  may  be  due  to  a  vasomotor  distrirbance  ;  otherwise  it 
follows  the  same  laws  that  it  does  in  other  pathological  states  of  the 
general  organism. 

-  Skiagraphy,  or  shadow  pictures  made  with  the  Rontgen  ray,  has 
added  a  most  valuable  aid  to  the  diagnosis  of  some  superficial  and 
even  deep  lesions  in  the  nervous  system.  Bullets  and  other  missiles 
liave  been  located  by  this  method.  Exostoses,  spiculje,  depressions  and 
fractures  in  the  inner  table  of  the  skull  have  been  thus  discovered  when 
there  were  no  external  signs  of  any  sort.  Many  tumors  and  growths 
can,  if  not  too  deeply  buried,  be  thus  outlined.  Cortical  growths  are 
•especially  discoverable  by  skiagraphy ;  basal  growths  are  perhaps  the 
least  so. 

The  examination  of  the  cerebrospinal  fluid  and  the  value  of  the 
"findings  will  be  referred  to  again  under  the  head  of  lumbar  puncture  in 
the  chapter  given  to  the  anatomy  of  the  spinal  cord. 

GENER.-\L  COXSIDER.\TIONS  UPON  THE  TREAT^IEXT  OF 
DISEASES  OF  THE  NERVOUS  SYSTE^I. 

I  hesitate  ver\-  much  to  write  the  following  chapter,  because  liter- 
ally there  are  no  general  principles  of  treatment  that  apply  to  all  pa- 
tients alike.  Human  beings  are  not  automata  nor  machines  built  upon 
exactly  the  same  plan  and  with  the  same  measurements.  Each  in- 
dividual has  his  own  peculiarities,  so  that  it  becomes  literally  true  what 
is  one  man's  meat  is  another  man's  poison.  In  the  nervous  system, 
wherein  resides  the  very  center  of  the  individual's  personality,  the 
constitutional  and  functional  differences  between  men  are  more  marked 
than  they  are  in  the  other  organs  of  the  body.  The  nervous  system  is 
the  immediate  source  of  all  human  activities.  From  the  creation  of  a 
Paradise  Lost  to  the  sweeping  of  a  public  highway,  the  nervous  system 
is  the  beginning  and  source  of  the  phenomena.  All  other  organs  de- 
velop and  functionate  nearly  in  the  same  way  in  all  men,  but  in  regard 
to  their  nervous  functions  the  differences  are  enormous.  It  is  the  fail- 
ure to  recognize  this  fact  that  leads  to  so  much  dissatisfaction  in  the 
management  of  these  affections.  The  greater  the  need  of  individualiz- 
ing in  any  kind  of  work  the  more  patience,  thought  and  concentration 
is  demanded  of  the  worker.  It  is  much  easier  to  think  mechanically 
and  machine-like,  to  have  a  single  formula  by  which  to  treat  all  hys- 
terias alike  and  another  by  which  to  label  ahvays  certain  general 
groups  of  symptoms  by  a  given  name.  It  saves  time  and  the  expendi- 
ture of  mental  force.  But,  alas !  it  is  usually  disastrous  to  the  patient's 
welfare  and  to  the  physician's  reputation.  Under  such  circumstances 
the  former  usually  turns  to  quackery,  while"  the  latter  rails  at  the  hor- 
rors of  ner\^ous  diseases. 

It  is  notorious  that  in  general  practice  pessimism  in  regard  to  the 


76  GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES 

prognosis  of  these  affections,  and  nihilism  in  regard  to  their  treatment 
are  all  too  common.  The  reason  for  this  is  often  too  obviously  in  the 
temperamental  and  mental  inadequacy  of  the  practitioner.  He  either 
lacks  the  proper  amount  of  patience,  his  trend  of  thought  is  too  mechan- 
ical, he  is  mentally  lazy  or  he  is  ill-informed  in  regard  to  the  newer 
discoveries  in  neurology. 

I  was  recently  asked  by  a  gentleman  of  large  practice  what  a 
neurone  was ;  another  informed  me  that  hysteria  was  nothing  but 
devilishness  in  the  woman ;  a  third  wanted  to  know  what  I  usually 
prescribed  for  paralysis ;  while  a  fourth  emphatically  declared  there 
was  no  such  thing  as  neurasthenia. 

Such  exhibitions  make  one  feel  that  there  are  worse  things  than 
nervous  diseases,  and  chief  among  them  are  the  dogmatism  of  ignor- 
ance and  the  assumption  of  egotism. 

On  the  average  the  prognosis  and  treatment  of  nervous  diseases. 
are  about  the  same  as  they  are  in  other  troubles.  All  of  the  self- 
limited  infections  are  beyond  the  pale  of  cure  in  the  sense  of  ceasing  at 
the  behest  of  the  physician.  The  latter  merely  controls  their  symp- 
toms, wards  off  complications  and  helplessly  lets  them  run  their  course 
and  terminate  themselves.  We  can  do  pretty  nearly  as  much  as  that 
in  locomotor  ataxia  and  a  great  deal  more  in  brain  tumor.  If  hys- 
teria is  incurable,  and  can  only  be  controlled  when  it  breaks  out  in 
exacerbations,  as  it  were,  what  are  we  to  say  of  the  rheumatic  diathe- 
sis, of  gout,  of  diabetes  and  the  other  constitutional  diseases?  Is  val- 
vular disease  of  the  heart  ever  cured,  or  advanced  pulmonary  tuber- 
culosis, or  certain  forms  of  renal  disease  ? 

As  among  other  affections  so  among  the  nervous,  we  have  the  in- 
herited, congenital  and  constitutional  troubles  that  can  only  be  con- 
trolled and  treated  symptomatica! ly,  whose  course  is  chronic,  and 
whose  termination  is  only  with  death. 

On  the  other  hand,  there  are  many  acquired  diseases,  like  chorea, 
neurasthenia,  syphilis  of  the  central  nervous  system,  multiple  neuritis, 
that  give  most  brilliant  results  under  proper  treatment. 

A  pessimistic  view  of  neurology  is  unwarranted  and  exposes  the 
holder  of  it  to  the  charge  of  being  too  badly  informed  to  make  an  ap- 
proximately correct  diagnosis,  too  inappreciative  of  the  close  relation- 
ship of  the  nervous  system  to  the  personality  of  the  patient,  too  gross 
and  mechanical  in  his  mode  of  thinking,  too  empirical  in  the  use  of 
his  remedial  agents,  and  too  oblivious  to  the  important  distinction  be- 
tween inherited  and  congenital  unalterable  disease  states  and  alterable 
and  acquired  temporary  states. 

The  purpose  of  this  chapter  will  be  to  point  out  a  few  general 
principles  of  neurological  therapy  m  order  to  more  particularly  empha- 
size the  unreasonableness  of  therapeutic  nihilism.  It  is  most  assuredly 
not  written  to  enable  any  one  to  concoct  a  fixed  scheme  of  treatment 
for  all  cases  of  nervous  disease  alike  and  thus  to  shirk  the  labor  and 
responsibility  of  studying  and  managing  each  individual  case  upon  its- 
own  merits. 

There  are  three  prominent  indications  in  the  treatment  of  nervous 
disease. 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  ^J 

In  the  first  place,  the  prevention  of  the  disease  itself,  its  return,  or 
its  exacerbation  should  always  be  attempted  by  the  aid  of  proper 
hygienic  and  prophylactic  measures. 

In  the  second  place,  every  endeavor  should  be  made  to  remove 
or  render  inactive  the  cause. 

Thirdly,  the  symptoms  should  be  controlled  in  the  hope  of  thereby 
removing  their  cause,  or  at  least  of  mitigating  the  distress  produced 
by  them. 

In  striving  after  these  various  ends  we  find  that  we  have  at  our 
•disposal  various  classes  of  agents.  They  are  the  psychic,  the  physical 
and  the  medicinal.    I  include  surgery  among  the  physical  measures. 

Psychic,  physical  and  even  medicinal  means  may  have  to  be  em- 
ployed in  the  prophylaxis.  The  putting  of  an  individual  into  the  best 
condition  to  ward  off  disease  means  the  putting  of  him  into  the  very 
best  mental  and  physical  hygienic  state.  Mind  and  body  must  be 
trained  to  make  for  health  and  not  for  disease.  Good  physical  and 
mental  food  is  a  necessity.  Proper  and  varied  exercise  is  a  prerequisite. 
Cleanliness,  system,  regularity,  moderation,  serenity  and  freedom  from 
irritation  and  exhaustion  are  desiderata.  Ignorance  of  the  laws  of 
liealth  is  not  so  widespread  as  indifference  to  them.  Ignorance  in  re- 
gard to  the  dangers  of  their  infraction  is  the  cause  of  much  of  this 
indifference.  It  becomes  the  duty  of  the  physician,  therefore,  to  warn 
as  well  as  to  instruct,  to  arouse  by  awakening  alarm  as  well  as  to 
calm  by  conveying  correct  information.  In  doing  thus  his  duty  he  may 
have  to  touch  upon  every  minutia  in  the  diet,  the  clothing,  the  habits, 
the  occupations,  the  amusements,  the  mentalization  even  of  his  protege. 
Nothing  is  too  insignificant  in  the  prophylaxis  of  nervous  diseases. 
Much  of  the  advice  which  he  is  to  give  is  commonplace  and  well  known, 
but  people  are  thoughtless  and  forgetful  and  he  has  assumed  the  role 
of  conservator  of  their  health ;  it  behooves  him,  therefore,  to  iterate 
and  reiterate  his  injunctions,  however  trite  they  may  seemx  to  be. 

One  of  the  most  important  cjuestions,  though  unfortunately  not 
one  of  the  most  frequent,  that  he  will  be  consulted  upon  is  that  of 
marriage  and  the  possible  effects  of  heredity.  In  no  branch  of  medi- 
cine is  heredity  so  prominent  a  factor  as  in  neurology.  Heredity  is  a 
tremendous  feature  in  etiology.  In  the  prevention  of  these  troubles 
it  must  receive  high  consideration.  If  not  for  their  own  good,  at 
least  for  the  good  of  society  and  future  generations,  the  unfit  should 
not  marry.  It  would  lead  me  too  far  to  mention  all  the  forms  of 
nervous  disease  that  ought  to  restrain  those  contemplating  marriage 
from  that  which  will  most  assuredly  give  to  the  world  more  defective 
and  more  diseased  offspring.  The  intermarriage  of  near  blood  rela- 
tions should  be  interdicted.  Two  nervously  afflicted  individuals  should 
not  enter  into  wedlock.  An  individual  who  has  a  form  of  nervous 
trouble  in  which  heredity  is  recognized  as  a  marked  element  ought  not 
to  beget  children.  S3^philitics  should  not  marry.  Members  of  fami- 
lies in  which  there  is  a  clear  psychopathic  taint  would  not  marry  if 
they  considered  the  welfare  of  others  besides  themselves.  Members  of 
families  in  which  there  is  a  traceable  neuropathic  taint  should  be  slow 
about  contracting  union,  or  if  they  do  marry  they  should  unite  in  a 


78'  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

family  where  there  is  a  history  of  exceptional  health  and  vigor  for 
several  generations  back.  The  children  of  a  neuropathic  ancestry 
need  close  observation,  but  coddling  should  be  most  strenuously  guard- 
ed against.  These  children  are  ofttimes. unfortunate  in  being  the  vic- 
tims of  both  a  bad  heredity  and  a  bad  discipline,  They  are  sometimes 
brilliant,  precocious,  entertaining  and  physically  weak.  They  are  the 
center  of  the  family  interest  and  sympathy.  They  are  therefore  over- 
indulged, injudiciously  humored  and  spoilt.  Their  physical  and  mental 
lives  are  all  but  riotous.  They  live  as  they  please,  eat  as  they  please  and 
think  as  they  please.  The  consequence  is  inevitable.  On  the  other 
hand,  I  sometimes  wonder  if  it  is  not  a  greater  evil  to  be  the  child  of 
self-opinionated,  narrow-minded,  ignorant  disciplinarians.  I  am  con- 
vinced that  in  too  many  cases  not  neglect  and  overindulgence  are  the 
bane  of  these  children  so  much  as  too  much  regulation — nagging,  in 
fact — by  anxious  and  loving  but  woefully  stupid,  ill-informed  and 
short-sighted  parents.  I  have  frequently  seen  young  neurotic  girls 
driven  almost  insane  by  the  imperious  attentions  of  a  mother  who 
meant  well,  but  who  was  incapable  of  seeing  things  from  her  daugh- 
ter's point  of  view.  A  school  for  parents  would  be  a  godsend  for  many 
neuropathic  children  and  its  curriculum  would  include  training  in  what 
not  to  do  as  well  as  in  what  to  do. 

These  children  of  neuropathic  parentage  need,  as  a  rule,  sys- 
tematic, wholesome,  evenly  balanced  lives.  All  shocks,  unusual  or 
one-sided  strains,  freakish  habits,  intemperance  in  thinking,  in  eating, 
in  drinking  and  in  everything  should  be  prevented.  A  steady  moral 
purpose  in  life,  a  wholesome  ambition  in  some  one  direction  and  a 
good  regime  in  living  should  be  inculcated.  Nerves  are  marvelously 
built  up  and  kept  strong  by  systematized  and  regular  mental  and  physi- 
cal activity. 

The  same  applies  to  adults  as  to  these  children.  Dissipation, 
irregularity,  extremes  are  disastrous  to  the  health  of  the  nervous  tis- 
sues. Proper  exercise  of  the  entire  personality,  mental  and  physical, 
in  a  manner  conducive  to  a  well-balanced  organism  is  a  necessity. 

It  is  more  solacing,  but  less  truthful,  to  say  that  hard  work  is  the 
cause  of  much  modern  nervousness  than  it  is  to  say  it  is  due  to  the 
distractions,  dissipations,  fuss  and  fume  that  are  allowed  to  accompany 
the  hard  work.  Hard  work  may  mjure  its  hundreds,  but  excessive, 
purposeless  motility,  mental  flightiness,  silly  rush  and  roar,  false  and 
foolish  identifying  of  mere  mental  and  physical  bombast  with  real  ac- 
complishment injures  its  thousands, 

The  use  of  alcoholics,  tobacco  and  noxious  beverages,  the  diet  and 
the  mode  of  eating  it,  the  frequency  and  the  style  of  bathing,  the  hours  of 
sleeping,  the  whole  life  of  the  adult  must  be  inquired  minutely  into, 
and  proper  suggestions  made  along  well-known  lines  to.  insure  against 
the  outbreak  of  a  possible  or  threatened  nervous  affection. 

The  dietetics  of  nervous  diseases  has  its  greatest  field  of  operation 
in  neurasthenic  and  allied  states.  As  I  have  treated  of  the  subject  in 
detail  under  the  head  of  neurasthenia,  I  will  not  speak  of  it  further 
here.  It  should  be  noted,  however,  that  for  neuropaths  generally  a 
wholesome  nitrogenous  diet,  with  the  drinking  of  abundance  of  water 


GENERAL    CONSIDERATIONS    UPON    NERVOUS    DISEASES  79 

between  meals,  is  to  be  employed.  It  includes  meats,  fowl,  fish,  eggs, 
milk,  buttermilk,  green  vegetables,  bread  and  butter.  As  a  rule  I  find 
that  neurotics  do  not  eat  enough  or  too  much  of  some  particular  sort 
of  food.  Especially  fats  do  they  seem  to  eschew.  They  overindulge 
in  stimulants,  tea  and  coffee.  I  am  convinced  that  in  these  cases  it 
is  not  so  important  to  advise  a  selected  diet  as  it  is  to  urge  a  generous 
one.  Whims  and  notions  often  confront  the  advice  of  the  physician, 
and  if  he  pays  much  attention  to  them  he  will  have  to  change  the 
dietary  every  few  days.  I  therefore  try  to  discover,  after  a  short  period 
of  observation,  about  what  agrees  best  with  the  patient  apart  from  any 
notions  that  he  may  himself  have.  I  then  urge  that  this  food  be  taken 
in  large  amount,  in  several  small  meals  a  day  if  necessary  at  first. 
Even  less  digestible  food  is  better  for  neurotics  than  little  or  no  food. 
The  stomach  can  always  be  assisted  in  the  disposing  of  it  with  proper 
agents. 

Food,  then,  the  best,  the  plainest  and  the  most  wholesomie  if  possi- 
ble, but  always  food,  more  food,  should  be  the  guiding  suggestion  in 
regard  to  the  dietary  of  most  nervous  people.  The  exceptions  are 
relatively  few  and  capable  of  being  easily  met. 

Athletes  are  not,  as  a  rule,  good  brain  workers,  nor,  on  the  other 
hand,  is  it  necessary  for  people  whose  nerves  are  under  a  high  tension 
to  strive  to  become  athletes  in  order  to  preserve  health.  It  is  amazing 
the  amount  of  ignorance  there  is  among  the  laity  in  regard  to  the  mat- 
ter of  physical  exercise.  Unused  muscles,  of  course,  with  an  over- 
worked brain  produce  an  unbalanced  organism.  A  certain  amount  of 
exercise,  therefore,  is  absolutely  imperative.  Among  real  brain  workers 
there  is  not  enough  exercise  taken,  as  a  rule,  and  among  a  large  class 
of  pseudo-brain-workers  there  is  entirely  too  much  exercise  indulged  in. 

No  exercise  is  of  much  benefit  that  fails  at  the  same  time  to  inter- 
est the  mind.  To  wearily  stand  and  swing  dumb-bells  or  Indian  clubs 
in  a  close,  stuffy  gymnasium  in  the  hope  of  gaining  health  is  almost 
ludicrous.  Long  forced  walks  in  which  one  is  longing  all  the  while  to 
return  home  are  not  conducive  to  health.  Such  exercises  merely  weary 
the  muscles  and  depress  the  mind.  It  is  my  observation  that  in  a  good- 
ly proportion  of  cases  too  much  mere  physical  exercise  is  taken.  I  am 
often  consulted  by  persons  who  are  on  the  verge  of  profound  nervous 
collapse  and  yet  who  wearily  force  themselves  every  day  to  take  a 
cold  plunge  bath  and  a  monotonous  measured  walk.  What  such  per- 
sons need  is  usually  rest  and  less  task-work ;  in  a  word,  very  moderate 
exercise  with  plenty  of  amusement. 

And  this  leads  me  to  state  another  point  I  also  believe  to  be  true, 
namely,  that  many  business  men  who  are  monotonously  confined  to 
their  offices  all  day  do  not  need  physical  outdoor  exercise  so  much  as 
they  need  relaxation  and  change  of  brain  activity.  The  grind  of  busi- 
ness develops  but  one  side  of  their  mental  faculties.  They  need,  there- 
fore, psychic  change  even  more  than  physical  change.  All  sorts  of 
outdoor  games  and  sports  are  commendable  therefore.  Moderation 
should  be  the  rule  always  even  here. 

The  hath  is  a  powerful  agent  for  good  or  for  evil,  hence  the  ground 
for  the  extremists  who  on  the  one  hand  spend  half  their  lives  in  watei', 


8o  GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES 

or  on  the  other  indulge  in  the  luxury  once  in  two  or  three  years.     Here 
as  everywhere  moderation  and  good  judgment  are  necessary. 

CleanHness  is,  of  course,  next  to  godliness  and  should  be  a  law : 
but  except  under  some  special  conditions  it  is  not  necessary  to  spend 
the  greater  part  of  one's  existence  in  the  bathtub  to  keep  clean.  I  am 
of  the  opinion  that  many  people  bathe  overmuch  as  well  as  that  man} 
bathe  not  enough.  Here  again  each  one  must  be  a  law  unto  himself. 
As  the  bath  is,  by  reason  of  its  deliglitful  after-effects,  a  sort  of  luxury 
as  well  as  necessity,  it  can  easily  be  overindulged  in. 

Human  beings  are  not  water  animals.  I  know  of  instances  where 
the  frequent  and  prolonged  immersion  of  the  body  in  water,  the  over- 
stimulation and  excitement  induced  in  a  delicate  organism  by  too  fre- 
quent cold  plunges,  the  tenderness  and  enervation  fostered  by  too  much 
employment  of  the  hot  water,  and  above  all  by  too  frequent  rasping  of 
the  skin  with  harsh  brushes,  rough  towels  and  dirty  soaps,  have  done 
positive  harm,  though  the  practice  had  been  persisted  in  because  it  gave 
a  temporary  pleasant  feeling  and  held  out  a  fatuous  hope  of  increased 
health.  Therefore,  while  a  daily  bath  is  to  be  commended,  it  is  to  be 
adjusted  to  the  individual.  His  constitutional  needs,  his  power  of 
reaction  and  his  general  vigor  must  be  taken  into  account  when  the 
questions  are  raised  as  to  the  frequency  of  the  bath,  the  proper  tem- 
perature of  the  water,  the  duration  of  the  immersion  and  the  various 
after  procedures.  Remember,  too  much  and  injudicious  bathing  are  as 
harmful  as  too  little  or  none  at  all. 

When  a  physician  is  consulted  by  an  individual  who  already  mani- 
fests the  symptoms  of  a  definite  nervous  trouble,  it  becomes  his  first 
duty  to  search  for  and  remove,  if  possible,  the  cause.  This  may  tax  his 
ingenuity  to  the  utmost  and  call  upon  all  of  his  mediate  and  immediate 
resources.  All  of  the  therapeutic  forces  may  have  to  be  brought  into 
play  here  to  banish  the  cause-  of  the  disease,  as  well  as  the  disease 
itself.  Psychic,  disciplinary  and  pedagogical  measures  can  remove  a 
false  mentalization  which  underlies  some  cases  of  the  psychosis  hys- 
teria. A  calming  manner,  an  assurance  that  ever^^thing  is  all  right, 
an  assistance  on  the  part  of  the  physician  in  banishing  trifling  worries 
and  at  times  an  autocratic  severity  with  positive  comm.ands,  wall  do 
more  than  bottles  of  medicine.  A  wx-ak  personality,  a  hesitancy  and 
uncertainty  begotten  of  want  of  knowledge,  or  an  exposure  of  the  fact 
on  the  part  of  the  attendant  that  he  is  not  perfectly  master  of  the  sit- 
uation wall  be  sure  to  heap  trouble  upon  trouble  for  him  and  will  send 
the  patient's  symptoms  into  an  exalted  degree  of  manifestation.  It  is 
the  difference  between  doctors  themselves  in  this  respect  that  often 
causes  the  apparent  differences  between  patients  in  regard  to  their 
responsiveness  to  treatment.  This  is  so  strikingly  true  that  it  under- 
lies the  wide  variations  of  opinion  among  medical  men  in  regard  to 
nervous  diseases  and  their  management.  It  is  so  true  that  a  practitioner 
who  finds  he  is  mentally  set  all  awry  and  meets  with  constant  discour- 
agement in  his  neurological  practice,  whose  cases  go  to  his  rivals  and 
remain  under  their  treatment  and  even  get  well,  will  do  wisely  to  blame 
himself  and  endeavor  to  find  out  and  correct  his  own  shortcomings. 

Change  of   environment,   change    of    companionship,   change  of 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  Si 

thought,  suggestion,  and  even  occasionally  hypnotism,  may  have  to  be 
resorted  to  in  order  to  lift  the  patient  out  of  the  mental  state  upon  which 
his  psychosis  and  neurosis  may  largely  depend. 

The  physical  causes  of  nervous  diseases  are  so  numerous  and 
the  methods  of  attempting  their  removal  are  so  commonplace  that  noth- 
ing but  a  bare  mention  of  them  need  be  made  here.  There  are  the 
intoxications,  for  instance,  such  as  alcohol,  arsenic,  lead,  morphine, 
cocaine;  the  infections,  like  syphilis,  tuberculosis,  pneumonia,  malaria, 
influenza.  These  will  all  have  to  be  attended  to  and  removed  before 
their  nervous  sequelae  can  be  expected  to  mitigate. 

Surgical  treatment  will  be  called  for  in  removing  distant  sources  of 
infection,  like  abscesses.  Tumors  and  deformities  and  exostoses  press- 
ing upon  the  nervous  tissues  will  demand  the  first  consideration.  I 
have  seen  simple  lateral  curvature  of  the  spine  cause  a  severe  hystero- 
neurasthenic  condition.  The  dependence  of  Jacksonian  epilepsy  upon 
injuries  to  the  skull  is  well  recognized  in  some  cases.  The  origin  of 
intracranial  abscess  from  mastoid  and  ear  disease  is  all  but  universal. 

Many  nervous  diseases  need  no  further  treatment  than  simple  re- 
moval of  the  cause.  It  is  positive  malpractice  to  go  on  plying  the  pa- 
tient with  analgesic  and  antispasmodic  remedies  without  attempting 
to  discover  and  remove  the  cause.  Only  when  the  latter  is  absolutely 
impossible  is  symptomatic  treatment  justifiable. 

The  symptomatic  therapy  as  applied  to  nervous  diseases  involves 
psychic,  physical  and  medicinal  measures. 

I  have  already  referred  sufficiently  to  the  general  psychic  influ- 
ences, which  are  the  same  here  as  they  are  when  employed  in  the  pre- 
vention of  disease.  Suggestion  and  hypnotism  will  be  treated  of  more 
in  detail  in  another  part  of  the  volume.  I  will  mention  here,  however, 
that  psychotherapy  is  of  wide  application  and  includes  much  more 
than  is  usually  credited  to  it.  I  do  not  refer  to  direct  psychotherapy, 
for  that  is  acknowledged  by  every  one  to  be  a  powerful  weapon  against 
diseases  of  a  certain  order.  What  I  mean  to  say  is  that  even  indirect 
psychotherapy  is  frequently  quite  as  forceful  in  accomplishing  good. 
I  am  convinced  that  not  a  little  of  the  benefit  obtained  by  both  physical 
measures  and  drugs  is  due  in  some  cases  to  the  change  of  mentaliza- 
tion  which  they  indirectly  induce  in  the  patient.  Metallotherapy,  elec- 
tricity, massage,  mechanical  exercises,  baths  are  almost  as  efficient  in 
affecting  the  patient's  mind,  in  awakening  new  hopes,  in  dispelling 
despair,  apart  from  their  mere  physical  effects,  as  is  music  or  change 
of  companionship  or  general  environment.  In  fact,  they  constitute  a 
part  of  the  change  of  environment  and  as  novelties  cause  a  novel  train 
of  thought.  They  are  all  legitimate  means  to  use,  in  properly  selected 
cases,  for  their  psychic  as  well  as  for  their  physical  influence. 

The  physical  agents  at  our  disposal  include  those  of  hydrotherapy, 
mechanic otherapy,  electrotherapy,  massage,  gymnastics  and  surgery. 
To  treat  exhaustively  of  any  one  of  these  would  take  more  space  than 
can  be  allotted  here  and  the  reader  is  therefore  referred  to  the  numer- 
ous special  treatises  upon  them.  Some  few  general  principles  may 
not  be  improperly  enunciated,  however,  at  the  beginning  of  a  volume 
upon  nervous  diseases. 


82  CEXERAL   CONSIDERATIONS   UPON    NERVOUS   DISEASES 

There  are  nian\-  kinds  of  baths  in  vogue  to-day  for  the  treatment 
of  disease,  as,  for  instance,  the  water,  the  electric  and  the  Hght  baths. 
Even  mud,  paradoxical  as  it  sounds,  is  now  the  constituent  of  a  bath. 

Hydrotherapy  means  the  employment  of  hot  and  cold  water  to 
stimulate,  quiet  and  otherwise  modify  the  functions  of  the  nervous 
elements.  The  ice  bag  is  to  be  included,  as  that  is  a  sort  of  local  appli- 
cation of  cold  hydrotherapy. 

There  is  much  refinenjent,  some  of  it  unnecessary  in  my  opinion, 
in  the  division  and  subdivision  of  baths  in  works  upon  hydrotherapy. 

Two  great  forces  underlie  all  forms  of  the  therapeutic  use  of  water 
in  this  way.  One  is  the  thermal  force,  the  other  is  the  mechanical.  To 
be  sure,  they  are  practically  both  the  same,  for  thermal  force  is  believed 
now  to  be  due  to  the  mechanical  activity  of  molecules. 

The  modes  of  applying  hydrotherapy  involve  the  consideration  of 
the  application  to  and  the  abstraction  from  the  body  of  heat,  and  stimu- 
lating, benumbing  and  other  effects  produced  upon  it  by  the  weight, 
force  and  shock  of  the  water.  As  a  general  rule  cold  baths,  however 
applied,  are  stimulating.  If  too  long  in  duration  or  if  the  patient's 
reactive  powers  are  weak,  stimulation  passes  over  into  exhaustion. 
Cold  baths  are  not  tonic  in  the  sense  that  they  are  frequently  supposed 
to  be.  If  brief  and  employed  in  persons  of  vigorous  constitution,  they 
first  contract  then  dilate  the  peripheral  vascular  apparatus.  This  sends 
the  blood  bounding  through  the  body  and  hastens  all  the  vital  processes  ; 
hence  the  exhilaration  that  usually  succeeds  a  plunge  into  a  tub  of 
water  at  60  or  70  degrees  F.,  followed  by  a  brisk  rub.  In  a  way  a  bath 
of  this  sort  is  like  all  other  stimulants,  even  alcohol.  It  is  not  a  tonic 
per  se.  It  uses  up  quickly  pabulum,  it  heightens  all  of  the  tissue  ac- 
tivities, it  excites  into  exalted  power  the  vital  organs,  it  enlivens  the 
whole  being  even  as  alcohol  does. 

The  value  of  such  an  agent  is  incalculable,  but,  like  a  double-edged 
sword,  it  can  cut  both  ways.  It  is  pitiful  to  see  how  often  nervous  sys- 
tems that  are  worn  out  and  in  need  of  rest,  that  are  crying  loudly  for 
more  nourishment  and  less  stimulation,  are  whipped  up  by  all  sorts 
of  irrational  methods  of  cold  bathing.  Great  harm  has  been  done» 
I  am  certain,  by  the  promiscuous  use  of  the  cold  bath,  and  all  of  its 
variations,  in  neurasthenia  and  other  states  of  depression  in  which 
malnutrition  is  a  prime  factor. 

The  mechanical  effect  of  the  water  is  added  to  that  of  the  cold  by 
applying  the  bath  in  the  form  of  a  shower,  a  solid  jet  (Charcot  douche) , 
a  rain  or  a  rapid  spurting.  Alternation  of  a  hot  and  cold  jet  thrown 
against  the  body  from  a  distance  of  ten  or  twelve  feet  constitutes  the 
Scottish  douche.  Other  modes  of  applying  cold  hydrotherapy  are  the 
wet  sheet,  the  cold  compress,  the  cold  rub,  the  cold  pack  and  the  ice 
bag. 

As  a  general  rule  all  such  applications,  even  the  full  or  partial  cold 
bath,  should  be  brief  and  followed  by  thorough  drying  and  toweling 
to  provoke  a  reaction.  Two  per  cent,  of  brine  may  be  judiciously  added 
to  the  water  sometimes,  thus  simulating  it  to  a  natural  sea  bath.  Many 
of  the  medicinal  springs  where  baths  are  employed  owe  their  virtue  to 
the  coldness  of  the  water. 


GENERAL    COXSIDERATIOXS    UPOX    XERVOUS    DISEASES  83 

Extremely  hot  baths  may  be  stimulating,  but  warm  baths  as  a 
rule  are  sedative  and  tonic.  The  temperature  of  the  water  should  be 
from  90  to  100  degrees  F.  Full  baths,  partial  baths,  sitz  and  foot  baths, 
hot  wet  packs,  hot  compresses,  sprays,  douches,  fomentations  and  hot 
water  bottles  are  some  of  the  ways  in  which  heated  water  may  be 
employed.  In  the  Turkish  bath  the  body  is  first  exposed  to  a  dry  tem- 
perature anywhere  from  130  to  200  degrees  F.,  and  then  plunged  into 
cold  or  gradually  cooled  \\ater.  In  the  Russian  bath  steam  vapor  is 
used  and  with  higher  temperatures  even  than  those  of  the  Turkish 
bath.  A  method  of  applying  heat  locally  dry,  even  to  the  height  of 
400  degrees  F.,  is  by  means  of  Beck's  various  apparatuses.  The  virtues 
of  the  hot  mud,  sand  and  other  baths,  as  well  as  those  of  hot  springs 
generally,  are  due  entirely  to  the  heat.  According  to  the  degree  of  heat 
there  is  first  a  contraction  then  a  dilation  of  the  peripheral  circulation, 
which,  however,  lasts  longer  than  it  does  after  the  cold  bath.  The 
sensibility  is  lessened  and  hence  hot  baths  are  sedative  in  irritable  and 
painful  states.  A  feeling  of  complete  relaxation,  languor  and  sleepiness 
usually  follows  them.  The  metabolism  is  slightly  increased  and  the 
urea  is  more  freely  excreted.  The  pulse  and  respirations  are  at  first 
rendered  more  rapid,  but  they  soon  become  calm  and  steady.  As  a 
sedative,  therefore,  a  warm  bath  is  most  valuable.  In  its  power  of 
provoking  gentle  and  prolonged  increase  of  the  vital  forces  without 
causing  excitement  and  high  stimulation,  the  warm  bath  is  more  tonic 
than  the  cold.  If  it  is  taken  too  frequently,  however,  too  hot  or  too 
long,  it  is  enervating.  As  a  continuous  therapeutic  measure  it  is  more 
generally  useful  than  cold  baths  in  weakened  states.  Its  effects  may 
not  be  so  immediately  noticeable,  but  they  are  more  lasting  and 
nutritional. 

Meclianico-therapy,  massage  and  passive  and  active  gynuiastics 
all  belong  to  the  same  general  category.  The  basic  principle  underly- 
ing them  is  muscular  and  vasomotor  movement  by  compression,  irrita- 
tion and  stimulation.  The  variations  upon  the  principle  are  innumer- 
able and  involve  all  sorts  of  mechanical  methods  and  contrivances. 
Exercise,  local  and  general,  passive  and  active,  is  the  foundation  of 
these  muscular  methods  of  cure.  In  various  institutions  throughout 
the  land  are  elaborate  machines  whereby  patients  are  rubbed  and 
shaken  and  twisted  and  slapped  and  punched  and  rolled  and  vibrated, 
until  one  wonders  whether  human  beings  after  all  are  nothing  but 
masses  of  impressionable  dough.  One  cannot  entirely  gainsay  these 
methods,  elaborate  and  ludicrous  as  they  sometimes  are.  In  supplying 
that  which  the  mental  inertia  of  the  patient  himself  makes  wanting, 
they  do  indeed  somewhat  stimulate  the  organs  and  tissues  of  the  body. 
Like  the  Kentucky  colonel's  infallible  cure  for  a  bad  liver — namely  a 
ride  on  a  bad  saddle  horse — they  do  shake  one  up,  and  even  a  shake  has 
its  advantages.  One  wonders  what  sort  of  a  pathology,  except  that 
which  goes  with  natural  laziness  and  acquired  aboulia,  is  that  which 
can  be  cured  by  shakes  and  slaps.  If  the  patients  enjoy  it,  however, 
and  their  faddish  propensities  are  satisfied,  we  can  at  least  attribute  a. 
large  amount  of  the  benefit  to  the  psvchic  effect.  Much  of  the  talk 
about  the  dissolution  of  adhesions,  of  the  absorption  of  adventitious 


84  GENERAL    COXSIDERATIOXS    UPON    NERVOUS    DISEASES 

matter  and  the  revivification  of  the  tissues  is  the  mere  twaddle  of  ad- 
vertisement and  has  no  basis  in  fact.  Massage  and  gymnastics  are 
real  and  valuable  aids  in  the  treatment  of  nervous  troubles  and  so  far 
as  the  steam-engine,  mechanico-machine  methods  can  be  made  to  imi- 
tate intelligent  massage  and  normal  gymnastic  movements  they  are 
not  to  be  condemned. 

Massage  is  a  local  exercise  of  the  muscles  entirely  passive  in  char- 
acter. It  has  been  systematized  and  more  or  less  elaborated.  In  pro- 
voking fine  muscular  movement,  in  eliminating  local  products  of 
metabolism  and  in  hurrying  on  the  flow  of  the  blood  current  it  lends 
itself  powerfully  to  the  relief  and  cure  of  nervous  diseases.  By  blunt- 
ing the  sensibility  it  relieves  pain,  warmth  is  created  in  the  muscles  and 
on  account  of  the  circulatory  phenomena  in  them  the  latter  maintain 
their  normal  development. 

Massage  should  never  be  employed  except  with  a  full  realization 
of  the  underlying  pathological  condition  and  the  end  to  be  attained  by 
it.  In  applying  it  the  hand  or  hands  of  the  operator,  previously  oiled 
with  olive  or  cocoanut  oil  or  not,  are  used  and  the  strokes  are  always 
made  toward  the  heart  or  centers  of  the  bodv.  In  a  general  massage  it 
is  always  best  to  begin  at  the  periphery  and  work  towards  the  body. 
The  movements  consist  of  gentle,  steady,  regular  rubbing,  pinching, 
squeezing,  pressing,  kneading  and  rolling  of  the  muscles  always  in  one 
direction.  The  pressure  may  be  gentle  or  firm,  superficial  or  deep, 
brief  or  prolonged.  The  patient,  of  course,  remains  all  the  ^^  hile  abso- 
lutely quiet. 

Gentle  stroking  or  effleurage  is  perhaps  the  most  generally  used 
manoeuvre  to  begin  with.  It  consists  of  quickl}'  and  lightly  tapping  the 
muscle.  \\'hen  the  strokes  are  more  energetic  with  one  hand,  while 
the  other  hand  rubs  the  surface  to  and  fro,  the  process  is  called  massage 
a  friction. 

Tapotoncnt  or  percussion  with  the  fingers  and  kneading  are  a 
couple  of  the  frequent  ways  of  employing  massage. 

The  patient  must  never  be  wearied  by  the  treatment.  As  a  rule 
a  seance  need  rarely  last  longer  than  a  half  or  three-quarters  of  an 
hour,  often  much  less.  Usually  a  restful  and  relaxed  feeling  follows. 
If  the  patient  is  inclined  to  sleep,  he  should  be  encouraged  to  do  so. 

It  is  a  good  thing  to  give  the  massage  usually  after  the  morning 
bath.  It  should  not  be  employed  too  soon  before  or  after  a  meal.  If 
gi\-en  m  the  evening  it  is  liable  to  disturb  the  night's  rest. 

Gymnastics  are  active  or  passive.  This  is  not  the  place  to  give 
an  elaborate  description  of  them.  Passive  movements  of  all  sorts  may 
be  given  while  the  patient  is  in  or  out  of  bed.  He  may  or  may  not  be 
told  to  resist  the  operator. 

Szvedisk  inovemenis  are  of  the  nature  of  gymnastics. 

Active  gymnastics,  calisthenics  are  all  well  known  and  need  but 
to  be  mentioned  here.  The  use  of  rubber  bands,  dumb-bells.  Indian 
clubs  are  advantageous  at  times.  JModeration.  gradual  increase,  en- 
tertainment and  plenty  of  good  fresh  air  must  be  enjoin.ed  while  under- 
going gymnastic  treatment.     As  soon  as  possible  the  patient  should 


GENERAL    CONSIDERATIONS    UPON    NERVOUS   DISEASES  85 

leave  gymnastic  exercise  for  the  final  and  more  natural  exertions  that 
accompany  outdoor  walks,  games  and  sports. 

For  a  discussion  of  the  nature  of  electricity,  the  apparatuses  em- 
ployed in  its  generation,  and  the  laws  in  regard  to  its  physics  the  reader 
should  consult  special  works  upon  the  subject.  Here  only  a  brief 
outline  of  its  use  in  therapeutics  can  be  introduced. 

There  is  much  glamor  surrounding  the  subject  of  electrothera- 
peutics and  much  mystery  kept  alive  by  the  use  of  a  lot  of  unnecessary 
details  and  formulae.  Not  so  much  harm  is  done  by  the  want  of  knowl- 
edge in  regard  to  volts  and  ohms  and  zvatts  and  electromotive  force 
as  by  the  inability  to  make  a  sufficiently  correct  diagnosis  so  as  to 
know  when  and  when  not  to  use  the  electricity.  As  a  natural  force  it 
is  the  same  always,  however  it  may  be  generated.  The  strength  and 
character  of  the  current  are  variously  modified  so  that  a  slightly  differ- 
ent effect  is  produced  upon  the  tissues  by  these  variations. 

The  necessary  electrical  outfit  for  neurological  work  is  not  elab- 
orate. As  a  part,  and  a  large  part  in  my  judgment,  of  the  benefit  of 
electrical  treatment  is  to  be  attributed  to  its  psychic  effect,  an  elaborate 
display  of  apparatus  has  its  advantages.  The  physician  may,  if  he 
chooses,  imitate  the  quacks  and  obtain  some  of  the  good  results  which 
they  thus  sometimes  obtain.  For  actual  physical  electrotherapeutics, 
however,  as  I  have  said,  not  much  of  an  apparatus  is  needed. 

The  first  requisite,  of  course,  is  a  good  generator  of  the  electricity. 

Static  electricity  is  obtained  from  the  well-known  static  machine. 

Faradic  and  galvanic  electricity  are  secured  from  the  zinc-carbon, 
the  dry  silver-chloride  or  other  form  of  galvano- faradic  battery.  In  an 
office  illuminated  by  electric  light  the  electricity  may  be  obtained  by 
tapping  the  wires  and  using  the  commercial  current  after  it  has  been 
passed  through  and  is  under  the  control  of  an  appropriate  rheostat. 
A  milliampermeter  is  necessary  to  measure  the  dosage,  and  various 
electrodes  and  an  insulating  stool  with  the  static  mach'ue,  are  needed 
to  administer  it.  All  kinds  of  ingenuity  have  been  displayed  in  the 
creation  of  electrodes.  What  will  be  actually  needed,  however,  are  a 
couple  of  plain  handles,  one  about  lo  cm.  and  the  other  about  40  cm. 
long,  a  third  handle  with  an  interrupting  attachment  to  it,  an  electrode 
about  5x15  cm.  square,  another  about  10  sq.  cm.  in  area,  and  a  third 
about  I  sq.  cm.  A  soft  wire  brush  and  a  rheostat  should  also  be  among 
the  fixtvires.  With  most  static  machines  a  regular  set  of  electrodes  is 
furnished.  High  frequency  ^currents,  now  being  used  with  some  degree 
of  success,  as  well  as  the  X-ray,  need  special  apparatus. 

Perhaps  a  few  definitions  here  of  electrical  terms  may  be  allow- 
able. The  anode  is  the  positive  pole ;  the  cathode  is  the  negative.  A 
current  is  spoken  of  as  stabile  when  the  electrode  is  held  steadily  in  one 
place,  as  labile  when  it  is  rubbed  or  moved  over  a  part.  An  ascending 
current  is  one  that  is  in  a  direction  contrary  to  the  course  of  the  usual 
nerve  impulse;  a  descending  current  follows  the  course  of  the  nerve 
impulse. 

In  regard  to  the  modus  operandi  of  electricity  we  know  little  be- 
yond the  fact  that  it  is  excitant  and  stimulant.  In  spite  of  the  at- 
tractiveness of  the  thought,  it  is  probably  not  true  that  nerve   force 


86  GENERAL    CONSIDERATIOXS    UPON    XER\OUS    DISEASES 

and  electric  force  are  the  same.  As  an  irritant  it  is  more  likely  that 
electricity  excites,  and  unites  with  or  completely  annihilates  nerve  force 
according  to  its  strength,  duration,  etc.  In  this  way  it  probably  acts 
precisely"  as  any  other  physical  agent.  In  moderate  dosage  it  is  a 
stimulant  tonic  :  in  large  dosage  it  is  a  violent  excitant :  in  overwhelm- 
ing dosage  it  is  a  physical  destroyer.  In  administering  electricity  this 
mechanical  effect  of  it  must  never  be  lost  sight  of  and  the  nature  of 
the  pathological  condition — in  a  word,  a  correct  diagnosis — must  be 
established.  I  once  saw  a  complete  paraplegic  who  had  been  rendere-d 
so  immediately  after  the  second  application  of  a  strong  galvanic  current 
to  his  spine  by  a  physician  who  diagnosed  his  trouble  as  rheumatism, 
though  the  entire  histcr}-  of  the  case  for  many  weeks  previously  showed 
that  a  myelitis  of  traumatic  origin  was  present.  The  patient  died  less 
than  a  year  later,  presenting  a  typical  clinical  picture  of  transverse 
dorsal  myelitis. 

Only  in  some  of  the  neuroses,  neuralgias  and  diseases  of  the  lower 
or  peripheral  neurones  is  electricity  of  much  avail.  In  the  neuroses 
and  neuralgias  all  forms  of  electricity  may  be  usefully  employed.  In 
the  degenerative  and  trophic  troubles  of  the  lower  neuro-muscular  ap- 
paratus galvanism  and  faradism  are  the  chief  forms  to  be  relied  upon. 
Treatment  should  be  given  as  a  rule  daily  or  every  other  day  for  six 
weeks  or  longer.  In  the  neuroses  the  middle  of  the  afternoon  seems 
to  be  the  best  time.  Seances  should  average  about  thirty  minutes ; 
longer  under  some  circumstances,  shorter  under  others.  The  proper 
dosage  and  other  details  of  administration  will  be  mentioned  under  the 
head  of  the  particular  diseases  in  which  it  is  recommended.  It  may  be 
stated  here,  however,  that  for  its  psychic  effect  and  superficial  influence 
the  static  current  with  its  spark  and  other  modifications  is  probably  the 
most  useful.  Therefore  it  is  to  be  commended  in  hysteria  and  certain 
other  mild  psychoses,  in  some  neurasthenias  and  neuralgias. 

The  galvanic  current  is  probably  the  most  generally  useful.  It 
reaches  the  deeper  parts,  though  not  to  the  same  degree  as  is  some- 
times imagined,  especially  about  the  head  and  in  the  spinal  cord,  when 
employed  in  moderate  or  safe  dosage.  It  is  well  to  remember  always 
that  the  anode  is  rather  soothing  in  its  effect,  whereas  the  cathode  is 
exciting  and  irritating.  Onlv  moderate  and  accurateh  measured  cur- 
rents should  ever  be  employed. 

The  faradic  current  is  more  superficial  in  its  influence  and  is 
generally  useful  in  peripheral  nerve  and  muscular  troubles.  There  is 
no  great  difference  between  the  eflects  of  the  electrodes,  but  the  sec- 
ondary current  is  stronger  and  more  irritating  than  the  primary.  The 
dosage  of  the  faradic  current  is  usually  regulated  by  the  sensations  of 
the  patient  and  the  am.ount  of  muscular  contraction.  Dana  tabulates 
the  special  methods  of  applying  the  galvanic  and  faradic  currents  thus : 

1.  General  galvanization  and  faradization  or  general  electriza- 
tion. 

2.  Local  electrization  by  galvanization  of  the  brain,  of  the  neck, 
of  the  spine,  of  the  special  senses,  limbs  and  viscera.  Or  by  faradiza- 
tion of  the  neck,  spine,  limbs  and  viscera. 

3.  The  combined  faradic  and  gah  anic  currents.     These  are  given 


GEXER.\L    COXSIDERATIOXS   UPON    XERVOUS   DISEASES  87 

by  means  of  the  De  Watteville  switch.    General  and  local  electrization 
can  be  given  in  this  way. 

4.  The  polar  method.  This  is  employed  chiefly  in  using  the  gal- 
vanic current.  The  indifferent  electrode  is  placed  on  the  sternum  or 
back  and  the  other  electrode  applied  wherever  indicated. 

5.  Cataphoric  electrization  by  means  of  Peterson's  electrode. 

6.  Electrolytic  applications  are  used  in  enlarging  strictures  and 
affecting  inflammatory  deposits  and  neoplasms. 

Electro-diagnosis  is  referred  to  in  the  chapter  on  symptomatology 
and  the  examination  of  the  patient. 

The  factors  that  enter  into  cliiuatothcrapy  are  largely  physical  in 
character  and  involve  barometric  pressure,  purity  of  air,  temperature, 
moisture,  sunlight,  wind,  social  and  endemic  conditions.  As  a  rule 
nervous  troubles  are  not  much  directly  aft'ected  by  these  conditions, 
though  the  underlying  diatheses  upon  which  they  depend  mav  be  ver\- 
greatly  so.  In  a  general  way  neurasthenics  prefer  a  warm,  marine 
climate.  Sea  voyages  are  good  for  them,  particularly  on  account  of 
the  enforced  rest  of  mind  and  body  that  they  involve.  If  stimulation 
is  needed,  high,  rarified  inland  climates  are  to  be  recommended.  Health 
resorts,  such  as  those  of  Colorado  and  southern  California,  the  West 
Indies,  the  Riviera  and  central  Germany,  are  popular,  but  a  new  and 
virgin  soil  is  sometimes  better,  aAvay  from  the  sight  and  thought  of 
the  presence  of  other  invalids.  A  wild  ranch  life,  a  roughing  of  it  in 
the  forests  of  Canada,  even  a  year  or  more  on  a  good  ^Mississippi  \'alley 
farm,  is  to  be  preferred  to  any  popular  resort,  with  its  crowded  cara- 
vansaries, its  social  competitions  and  its  gaudy  and  shallow  artificiali- 
ties. What  a  neurasthenic  generally  needs  above  all  else  is  radical 
change  of  environment  and  of  thought  with  rest.  This  is  hard  to  ob- 
tain at  the  established  resorts. 

Little  need  be  said  here  in  regard  to  the  medicinal  treatment  of 
diseases  of  the  nervous  system.  Except  for  the  control  of  symptoms, 
medicines  play  but  a  minor  role.  Infections  and  underlying  diatheses, 
such  as  tuberculosis,  syphilis,  gout,  rheumatism  and  malaria,  call  for 
their  special  medication.  So  do  anzemia  and  other  blood  conditions. 
The  laity  have  not  yet  learned,  and  some  physicians  also,  how  little 
medicine  does  in  some  diseases ;  for  on  goes  the  expenditure  of  monev 
and  the  swallowing  of  all  sorts  of  patent  nostrums,  in  spite  of  the  fact 
that  the  pathological  conditions  show  the  utter  uselessness  of  it.  A 
badly  disciplined  girl  is  plied  with  valerian  and  asafoetida ;  an  ad- 
vanced tabetic  takes  hundreds  of  pills  of  so-called  alteratives ;  and 
hemiplegics  go  on  begging  for  some  magic  elixir  which  will  relieve 
them  of  their  imperfect  speech.  It  is  astonishing  what  crudity  of 
Ideas  and  credulity  of  belief  are  exhibited  thus  in  connection  with  dis- 
eases of  the  nervous  apparatus.  A  man  is  reconciled  to  an  amputated 
limb,  but  for  a  lost  memory  he  hunts  the  world  up  and  down  for  a 
restorative.  AA'hen  he  is  told  by  competent  authority  that  he  has  an 
incurable  valvular  heart  lesion  he  seeks  for  relief,  but  not  cure ;  when 
equal  authority  tells  him  he  has  an  incurable  optic  atrophy,  he  offers 
a  million  dollars  for  a  remedy  and  consults  with  the  most  ignorant 
and  superstitious. 


88  GENERAL    COXSIDERATIOXS    UPON    NERVOUS    DISEASES 

In  no  class  of  diseases  is  the  doctrine  of  laissez-faire  and  the  maxim 
of  ;///  noccrc  more  to  be  remembered  than  in  those  of  the  nervous  sys- 
tem. There  is'ahvays  less  danger  in  doing  too  H'ttle  than  in  doing  too 
much.  The  power  of  self-restraint  and  the  maintenance  of  a  masterly 
inactivity  should  be  learned  by  the  physician  here  if  anywhere  at  all. 
If  patients  are  clamorous,  as  they  usually  are.  that  something  should 
be  done,  be  honest  with  them.,  or  at  least  with  their  family,  and  state 
the  utter  uselessness  of  treatment  if  it  is  useless.  One's  reputation  is 
thus  guarded  and  his  conscience  put  at  ease.  If  still  the  patient  de- 
mands something,  inform  the  family  that  you  will  prescribe  a  placebo 
for  its  psychic  effect.  Everybody  will  be  happy  then,  so  far  as  hap- 
piness can  be  attained  under  the  circumstances. 

Under  no  circumstances  carry  on  a  deception  with  yourself  on 
the  one  side  as  the  deceiver  and  the  patient  and  all  his  family  on  the 
other  as  the  deceived.  Let  the  burden  be  shared  partly  by  the  family. 
It  is  legitimate  to  proceed  in  this  way  often  to  keep  a  foolish  and  self- 
willed  individual  from  the  hands  of  ignorant,  greedy  and  unscrupulous 
quacks,  both  medical  and  religious. 

Serum  Therapy  and  organotherapy  seem  to  have  a  limited  field 
of  usefulness  in  neurology.  They  are  still,  however,  in  the  experi- 
mental stage ;  except  perhaps  the  use  of  the  thyroid  gland  and  its  ex- 
tract in  cretinism  and  myxcfidema,  where  organotherapy  has  afforded 
most  brilliant  results. 


SECTION    B. 


THE    NEURONIC    DISEASES. 


Parenchymatous  Functional  and  Degenerative  Troubles. 


THE  NEURONE  AND  THE  NEURONIC  STRUCTURE  OF  THE 
NERVOUS  SYSTEM. 

I  have  already  referred  to  the  fact  that  the  nervous  system,  as  it 
is  known  in  general  anatomy,  is  a  large,  complex,  compound  organ 
with  a  more  or  less  uniform  structure  and  function  throughout  all  of 
its  parts,  but  with  an  apparent  difference  of  function  in  different  parts 
on  account  of  the  dift'erent  sorts  of  end-organs  and  tissues  with  which 
those  parts  are  respectively  connected.  Viewed  thus  as  a  single  organ, 
we  find  the  nervous  system  composed  everywhere  of  three  distinct  sets 
of  histological  elements  dividing  between  them  two  important  func- 
tions. 

The  exhibition  of  nerve  force  is  the  specific  function  of  the  nerve- 
cells  which  with  their  processes  are  now  called  neurones.  The  nour- 
ishment and  support  of  these  nerve-cells,  and  the  holding  of  them  to- 
gether in  ganglionic  masses,  constitute  the  specific  function  of  the 
neurogliar  and  connective  tissue,  blood-vessels,  lymphatics  and  epithe- 
lium. 

The  former  are  the  real  functionating  parts  of  the  nervous  system 
and  so  far  are  to  be  regarded  as  the  neural  tissues.  The  latter  does 
not  functionate  in  any  specific  way  and  accordingly  may  be  looked  upon 
as  a  non-neural  tissue. 

Neuroglia  is  not  found  outside  of  the  nervous  system  and  will 
therefore  need  a  little  further  explanation  after  I  have  considered  the 
nerve-cells. 

The  connective-tissue,  blood-vessels,  lymphatics  and  epithelium 
do  not  differ  from  the  same  elements  in  other  parts  of  the  body  and 
hence  need  no  further  description  here.  The  various  end-organs  and 
tissues  with  which  the  nerve-cells  are  in  communication,  and  through 
which  they  reveal  their  activities,  are  included  in  the  descriptions  of 
the  skin,  the  muscles,  the  organs  of  special  sense,  etc.,  in  works  upon 
general  anatomy  and  histology. 

The  Neurone  and  Neurone  Doctrine. 
Of  all  the  generalizations  of  science  none  have  been  more  brilliant, 
more  illuminating,  more  practical  than  the  Neurone  Doctrine.     Likf 


90  THE    XEUKOXIC    DISEASES 

all  these  great  scientific  generalizations,  as  for  mstance,  the  law  of 
gravitation,  the  atomic  theory  of  chemistry,  evolution,  the  nebular 
hypothesis  and  the  undulator\-  theory  of  light,  it  is  an  inference  merely, 
drawn  from  and  propounded  to  harmonize  a  great  mass  of  seemingly 
anomalous  and  unrelated  facts  and  phenomena.  It  is  not  put  forth  as 
an  infallible  truth.  It  is  open  to  future  modification,  and  if  need  be 
to  entire  annihilation,  should  future  discoveries  be  made  that  contra- 
dict its  present  teachings. 

Science,  to  be  worthy  of  the  name,  must  be  something  more  than 
a  catalogue  of  disjointed  observations.  If  it  hopes  to  escape  chaos,  or 
to  make  real  progress,  it  must  have  a  working  basis,  a  theory,  a  plan. 
a  rational  and  well-founded  idea  whereon  to  advance.  Such  is  the 
neurone  concept  first  clearly  stated  by  Waldeyer,  of  Berlin,  in  1891, 
and  modified  and  elaborated  by  the  work  of  Golgi,  Raymon  y  Cajal, 
Van  Gehuchten.  Schafer,  Sherrington,  Bethe,  Apathy.  Batton,  Held, 
Hodge,  Vas,  Barker  and  others. 

The  special  value  of  the  doctrine  lies  in  the  fact  that  it  puts  many 
hitherto  unexplained  phenomena  in  the  nervous  system  upon  a  satis- 
factorv  anatomical  basis ;  and  it  enables  one  to  comprehend  and  to 
teach  better  than  has  hitherto  been  possible,  the  various  nervous  pro- 
cesses whether  physiological,  pathological  or  psychological. 

Neurosis  and  psychosis,  organic  and  functional,  inflammatory  and 
degenerative,  are  some  of  the  terms,  bandied  about  in  neurological 
patholog}'  that  indicate  the  unsettled  state  of  much  of  our  knowledge 
even  to-day  of  the  real  nature  of  neurological  processes.  Like  a 
mariner  without  a  compass,  we  have  been  buffeted  about  upon  the 
parenchymatous  and  interstitial,  the  nuclear  and  protoplasmic,  the 
fibrous  and  cellular,  the  vasomotor  and  molecular  waves  until  we  have 
almost  despaired  of  ever  reaching  terra  firina.  The  simultaneous  ap- 
pearance of  peripheral  and  central  manifestations  in  tabes,  the  galvano- 
faradic  dissimilarities  between  the  central  and  peripheral  palsies,  the 
very  raison-d'etre  of  the  so-called  systemic  and  non-systemic  diseases 
have  hitherto  received  but  scant  explanation.  And  as  far  as  the  pathol- 
ogy of  the  hcte-noire  of  medicine,  hysteria,  the  imagination  has  toved 
in  our  ignorance  riotously  with  it  or  in  hopeless  despair  left  it  severely 
alone. 

The  neurone  theory,  with  all  its  imperfections  and  unanswered 
questions,  and  founded  as  it  is  upon  a  limited  number  of  facts,  sends 
a  brilliant  ray  of  light  into  this  mass  of  darkness  and  promises  con- 
gruity  where  all  has  been  incongruous.  The  following  statements  in 
connection  with  the  theory  seem  to  be  warrantable  at  the  present  time : 

a.  The  nervous  system  is  not  a  uniformly  continuous,  united 
entity,  but  is  made  up  of  a  mass  of  distinct  and  disconnected  nervous 
units.    Discontinuity  is  the  rule. 

h.  These  nervous  units  (neurones),  each  consisting  of  a  cell- 
body  with  processes,  have  taken  the  place  of  the  cells  and  fibres  of  the 
older  histology. 

c.  Xo  cell-body  is  connected  with  any  other  cell-body :  nor  do  its 
processes  anastomose  with  those  of  its  neighbors. 

d.  The  terminal  processes  of  neighboring  neurones  intermingle 


THE    XEUROXIC    DISEASES  gi 

^without  anastomosing.  Sometimes  the  terminal  branches  of  the  pro- 
cesses of  one  neurone  surround  and  immesh,  as  in  a  net,  the  body  of  a 
neighboring  neurone.  This  is  spoken  of  as  an  arborization,  a  teloden- 
-drion,  or  a  synapse. 

e.  The  ceh-body  is  for  the  nutrition  of  the  neurone  while  its  pro- 
■cesses  are  for  the  transmission  of  nervous  impulses. 

The  following  deductions  form  parts  of  the  theory,  but  as  }'et  have 
not  been  completely  established : 

a.  In  some  instances,  minute  neuroiibrils  may  anastomose  and 
■connect  directly  sensory  with  motor,  and  motor  with  sensory  elements. 

b.  Xerve  force  or  nervous  excitability  is  a  quality  of  the  entire 
neurone  (cell-body  with  its  processes)  and  is  not  merely  a  force  evolved 
hy  the  cells  alone  and  then  sent  out  along  various  nerve  fibres. 

c.  Afferent  and  efferent  are  relative  terms,  since  strictly  speaking 
there  are  no  currents  in  the  neurones,  but  merely  states  of  excitability. 

d.  Neurones  are  sensory  or  motor  in  ftmction.  solely  according 
to  the  nature  of  the  end-organs  with  which  they  are  respectively  con- 
nected. 

e.  Xervous  excitability  or  nervous  impulse  is  in  all  probability 
a  molecular  force,  involving  changes  within  the  substance  of  the  neu- 
rone. 

f.  The  neurones,  or  at  least  their  terminal  processes,  are  en- 
•dowed  with  a  low  grade  of  amoeboid  movement.  This  is  very  ques- 
tionable. 

g.  By  means  of  this  amoeboid  (expansion  and  contraction)  move- 
ment, the  terminations  of  neighboring  processes  are  made  to  approxi- 
mate and  separate  from  one  another.  This  enables  one  neurone  to 
■excite  or  transmit  its  owm  excitability  to  the  neighboring  neurones. 
This  is  extremely  doubtful. 

h.  In  some  instances,  this  nervous  excitability  may  be  transmit- 
ted from  one  process  to  a  neighboring  process  by  means  of  the  inter- 
"vening  neurogliar  elements  which  are  derived  from  the  same  blasto- 
■dermic  layer  as  the  neurones  themselves  are. 

The  Neurone.  The  neurone  or  nerve-unit  consists  of  a  nucleated 
■cell-body  with  a  dozen  or  more  processes.  These  processes  are  not 
nerve  fibres,  but  extensions  from  the  cell-body.  One,  or  at  most  two, 
•of  them  are  very  long  and  are  called  neuraxones:  the  others  are  shortand 
are  named  protoplasmic  processes  or  dendrites.  A  neuraxone  consists 
•of  an  axis-cylinder  surrounded  by  a  medullary  substance.  Outside  of  the 
central  nervous  system,  the  medullary  substance  is  again  surrounded 
"by  a  nucleated  covering  known  as  the  neurilemma.  Each  axis-cylinder 
IS  composed  of  a  number  of  primitive  fibrils,  held  together  by  a  kind  of 
cement-like  substance.  Obersteiner  has  coimted  as  many  as  fifty  fibrils 
in  one  axis-cylinder  of  the  sciatic  nerve  oh  a  frog.  It  is  readily  under- 
-stood,  therefore,  how  the  distal  ends  of  the  neuraxones  may  split  up 
into  numerous  brush-like  branches  (arborization),  and  how  along  their 
•course  they  may  give  off  at  right  angles  short  lateral  branches  (col- 
laterals), which  also  terminate  in  an  arborization.  These  primitive 
fibrils  of  the  axis-cylinder,  when  traced  backward  into  the  cell-body, 
are  seen  to  pass  without  interruption  through  the  cell-substance,    or 


92 


THE    XEURONIC    DISEASES 


FIGURE  17. 


Diagram  of  a  lower  motor  neurone.  (After  Barker.)  D,  a  motor  cell  from 
anterior  horn  of  the  cord  with  its  protoplasmic  processes.  Ax,  axis-cj^Iinder 
process.  S  F,  collaterals.  M,  medullar}'  sheath.  X  R,  node  of  Ranvier.  N  of 
N,  nucleus  of  neurilemma.  Tel,  the  ending  in  striped  muscle-fibre,  M'.  N,  the 
nucleus,  and  N'  nucleolus  of  the  cell-bodv. 


THE    NEURONIC    DISEASES 


93 


to  bend  within  the  cell-body  and  terminate  in  one  or  more  of  the  short 
processes  or  dendrites.  On  the  other  hand,  the  fibrils  of  the  dendrites 
do  not  all  pass  into  the  nenraxone  but  some  of  them  cross  through  the 
•cell-body  and  continue  on  into  the  other  dendrites. 

The  cell-body  itself,  sometimes  called  the  perikaryon,  consists  of 
a  mass  of  protoplasm  inclosing  a  nucleus  and  a  nucleolus.  It  measures 
from  1-3500  to  1-250  of  an  inch  in  diameter.  Its  contents  are  com- 
posed of  a  semifluid  albuminous  substance,  like  the  white  of  an  &gg, 
and  is  spoken  of  as  the  protoplasm  or  cytoplasm.  Within  this  cyto- 
plasm lies  the  nucleus,  inclosing  the  nucleolus.  The  cell-body  proper 
is  a  network  of  granular  fibres,  between  which  is  the  viscid  fluid  called 
the  paraplasm.     In   this   network   are   the   chi'omophyUic   granules   of 

FIGURE  18. 


Golgi  cell  of  Type  I.  From  the  optic  tract  of  a  cat.  The  axis-cylinder  or 
neuraxone  is  only  moderately  branched,  giving  off  collaterals  at  points  marked  c. 
The  dendrites  are  numerous  and  abundantly  branched.     (After  Kolliker.) 

Nissl  which  stain  deeply  with  aniline  dyes.  Not  all  cells  possess  these 
granules.  Those  that  do  not  are  called  somatochromes,  while  the  others 
are  named  karyochromes.  These  granules  are  thought  to  contain  the 
nutrient  substance  of  the  cell-body,  while  its  functional  activity  is  sup- 
posed to  depend  upon  the  paraplasm.  A  trace  of  pigment  is  usually  a 
•constituent  of  the  cell-body. 

The  nucleus  and  nucleolus  are  both  likewise  reticulated  and  stain 
deeply.  Such  in  brief  is  the  minute  anatomy  of  a  neurone,  the  ultimate 
unit  of  the  functionating  or  excitable  part  of  the  nervous  system. 

There  are  three  types  of  neurones,  which  differ,  however,  more 
in  degree  than  in  kind.  They  are  the  motor,  the  sensory  and  the  sym- 
pathetic. 

The  motor  is  the  simplest.  An  example  of  it  may  be  seen  in  the 
cell-body  found  imbedded  in  the  anterior  horn  of  the  spinal  cord,  with 
its  dozen  or  more  dendrites  extending  for  a  short  distance  in  all  direc- 
tions, even  into  the  posterior  horn,  and  its  single,  long  neuraxone  pass- 
ing out  through  the  anterior  root  to  its  termination  in  some  distant 
muscle-plate  or  motor  end-organ. 


94  THE    NEURONIC    DISEASES 

The  sensory  neurone  is  somewhat  more  complex.  It  may  be  seert 
with  its  cell-body  resting  midway  in  its  make-up  in  the  ganglion  of 
the  posterior  spinal  root  and  its  two  processes  extending  in  opposite 
directions,  one  going  out  to  the  skin  or  distant  special  end-organ  of 
sense,  and  the  other  passing  up  through  the  posterior  root  into  the 
cord  as  far  even  as  the  medulla  oblongata.  This  neurone  is  sometimes- 
described  as  though  its  neuraxone  were  bifurcated  shortly  after  it  had 
left  the  cell-body  and  the  two  branches,  T-like,  were  directed  in  oppo- 
site ways.  It  is  better,  however,  to  regard  the  central  process  as  the 
neuraxone  and  the  peripheral  process  as  a  modified  dendrite. 

The  sympathetic  neurone  partakes  of  the  nature  of  both  of  those 
just  described,  but  its  neuraxone  is  non-medullated. 

FIGURE  19. 


Golgi  cell  of  Type  II.  From  the  cerebrum  of  a  cat.  (a)  Axis-cylinder  is  very 
much  branched.  The  dendrites  are  coarse  and  are  covered  with  "thorns"  or 
"gemmules."     (From  KolHker.) 

The  accompanying  illustrations  will  show  some  other  character- 
istics and  other  subsidiary  types  of  neurones.  Note  the  enormous  num- 
ber of  dendrites  in  the  Golgi  cell  of  this  author's  type  I  and  the  pecu- 
liar "thorns  or  "gemmules"  on  some  of  them  in  his  type  II.  Observe 
the  enormously  complex  arborization  of  the  Purkinje  cell  process  illus- 
trated by  Van  Gehuchten. 

In  regard  to  the  physiology  of  the  neurone,  the  experiments  of 
Hodge,  Xissl,  Vas,  Mann,  and  others  are  fascinating  in  the  extreme. 
The  movements  of  the  so-called  chromatin-bodies  and  of  the  peculiar 
dumb-bell-shaped  objects  in  the  midst  of  the  mass  of  crossing  and  re- 
crossing  fibres  within  the  cell  have  been  distinctly  observed  and  por- 
trayed. Nissl  even  goes  so  far  as  to  assert  that  the  arrangement  and 
movements  of  these  intracellular  fibrils  and  chromatin-bodies  enable  us 
to  distmguish  motor  from  sensory  cells.     His  views  in  this  respect. 


THE    NEURONIC    DISEASES  95 

however,  have  not  been  universally  accepted.  The  activity  of  the  neu- 
rone results  in  a  diminution  in  the  size  of  its  cell-body,  a  lessened 
power  for  absorbing  stains  (diminished  power  of  assimilation),  vacuo- 
lation  (the  using  up  of  its  own  substance)  and  a  marked  alteration  in 
the  contour  of  the  nucleus  from  a  smooth  and  round  to  an  irregular 
and  jagged  edge.  Gentle  stimulation  of  the  cell  causes  it  to  swell  and 
the  chromatin  bodies  to  move  towards  its  periphery.  Overstimulation 
results  in  a  shriveling  up  of  the  celh  and  a  complete  or  almost  com- 
plete disappearance  of  the  chomatin  bodies.  The  dumb-bell  bodies, 
under  the  same  conditions,  stain  more  deeply  and  do  not  disappear. 
Mere  activity,  over-exhaustion,  poisoning  from  retained  excrementi- 
tious  products  (auto-intoxication)  or  from  toxins  introduced  from 
without,  such  as  alcohol,  absinthe  and  nicotine  will  all  provoke  the 
same  histological  changes  in  the  neurone.  Rest  restores  its  normal  ap- 
pearance, but  only  after  a  considerable  lapse  of  time.  This  goes  a  long 
way  to  prove  that  the  main  function  of  the  cell-body  is  the  nutrition  of 

FIGl^RE  20. 


A  Purkinje  cell  of  the  cerebellum,  illustrating  a  marvellously  complex  abori- 
zation  of  a  single  neuraxone  pr.  cyl.      (After  Van  Gehuchten.) 

the  entire  neurone.  It  likewise  is  not  a  little  suggestive  of  the  true 
nature  of  many  of  the  nervous  diseases,  of  the  cause  of  many  of  their 
peculiar  manifestations,  and  the  direction  in  which  a  restoration  of  the 
integrity  of  the  nervous  apparatus  is  to  be  looked  for. 

The  neurones  are  developed  from  the  neuroblasts  of  the  embryo, 
which  in  turn  are  evolved  from  the  epiblastic  layer  of  the  developing 
jvum.  The  figure  after  J-  Kollmami  shows  admirably  the  different 
stages  of  the  development  of  the  neurones. 

The  neuroglia  consists  of  a  peculiar  variety  of  cells  which  are 
found  only  in  the  nervous  system  and  which  are  developed  from  the 
spongioblasts  of  the  embryo.     These  cells  seem  to  have  no  other  func- 


96 


THE    NEURONIC    DISEASES 


tion  than  to  form  a  supporting  network,  scaffolding  as  it  were,  for  the 
neurones.  Until  quite  recently  the  neuroglia  was  spoken  of  as  a 
variety  of  connective  tissue.  It  is  unlike  the  latter,  however,  in  be- 
ing developed  from  the  epiblastic  instead  of  the  mesoblastic  layer  of 
the  growing  ovum,  and  in  containing  the  peculiar  chemical  substance 
neurokeratin,  which  is  a  variety  of  the  keratin  seen  in  the  hair,  nails 
and  epidermis. 

The  neurogliar  cells  are  sometimes  called  "spider  cells"  because 
of  the  relatively  small  size  of  the  body  and  tlie  very  numerous  and 

FIGURE  21. 


Epcndyma   ...X^^i. 


Spongioblast 
Cermiaul  cell 


Mfdullary  tube V 


^ . Substantia 

grisea: 

A 


—  Substantia 
alba. 


-  Dendrites 


Axones  of  (mo- 
/     tor)     ventral 
root. 


''-  Neuroblast. 


Transverse  section  of  the  spinal  cord  of  the  chick  to  show  the  neurones  in 
the  different  stages  of  development.  Right  side  is  from  a  five  day  chick ;  the 
left  side  from  a  two  day  chick.     (After  Kollmann.) 

highly  ramified  processes.  The  body  is  varied  in  size  but  is  more  or 
less  round  in  shape.  It  consists  of  granular  protoplasm  in  which  is 
imbedded  a  large  nucleus  with  a  nucleolus.  So  fine  and  numerous  are 
the  processes,  that  where  the  neuroglia  is  found  in  abundance,  as  for 
instance,  around  the  central  canal  of  the  spinal  cord,  in  the  periphery 
of  the  cord,  beneath  the  ependyma  of  the  ventricles  of  the  brain  and 
below  the  pia  mater,  the  tissue  resembles  almost  a  homogeneoius  matrix. 
According  to  Weigert  the  processes  stain  differently  from  the  cell- 
body  and  thus  would  seem  to  have  a  different  composition  both  chem- 
ically and  physically.  In  states  of  inflammation  the  neurogliar  cells 
are  seen  to  swell  up  and  serve  as  scavenger  cells  in  carrying  off  noxious 
products. 

The  Neuronic  Architecture  of  the  Nervous  System. 

Having  now  studied  the  elements  that  enter  into  the  composition 
of  the  nervous  system  and  learning  that  the  functionating  neurones, 
according  to  Donaldson,  make  up  fifty-three  per  cent,  of  its  bulk  (at 
least  in  the  brain  and  spinal  cord),  while  forty-seven  per  cent,  con- 
sists of  the  sustentacular  tissue   (neuroglia  and  connective  tissue  net- 


THE    XEL'ROXIC    DISEASES 


97 


work),  it  remains  to  be  seen  how  these  elements  are  arranged  in  rela- 
tion to  one  another  in  the  architecture  of  the  sum  total  or  completed 
apparatus. 

Imbedded  in  the  sustentacular  tissue  everywhere  are  the  innu- 
merable neurones.  Each  neurone  constitutes  a  unit  in  itself,  so  that 
it  is  quite  improper  to  speak  of  nerve-cells  and  nerve-fibres  as  distinct 
and  separate  structures. 

The  aggregate  of  all  these  countless  neurones  constitutes  the  real 
functionating  nervous  apparatus  and  their  disease  alone  constitutes 
real  inherent  nervous  disease.  They  are  not  scattered  promiscuously, 
however,  throughout  the  meshwork  of  supporting  tissue  but  are  more 
or  less  regularly  grouped  and  arranged,  both  in  relation  to  particular 
parts  of  the  body  and  in  relation  to  one  another. 

FIGURE  22. 


Glia  cells  from  the  cerebral  cortex  of  a  rabbit.     (After  Benda.) 


Upon  this  grouping  we  have  established  certain  artificial  gross 
anatomical  divisions  of  the  nervous  system,  such  as  the  brain,  the  spinal 
cord,  the  peripheral  nerves  and  the  sympathetic  system.  These  divis- 
ions, however,  are  arbitrary,  for  the  neurones  which  we  find  in  them 
are  alwa_ys  the  same  in  all  essentials. 

Somewdiat  more  significant  than  these  gross  anatomical  sub- 
divisions of  the  nervous  system,  is  its  obvious  arrangement  into  masses 
of  gray  and  vjhite  matter.  A  close  examination  of  this  reveals  the  fact 
that  what  is  called  gray  matter  is  only  the  anatomical  bunching  together 
of  the  bodies  of  the  neurones,  while  the  white  matter  represents  the 
assemblage  in  close  proximity  of  their  neuraxones.  In  the  sympa- 
thetic ganglia,  in  the  ganglia  on  the  posterior  spinal  nerve  roots,  in  the 
:gray  matter  of  the  central  cord,  in  the  ganglia  and  nuclei  of  the  cranial 
nerves,  in  the  optic  thalami  and  corpora  striata,  in  the  cortex,  and  in 
fact  wherever  this  so-called  gray  matter  is  found,  there  are  congre- 
•gated  in  close  quarters  the  bodies  of  the  neurones.  In  the  spinal 
nerves,  in  the  white  columns  of  the  cord,  in  the  centrum  ovale  of 
the  brain,  and  wherever  else  so-called  white  matter  is  observed,  there 


gS  THE    NEURONIC    DISEASES 

run  the  neuraxones  extending  out  from  the  cell-bodies  of  the  neu- 
rones. It  is  obvious,  therefore,  that  there  is  no^  very  great  signifi- 
cance to  be  attached  to  this  subdivision  of  the  nervous  tissue,  namely, 
into  gray  and  white  matter. 

It  is  clear  that  the  anatomical  and  functional  relationship  of  the 
individual  neurones  themselves  to  one  another  is  the  great  and  im- 
portant underlying  fact  in  the  structure  and  specific  activity  of  the 
nervous  system.  There  is  no  single  neurone  anywhere  in  the  body 
whose  extent,  with  the  aid  of  its  neuraxone  and  dendrites,  is  so  enor- 
mous that  it  can  reach  from  one  extreme  end  of  the  nervous  system 
to  the  other.  And  yet  we  know  that  both  afferent  and  efferent  im- 
pulses traverse  the  entire  length  and  breadth  of  the  body.  They  must 
clearly,  therefore,  pass  over  several  successive  neurones  in  their  long 
journeys.  There  is  an  end-to-end  arrangement  of  the  neurones  of  the 
A^arious  functional  pathways  along  which  the  impulses  travel  between 
center  and  periphery.  It  is  necessary  to  be  familiar  with  the  construc- 
tion of  these  afferent  and  efferent  pathways,  to  know  just  where  and 
how  their  constituent  neurones  begin  and  terminate,  and  to  comprehend 
what  functional  relationship  one  neurone  bears  to  its  neighbor  when 
both  are  constituents  of  the  same  direct  and  single  pathway. 

In  an  earlier  paragraph  I  described  three  typical  forms  of  neu- 
rones and  showed  that  whereas  their  differences  were  not  essentially 
important,  they  subserved  respectively,  motor,  sensory  and  sympathetic 
functions.  Other  types  of  neurones  might  have  been  described,  espe- 
cially in  the  cortex,  the  commissural,  and  the  association  tracts  of 
the  brain.  In  all  essentials,  however,  they  are  practically  the  same. 
If  I  describe  the  afferent  and  efferent  projection  paths  upon  the  basis 
of  their  neuronic  constituents,  it  will  suffice  to  indicate  the  general 
neuronic  architecture  of  the  entire  nervous  system.  The  principle 
imderlying  it  will  have  been  portrayed.  Future  discoveries  may  en- 
large our  ideas  but  it  hardly  seems  probable  that  any  very  great  alter- 
ation in  the  general  principle  of  construction  will  ever  hereafter  be 
made. 

The  entire  length  of  the  pathway  for  all  motor  impulses  from 
brain  to  muscle  seems  to  be  made  up  of  two  long  neurones,  placed 
end-to-end.  Of  course  it  must  be  understood  that  the  aggregate  motor 
tracts  are  constituted  of  a  great  number  of  neurones  lying  side  by  side. 
Longitudinally  considered,  however,  each  individual  outgoing  impulse 
must,  after  it  leaves  the  brain,  traverse  two  neurones  before  it  ex- 
pends itself  upon  the  appropriate  muscle.  The  first  or  central  neurone 
has  its  body  imbedded  in  the  cortex  near  the  fissure  of  Rolando  and 
projects  its  neuraxone  down  through  the  cerebral  crura  and  the  pvra- 
midal  tracts  of  the  cord,  to  its  termination  in  an  arborization  around 
some  cells  in  the  cranial  nuclei  of  the  medulla  or  in  the  anterior  horns 
of  the  cord.  The  second  or  peripheral  neurone  has  its  body  nestling 
in  a  cranial  nucleus  or  anterior  horn  and  extends  its  neuraxone  out 
through  the  nerve  to  the  end-plate  of  the  muscle  it  is  created  to  sub- 
serve. 

The  two  sections  of  this  pathway  may  well  be  named  cortico-spinal 


THE    NEURONIC    DISEASES 


99 


and  spino-muscular  respectively.  The  central  neurone  inhibits,  stimu- 
lates, controls  and  regulates  the  action  of  the  peripheral  neurone.  It 
moreover  assists  in  maintaining  its  nutrition.  The  peripheral  neurone 
on  the  other  hand  stimulates  the  contractions  of  the  muscle  and  pre- 
sides over  its  nutrition. 


A.C.N 


FIGURE  23. 


Multipolai 

Cell  of  Ant 

Horn 


Schema  of  the  relationship  of  the  neurones  in  the  sensory  and  motor  path- 
ways between  the  brain  and  the  periphery.     (After  Halliburton  and  Mott.) 


The  pathway  for  the  afferent  or  sensory  impulses  is  inore  com- 
I)lex  and  as  a  rule  is  made  up  of  a  number  of  end-to-end  neurones. 
The  outermost  or  peripheral  neurone  has  its  body  hidden  away  in  the 
ganglion  on  the  posterior  spinal  nerve-root.  As  a  modified  dendrite' 
one  of  its  processes  extends  outward  in  the  nerve  to  the  skin,  or  some 
special  end-organ,  while  the  neuraxone  passes  inward  and  upward  to 


lOO  THE    NEUROXIC    DISEASES 

the  spinal  cord  to  terminate  in  an  arborization  around  the  cells  at 
the  top  of  the  column  of  JJurdach  and  Goll.  These  ceils  constitute  the 
bodies  of  the  next  succeeding  neurones  whose  neuraxones  again  pass 
upward  to  terminate  in  an  arborization  around  the  cells  found  lying  in 
the  optic  thalamus.  These  cells  once  more  extend  their  neuraxones  up- 
ward to  terminate  and  arborize  around  the  cell-bodies  of  other  neurones 
imbedded  in  the  cerebral  cortex. 

There  are  great  variations  in  the  neuronic  arrangement  of  the 
sensory  paths.  They  will  be  discussed  somewhat  more  in  detail  when 
the  anatomy  and  physiology  of  the  brain  and  spinal  cord  are  taken 
up.  Here  I  merely  wish  to  call  attention  to  the  fact  that  the  afferent 
and  efferent  paths  between  the  brain  and  the  periphery  are  formed 
of  a  series  of  neurones  placed  end-to-end.  that  make  the  progress  of 
the  impulse  a  step-like  one.  There  are  special  neurones  and  neuronic 
paths  that  do  not  emerge  from  the  central  nervous  system  at  all  but 
serve  to  connect  different  parts  of  it  together  and  to  approximate  the 
inner  ends  of  the  various  projection  paths.  In  fact  we  are  only  on 
the  threshold  of  knowledge  in  regard  to  the  bewildering  interlacement 
of  all  these  countless  neurones.  It  is  hardly  probable  that  what  we 
denominate  commissural,  associative  and  projection  tracts  contain 
all  of  the  neurones  that  it  is  possible  for  us  to  know  later.  Indeed  we 
have  still  a  goodly  amount  to  learn  in  regard  to  these  even,  and  the 
future  will  doubtless  reveal  to  us  greater  complexities  in  the  innumer- 
able pathways  by  which  impulses  travel  hither  and  yon  and  in  and  out  of 
the  nervous  system.  When  we  will  have  learned  more  of  these  pathways, 
we  will  doubtless  be  able  to  understand  some  diseases  that  are  now  un- 
explainable.  Already  we  are  sufficiently  acquainted  with  some  of  them 
to  enable  us  to  classify  some  organic  and  functional  troubles  in  accord- 
ance with  their  location. 

There  are  some  diseases  that  seem  to  have  their  seat  entirely 
within  the  neurones.  Pathologically  and  symptomatically  they  are,  in 
the  literal  sense  of  the  word,  nervous  diseases.  The  surrounding  tis- 
sues may  not  be  affected  at  all  in  them  or  only  secondarily  so  later  on. 
Etiologically,  heredity,  toxsemic  and  general  cachectic  states  play  the 
most  important  role  in  their  development.  Sometimes  the  heredity 
is  direct,  at  other  times  it  is  indirect.  The  inheritance  may  range  all 
the  way  from  a  mere  neuropathic  tendency  to  an  actual  and  gross  de- 
fect. So  influential  are  the  inherited  and  congenital  conditions  in  the 
development  of  these  diseases  that  it  is  doubted  by  some  whether  with- 
out such  a  neuropathic  predisposition  these  diseases  would  ever  appear 
as  a  result  of  the  exciting  causes  usually  given  for  their  appearance. 
It  is  not  believed  by  many  that  mere  strain,  exposure,  overexertion, 
intoxication  or  infection  would  ever  induce  a  pure  neuronic  disease  if 
the  neurones  themselves  were  not  previously  predisposed  by  an  inher- 
ited weakness.  It  is  contended  that  such  active  causes  would  produce 
in  those  who  were  endowed  with  a  vigorous  heredity,  diseases  of  the 
other  tissues  also,  such  as  hemorrhage  and  inflammation. 

We  divide  these  diseases  nevertheless  into  the  inherited  and  the 
acquired.     This  is  a  convenient  division  for  practical  purposes  but  it 


THE    NEURONIC    DISP:ASES  IOI 

is  about  as  strictl_y  scientific  and  logical,  in  view  of  what  we  already 
know,  as  would  be  their  division  into  organic  and  functional. 

All  diseases  in  their  last  analysis  must  logically  be  assumed  to  be 
organic.  A  change  of  function  to  that  which  is  non-function  presup- 
poses by  all  the  laws  of  reason,  a  change  m  the  functionating  substance. 

Organic  and  functional  are  relative  terms  to  indicate  the  efficiency 
and  inefficiency  of  our  present  means  of  investigation.  The  pains  of 
tabes  differ  only  in  degree,  and  sometimes  not  at  all,  from  the  pains  of 
idiopathic  neuraglia,  and  yet  merely  because  we  can  see  the  degen- 
erated conditions  in  the  former  we  speak  of  it  as  an  organic  disease, 
while  the  unseen  changes  in  the  latter  we  denominate  functional. 

Pathologically  there  is  in  all  probability  a  mere  difference  of  de- 
gree rather  than  of  kind  between  the  so-called  organic  and  functional 
neuronic  diseases.  A  neurosis  is  a  degenerative  trouble  as  truly  as 
is  a  wasted  condition  of  the  neurones  in  some  form  of  systemic  disease. 
It  may  be  a  more  widely  diffused  or  a  lesser  degree  of  degeneration, 
but  that  it  is  a  condition  of  functional  and  therefore  inherent,  degen- 
eracy can  not  be  reasonably  gainsaid.  To  conform  with  popular  usage, 
however,  particularly  as  we  are  in  need  of  many  data  to  make  our  con- 
tention absolutely  undeniable,  J  will  continue  to  divide  the  neuronic 
affections  into  the  organic  and  functional.  As  some  of  the  former  con- 
fine themselves  to,  or  at  least  begin  in,  a  particular  set  of  neurones,  they 
may  be  further  subdivided.  In  a  gross  way  the  same  is  true  of  the 
neuroses. 

The  following  seems  to  me  to  be  a  warrantable  classification  of  the 
pure  neuronic  diseases: 

The  Functional  Neuronic  Diseases. 

(Neuroses  and  Psychoneuroses.) 

1.  Those  of  the  Cerebrospinal  System. 

2.  Those  of  the  Sympathetic  System. 

The  Organic  Neuronic  Diseases. 

(System  Diseases.) 

1.  Those  of  the  Aff'erent  System. 

2.  Those  of  the  Efferent  System. 

3.  Those  of  the  Afferent  and  Efferent  Systems. 

FUNCTIONAL  NEURONIC  DISEASES. 

THE  NEUROSES. 

All  disease  must  be  functional  in  its  incipiency.  Some  diseases 
remain  functional ;  others  go  on  to  cause  slight  or  minute  changes  un- 
discoverable  by  our  present  means  of  investigation ;  while  still  others 
advance  to  the  production  of  gross  microscopic  and  macroscopic  altera- 
tions, much  destruction,  and  even  annihilation  of  tissue.  The  latter 
changes  we  can  see  and  so  we  call  them  Organic ;  the  former  we  cannot 
see,  and  so  we  still  must  denominate  them  Functional. 

This  use  of  the  term  functional  has  come  to  be  specific.  We  do 
not  include  the  gross  organic  diseases  in  the  class  of  functional  troubles, 


102  IIIE    N'L-L'[<OXIC    DISF.ASKS 

thoug-h  as  a  matter  of  fact  they  involve  even  greater  functional  dis- 
turbances than  do  the  latter. 

The  specifically  called  functional  diseases  are  sometimes  denomi- 
nated the  Amauroses.  As  these  diseases  are,  so  far  as  we  can  deter- 
mine, the  result  of  hereditary,  nutritional,  hygienic  and  general  toxsemic 
influences,  they  implicate  all  of  the  neurones.  They  are  diseases, 
therefore,  of  the  nervous  apparatus  more  or  less  /;/  toto.  and  from  their 
inherent  nature  are  the  most  specific  of  all  those  of  the  nervous  system. 
They  are  dififuse  affections  within  the  neuronic  network.  They  there- 
fore are  sometimes  called  the  Psychoiieuroscs.  They  do  not  all  present, 
for  some  reason  unknown  to  us,  exactly  the  same  degree  of  vividness 
in  their  mental,  sensor}-  and  motor  manifestations.  Some  of  them,  like 
hysteria,  take  on  a  psychic  complexion ;  others,  like  hemicrania,  lead 
with  sensory  phenomena ;  still  others,  like  the  myospasms,  seem  almost 
to  be  entirely  motor. 

The  characteristic  of  these  neuroses  or  psychoneuroses  is  that 
they  all  present  a  clinical  picture  in  which  all  forms  of  nen^ous  symp- 
toms appear,  though  not  in  all  patients  nor  in  all  periods  of  the  disease. 
Their  dift'use  localization  is  well  represented  in  the  name  psycho- 
neuroses. 

The  hereditary  psychoneuroses  are  of  the  nature  of  biological 
defects.  They  are  instances  of  racial  or  familial  degeneracy.  Thev 
bespeak  a  functional  inadequacy  in  the  neurones  as  a  result  of  an 
embryological  degenerative  inferiority  in  their  structure.  As  diseases 
they  are  therefore  not  hopeful  from  the  standpoint  of  prognosis  or 
therapy. 

The  congenital  psychoneuroses  are  hardly  much  more  favorable. 

The  acquired  psychoneuroses  are  somewhat  more  encouraging, 
though  as  some  heredity,  less  in  intensity  perhaps,  plays  a  role  in  their 
evolution,  they  are  at  times  obstinate  and  need  both  judicious  and 
decisive  management.  Their  prognosis  under  given  conditions  is  ex- 
ceedingly bright. 

We  can  conveniently  divide  the  psychoneuroses  into  those  whose 
symptoms  point  most  prominently  to  the  cerebrospinal  apparatus  on  the 
one  hand,  or  to  the  sympathetic  system  on  the  other.  The  functions 
of  the  latter  are  so  markedly  distinctive  that  when  they  are  deranged 
we  sometimes  refer  to  them  as  angioneuroses  or  trophoneuroses.  It 
goes  without  saying,  of  course,  that  this  classification  is  liable  to  modi- 
fication under  the  development  of  future  knowledge. 

A.      THE  CEREBROSPINAL  XEUR(JSES.      PSYCHONEUROSES. 

HYSTERIA. 

Hysteria  is  recognized  at  the  present  day  as  a  mental  trouble, 
which,  unlike  the  forms  of  psychosis  usually  classified  under  the  old 
term  insanity,  reveals  itself  more  distinctively  through  the  motor, 
sensory  and  trophic  apparatuses  than  they  do.  The  paralyses,  anesthe- 
sias and  other  stigmata  of  the  disease  are  clearly  mental  in  origin. 
Moreover,  the  disturbances  of  the  memory,  volition  and  intellect,  caus- 


THE    NEURONIC    DISEASES 


103 


ing  a  greater  or  less  transformation  of  the  patient's  personality,  the 
ego,  indicate  the  psychic  nature  of  the  disease. 

The  resemblance  of  many  of  the  phenomena  allied  to  hysteria, 
such  as  the  histrionic  manifestations,  the  mimicries,  the  hypnoses,  the 
catalepsies,  the  somnambulistic  actions,  as  well  as  the  character  of  the 
typical  hysterical  symptoms  themselves,  have  inclined  most  authors  to 
regard  the  trouble  as  largely  a  disturbance  of  the  higher  psychic  or 
cortical  inhibition,  with  a  relaxation  of  the  lower  or  subcortical,  or 
ganglionic  activities.  It  is  assumed  that  there  are,  so  to  speak,  two 
minds,  the  conscious  and  the  subconscious,  the  seat  of  whose  activity 
is  not  known  positively,  though  the  former  is  supposed  to  be  dependent 
chiefly  upon  the  cortex  and  the  latter  upon  the  lower  layers  of  the 
cortex  or  basal  ganglia. 

Janet  speaks  of  hysteria  as  bemg  the  result  of  a  "contraction  of 
the  consciousness.""  From  this  point  of  view  hysteria  may  be  not 
inaptly  compared  to  the  well-known  spastic  paralyses  of  organic  cerebral 
disease;  only  in  hysteria  the  failure  of  inhibition  from  above  and  the 
spasticity  from  below  are  entirely  and  completely  in  the  mental  or 
psychic  sphere  and  not  in  the  organic.  While  admitting  that  much  of 
this  is  purely  theoretical,  the  theory  explains  and  covers  a  larger 
amount  of  hysterical  phenomena  than  any  explanation  hitherto  ad- 
vanced. 

Etiology. — The  first  thing  that  must  be  observed  under  the  head 
of  the  etiology  of  hysteria  is  that  most  of  the  causes  assigncu  uy  the 
older  writers  are  no  longer  regarded  as  such.  The  uterus,  on  account 
of  which  the  disease  received  its  name,  is  not  the  cause :  nor  are  any 
of  the  sexual  organs,  or  the  sex  of  the  individual.  Not  upon  any  single 
organ  or  tissue  of  the  body  can  the  blame  be  laid  for  the  hysterical 
condition,  though  upon  one  or  all  of  them  may  depend  the  outbreak 
of  an  attack.  The  primary  cause  of  hysteria  is  to  be  found  in  the 
patient's  mental  make-up,  his  temperament,  his  mental  instability, 
which  is  more  or  less  congenital  and  constitutional.  The  secondary 
causes  that  may  precipitate  an  attack  of  hysteria  or  arouse  the  latent 
temperament  into  a  more  or  less  continuous  objective  reality  are  in- 
numerable and  include  such  factors  as  early  education,  discipline,  en- 
vironment, physical  abnormalities  and  local  diseases. 

From  what  has  just  been  said,  it  will  be  readily  surmised  that 
heredity  plays  the  greatest  role  among  the  predisposing  causes  of  hys- 
teria. The  heredity  is  usually  direct  and  transmitted  through  the 
maternal  ancestry.  The  mother,  or  grandmother,  or  maternal  aunts 
of  the  patient  will  be  found  to  have  been  hysterical.  Frankly  admitting 
the  force  of  suggestion  and  close  companionship  between  mother  and 
child  in  the  development  of  hysteria  in  the  latter,  it  is  nevertheless  true 
that  the  hysterical  predisposition  is  chiefly  pre-natal  in  origin.  The 
heredity  is  not  always  direct  and  occasionally  it  is  transmitted  by  the 
father.  Chorea,  epilepsy,  extreme  neurasthenia  or  mental  disease  may 
have  been  the  trouble  in  the  ancestry.  Chronic  alcoholism,  excessive 
use  of  tobacco  and  dissipation  involving  nervous  strain  may  transmit  to 
the  offspring  the  neuropathic  temperament  that  needs  but  an  exciting 
cause  to  provoke  a  genuine  attack  of  hysteria. 


I04  THE    JSIEURONIC    DISEASES 

Next  to  heredity  the  great  predisposing  cause  is  a  false  early  edu- 
cation. The  child  being  more  or  less  neuropathic,  its  irritability,  over- 
sensitiveness,  flashes  of  what  seem  like  mental  brilliancy,  high  emo- 
tionalism and  general  abnormality  are  fondly  mistaken  by  parents  for 
evidences  of  exceptional  talent  or  even  genius.  It  is  pampered  and 
coddled,  all  its  whmis  are  humored,  its  doings  and  sayings  are  lauded, 
and  all  systematic  discipline  and  irksome  routine  are  completely  omit- 
ted. The  child  becomes  egoistic  and  tyrannous ;  it  loses  all  idea  of  the 
proper  relationship  it  should  bear  to  society ;  it  feels  aggrieved  at  every 
little  opposition  it  meets ;  and  as  a  result  it  grows  into  adult  age  com- 
pletely unfitted  to  meet  the  disappointments,  discouragements  and  trials 
of  life.  This  provokes  a  spirit  of  revolt  and-  a  tendency  to  be  moody 
and  unsocial.     It  may  break  into  a  violent  and  emotional  excitation. 

For  a  long  time  it  was  believed  that  hysteria  was  a  disease  of 
women  only.  This  was  the  result  largely  of  locating  the  cause  of  the 
trouble  in  the  uterus.  The  same  symptoms  in  men  were  not  deemed 
hysterical.  Since  we  have  given  up  this  old  pathology  and  pathogenetic 
explanation  of  the  symptoms,  more  care  has  been  taken  in  studying" 
and  comparing  them  and  as  a  result  we  find  that  hysteria  is  a  disease 
of  both  sexes  and  of  all  ages. 

The  trouble  appears  more  frequently  among  women  than  among" 
men  in  the  proportion  of  about  ten  or  six  to  one,  not  because  of  their 
sexual  but  because  of  their  nervous  and  mental  dififerences.  Woman's 
nervous  system  is  more  mobile  and  less  inhibited  normally  than  is 
man's.  Some  of  the  most  typical  cases  of  hysteria  that  I  have  seen  have 
occurred  in  men. 

The  dependence  of  the  disease  upon  nervous  instability  is  further 
emphasized  by  the  fact  that  it  so  frequently  breaks  out  in  its  most 
violent  forms  about  the  time  of  puberty,  and  from  this  period  up  to  the 
thirtieth  or  fortieth  year.  Many  of  the  neurotic  symptoms  of  the 
climacteric  are  hysterical. 

It  occurs  in  childhood  and  has  been  seen  as  early  as  two  years  of 
age.  Passionate  outbursts  of  temper  and  such  manifestations  as  chorea 
and  certain  subjective  sensory  phenomena  in  childhood  are  occasionally- 
hysterical  in  character. 

Hysteria  is  rare  after  the  climacteric  and  in  old  age,  though  some 
authors  speak  of  a  senile  hysteria. 

Certain  races  and  nations  seem  to  be  more  prone  to  the  disease 
than  others.  It  is  very  common  among  the  Latin  races,  especially  the 
French,  from  whom  we  have  learned  most  about  it.  The  Jews  are 
very  liable  to  it  and  it  has  been  observed  among  certain  barbarian  tribes. 
The  Anglo-Saxon  is  probably  the  least  subject  to  it  among  the  civilized 
races. 

There  are  certain  exciting  causes  that  may  arouse  a  latent  hysteria. 
Foremost  among  them  are  emotional  shocks  and  strains,  such  as  terror, 
anxiety,  disappointed  love  or  what  may  be  termed  psychic  traumata  of 
every  sort.  The  symptoms  following  lightning  stroke,  earthquakes, 
railroad  accidents  and  collisions  are  often  purely  hysterical. 

Sudden  irritative  and  imitative  impulses  may  excite  a  hysteric 
outbreak.    This  occurs  in  epidemics  and  among  masses  of  people.    The 


THE    XEUROXIC    DISEASES  IO15 

medigeval  semi-religious  pilgrimages,  dances,  the  New  England  witch- 
craft, modern  revivals,  stampedes,  religio-medical  followings  of  quack- 
ery and  peculiar  beliefs  of  all  sorts,  many  strange  antics  of  the  inmates 
of  monasteries,  convents,  boarding  schools  and  factories  are  all  more 
or  less  attributable  to  the  hysterical  tendency.  The  history  of  these 
epidemics  and  outbreaks  affords  most  interesting  and  sad  reading.  The 
folly  and  weakness  of  human  nature  is  its  most  obtrusive  lesson. 

Organic  diseases  and  traumatic  injuries  may  woric  through  the 
mind  and  nervous  system  to  provoke  and  maintain  a  hysterical  at- 
tack in  one  who  is  already  predisposed.  By  themselves  they  are  not 
causative  of  hysteria.  This  should  be  carefully  remembered,  for  it 
explains  how  a  removal  of  these  exciting  causes,  by  surgical  or  other 
means,  often  results  in  a  return  of  the  hysteria  or  hysterical  tempera- 
ment into  a  latency  which  is  too  often  interpreted  as  a  cure,  but  which 
only  awaits  another  powerful  excitant  to  awaken  it  into  activity.  Just 
as  hysteria  is  often  symptomatically  imitative  of  known  forms  of 
organic  disease,  so  in  those  already  predisposed  it  is  etiologically  imita- 
tive of  them. 

Symptoms. — As  Alobius  well  says,  hysteria  is  a  state  in  which 
ideas  exert  an  influence  to  bring  about  morbid  changes  in  the  func- 
tions of  the  body.  The  ideas  or  mental  state  of  the  patient  constitute 
the  most  important  symptoms  therefore,  and  though  not  always  the 
most  obtrusive  or  the  most  easily  elicited,  they  should  in  every  clinical 
examination  be  most  earnestly  and  persistently  sought  for.  Certain 
facts  stand  out  very  prominently  in  regard  to  a  hysteric's  psychic 
condition.  The}-  are  irritability  and  instability,  abnormal  emotionalism, 
altered  volition  and  inhibition,  and  increased  power  of  imagination. 
The  mental  power  is  not  weakened,  the  memory  is  usually  intact,  and 
the  will  and  intellect  are  about  up  to  the  patient's  normal  capacity. 
This  leaves  the  imagination  as  the  chief  faculty  at  fault,  and  yet  the 
increase  in  the  power  of  the  imagination  is  rather  the  result  of  the 
weakened  power  in  the  higher  or  controlling"  inhibition.  Abnormal 
irritability  with  changeability  of  ideas,  all  the  result  of  a  congenital 
defect  in  the  cortical  structures  underlying  the  function  of  mentaliza- 
tion  and  of  au' educational  failure  in  the  development  of  the  associational 
paths  supporting  the  proper  concepts  of  life  and  its  thousand  and  one 
relationships,  is  the  hysterical  mental  condition. 

This  abnormal  irritability  is  both  centripetal  and  centrifugal  in  its 
action.  It  is  provoked  abnormally  by  every  slight  inpouring  impulse 
and  it  provokes  abnormally  every  function  of  the  body,  motor,  sensory 
and  vasomotor. 

As  Oppenheim  points  out,  this  abnormal  irritability  reveals  itself 
in  the  sudden  variations  in  disposition  and  in  the  pathological  increase 
of  normal  actions.  Laughing  and  crying  becomie  spasmodic.  The 
transient  normal  inhibition  produced  by  fear,  anxiety,  becomes  paraly- 
sis. Indifference  and  insensibility  from  the  same  cause  become  stupor, 
delirium  and  anaesthesia.  Imaginary  thoughts  develop  into  hallucina- 
tions. Motor  activity  passes  into  spasms,  contractures  and  cataleptic 
rigidity. 

This  irritability  and  heightened  influence  of  the  mind  are  produced 


I06  THE    NEURONIC    DISEASES 

by  the  most  insignificant  circumstances  and  often  by  no  known  reasons. 
It  shows  itself  in  unwarrantable  outbursts  of  anger,  joy,  vexation, 
depression  and  terror.  The  memory  may  participate  in  this  irritability, 
causing  past  events  and  sights  to  be  recalled  with  such  vividness  as  to 
throw  the  patient  into  a  confused  and  dream-like  state  and  to  make  it 
appear  as  though  he  were  living  in  another  world  or  in  another  period 
of  time.  With  all  this  irritability  there  is  a  most  obvious  loss  of  the 
power  of  mental  inhibition  and  self-control,  especially  over  the  emo- 
tions. There  is  not  strictly  any  loss  of  volitional  power,  or  alx)ulia, 
but  rather  perversion.  When  the  patient  declares  she  cannot  act,  she 
frequently  exhibits  at  the  same  moment  an  astonishing  power  of  voli- 
tion in  other  ways.  The  ideas  which  are  passing  through  her  mind  at 
the  instant  have  so  altered  her  motives  for  action  that  her  power  of 
volition  is  shown  not  in  the  desired  but  in  other  and  unexpected  ways. 
Instead  of  loss  of  will,  therefore,  it  is  nearer  the  truth  to  speak  of 
perversion  of  the  will.  There  is  no  distinct  weakening  of  the  mental 
power,  though  feeble-minded  people  may  be  attacked  by  the  disease. 
As  a  matter  of  fact,  hysteria  occurs  more  frequently  among  intelligent 
than  among  ignorant  individuals,  a  truth  which  has  its  bearing,  in  the 
management  of  these  cases,  upon  the  relationship  of  the  physician  to 
the  patient. 

The  alterations  of  character,  the  oft-times  senseless  and  purpose- 
less acts,  the  prevarication,  the  instability  and  unreliability,  the  tout 
'ensemble  picture  which  so  often  arouses  disgust  and  even  anger  among 
the  bystanders,  are  not  the  result  of  mental  enfeeblement,  but  rather  of 
the  abnormal  irritability,  rapid  changeability,  perverted  memory  and 
vivid  imagination  which  cause  a  swift  passage  of  ideas  through  the 
patient's  mind.  There  is  no  fixity  in  her  motives  and  she  is  the  prey  to 
every  gust  that  whirls  down  upon  her  mental  horizon.  She  acts  logi- 
cally in  accordance  with  her  motives,  albeit  the  acts  themselves  appear 
to  be  bizarre,  willful  and  without  rhyme  or  reason. 

To  understand,  therefore,  the  attitudes,  the  speeches,  the  sensa- 
tions, the  whole  outward  manifestation  of  these  patients  one  must 
closely  recognize  the  state  of  mental  irritability  and  then  as  far  as 
possible  trace  the  underlying  ideas  to  their  source. 

Hysteria  being  in  that  ill-defuied  borderland  between  sanity  and 
insanity,  its  mental  m.anifestations,  which  are  always  present,  assume 
the  most  varied  forms.  Some  hysterics  are  undcubtedly  insane  in  the 
common  acceptation  of  the  term,  while  others  are  onlv  weak  and  irre- 
sponsible, especially  in  the  moral  sphere,  but  would  not  be  commonly 
regarded  as  insane. 

Hysterics  exhibit  the  hallucinations,  delusions  and  illusions  of  the 
most  profound  forms  of  mental  alienation,  down  to  mere  prevarica- 
tion, secretiveness  and  other  slight  forms  of  moral  delinquency. 

It  is  in  the  ethical  and  emotional  spheres  that  hysteria  indicates  its 
relationship  to  mental  troubles  most  distinctly.  Certain  mental  mani- 
festations that  occasionally  occur  v/ith  hysteria  should  not  be  looked 
upon  as  a  part  of  the  disease.  They  are  mere  complications ;  the  two 
conditions  are  merely  associated  forms  of  disease  due  to  the  same 
cause.     A  melancholia,  mania,  paranoia  will  sometimes  break  out  in 


THE    NEURONIC    DISEASES  lOJ 

the  course  of  hysteria  and   be  erroneously  named   hysterical   melan- 
cholia, hysterical  mania,  etc. 

The  prognosis  of  such  cases  depends  not  upon  the  hysteria,  but 
upon  the  insanity,  and  as  a  rule  it  is  bad  for  recovery.  A  clear  appre- 
ciation of  this  distinction  will  lead  to  better  results  in  the  management 
of  h3'Steria  and  to  more  prompt  asylum  confinement  in  the  cases  com- 
plicated by  insanity. 

Other  symptoms,  often  classified  as  hysterical,  such  as  the  impera- 
tive conceptions,  phobias,-  like  agoraphobia,  pyrophobia,  manias,  like 
dipsomania,  morphino-mania,  kleptomania,  are  comphcations  and 
should  not  be  regarded  as  a  part  of  the  disease  we  are  now  referring  to. 
They  are  expressive  of  a  phrenasthenia  and  represent  a  mental  de- 
pression, congenital  or  acquired.  They  often  occur  in  hysteria,  but 
they  are  not  symptomatic  of  it.  As  mental  troubles  they  may  be  modi- 
iied  and  colored  by  the  hysteria  that  is  present,  and  the  association  of 
the  two  sets  of  symptoms  may  be  so  close  that  one  may  have  much 
difficulty  in  determining  which  is  the  predominating  and  more  im- 
portant disease.  Here  doubtless  belongs  the  astasia-abasia  so  much 
studied  in  recent  years  by  European  neurologists.  Standing  and  walk- 
ing are  impossible,  though  there  are  absolutely  no  signs  of  disturbance 
of  motility,  of  sensibility  or  of  coordination  when  the  patient  is  lying 
down.  Only  when  he  gets  up  and  attempts  to  walk  does  rlie  difficulty 
reveal  itself.  Moving  on  all  fours,  swimming  and  other  forms  of 
movement  may  still  be  performed. 

There  are  several  possible  explanations.  It  is  clearly  psychic  in 
origin  and  may  be  a  sort  of  specific  psychic  ataxia  or  special  form  of 
mental  incoordination,  loss  of  the  memory  pictures  for  walking. 

A  somewhat  similar  condition  obtains  in  some  of  the  occupation 
neuroses. 

True  hysteria,  uncomplicated,  is  characterized  by  three  particular 
forms  of  psychic  disturbance  observed  mostly  in  paroxysms. 

The  first  is  an  indefinite  sense  of  fear^  unaccompanied  by  definite 
conceptions  such  as  occur  in  the  well-known  phobias.  With  this  sense 
of  fear  is  a  feeling  of  precordial  oppression  and  cardiac  palpitation. 

The  second  is  a  state  of  hallucinatory  delirium,  in  which  the  patient 
shows  the  manner  and  fancies  of  one  under  the  influence  of  frightful 
dreams  or  visions.  He  slinks  away  or  strikes  at  the  attendant.  From 
this  half-dreaming  state  a  dash  of  cold  water  or  other  forcible  form  of 
stimulation  may  arouse  him. 

The  third  state  is  that  in  which  somnambulism,  hypnotism, 
lethargy,  catalepsy,  etc.,  obtain. 

All  of  these  three  states  are  typically  hysterical  and  are  dependent 
largely  upon  the  abnormal  activity  of  the  aflrective  faculties,  the  feel- 
ings, emotions  and  imagination. 

Next  to  the  mental  state  in  frequency  and  importance  are  the 
presence  and  the  character  of  the  sensory  symptoms.  Though  these 
symptoms  are  subjective,  like  the  mental,  and  are  therefore  that  much 
less  valuable  as  positive  indications  of  disease,  they  can  be  examined 
and  tested  objectively  or  at  least  made  to  provoke  objective  signs  that 


io8 


THE    XEURONIC    DISEASES 


FIGURE  24. 


Hysterical   anjesthesia. 


THE    NEURONIC    DISEASES  lOQ 

are  most  valuable  in  indicating  not  only  the  presence  of,  but  the  real 
nature  of  the  trouble. 

The  first  great  law  to  be  remembered  in  regard  to  hysterical  sen- 
sory phenomena  is  that  they  are  physiologically  and  anatomically 
mental  and  not  neural.  They  do  not  localize  themselves  in  accordance 
with  nerve  distribution  or  cortical  limitations ;  they  involve  those  parts 
of  the  body  known  only  to  the  patient's  ego,  or  his  consciousness. 
They  are  therefore  more  or  less  co-extensive  with  the  segments  of  the 
body  and  not  with  the  mere  cutaneous  area  of  this  or  that  set  of  nerves. 
The  hand,  the  arm,  the  leg,  the  half  of  the  body,  the  glove  or  stocking 
type  of  distribution  indicate  the  areas  aflected.  The  special  senses 
show  the  same  peculiar  mental  disturbance.  In  hysterical  blindness  it 
is  mental  vision,  not  actual  vision  that  is  affected. 

A  second  law  to  be  remembered  in  regard  to  these  sensory  phe- 
nomena is  with  regard  to  their  great  changeableness  and  instability. 
They  come  and  go  with  rapidity  and  uncertainty.  They  may  be  mild 
or  marked  throughout  their  entire  extent  and  continuance,  or  they 
may  be  mild  in  one  part  of  the  body  while  severe  in  another.  One 
side  may  show  hypersesthesia,  the  other  anaesthesia.  The  visual  field 
of  one  eye  may  be  immensely  more  altered  than  that  of  the  other.  A 
reversal  of  the  conditions  may  even  take  place  at  a  most  unexpected 
moment.  It  is  this  fact  that  renders  hysterics  the  walling  and  self- 
deceived  dupes  of  religio-medical  quacks,  to  whom  they  give  fulsome 
testimonials  of  astounding  cures. 

All  forms  of  sensation  may  be  affected  in  hysteria.  Smell,  taste, 
hearing  and  sight  of  the  special  senses  and  tactile,  temperature  and  pain 
of  the  cutaneous  senses,  and  even  the  muscular  sense  may  be  altered. 
The  sense  disturbance  itself  may  be  exactly  that  of  an  organic  disease ; 
the  only  way  it  can  be  determined  as  hysterical,  mental  or  functional 
is  by  carefully  considering  its  distribution  and  noting  its  great  change- 
ableness and  instability. 

The  pain  sense  is  probably  the  one  most  frequently  reported.  In 
fact,  more  or  less  pain  is  complained  of  in  every  case  of  true  hysteria. 
To  attempt  to  give  a  complete  description  of  the  pains  of  hysteria  would 
be  to  write  a  volume  upon  every  kind  of  pain  known  to  the  human 
mind. 

The  pains  of  hysteria  may  be  of  every  sort  and  of  every  degree  of 
severity ;  they  may  be  located  in  any  or  all  parts  of  the  body ;  and 
they  may  act  exactly  as  any  other  sort  of  pain  acts.  Then  how  are  we 
to  determine  the  hysterical  character  of  these  pains  ?  Often  we  cannot. 
Less  frequently  we  can  do  so  only  by  their  association  with  other  symp- 
toms and  conditions  suggestive  of  hysteria,  and  still  less  frequently 
by  certain  peculiarities  that  in  a  few  hysterics  do  characterize  and  dis- 
tinguish them  from  other  forms  of  pain. 

In  the  head  there  is  with  the  pain  an  occasional  hyperzesthesia. 
The  patient  dislikes  combing  of  the  hair.  Often  there  is  a  distinct 
clavus  or  sharp  circumscribed  area  of  pain  at  the  vertex,  a  position 
not  commonly  selected  by  headaches  from  other  causes.  Rarely  this 
pain  is  dull  and  spreads  over  the  whole  cranium  or  is  limited  to  one 
side.     In  such  instances  neurasthenia  or  migraine  should  be  carefully 


no 


TIJK    XKUKOXJC    DISEASES 


FIGURE  25. 


Hysterical   anaesthesia. 


THE    NEURONIC    DISEASES  III 

eliminated  before  a  diagnosis  of  hysteria  is  made.  With  hysterical 
clavus,  lasting  several  hours  or  days,  there  is  not  unfrequently  vertigo, 
nausea  and  vomiting.  Remember  that  hysterical  headache,  whether  it 
is  vertical,  occipital,  temporal  or  of  the  entire  head,  shows  a  tendency 
to  be  influenced  by  the  mental  condition  of  the  patient.  In  this  it  differs 
from  other  forms  of  cephalalgia. 

Spinal  pains  are  a  part  of  the  hysterical  condition.  I  have  not 
found  them  equally  distributed  along  the  entire  spine  so  regularly  as  I 
have  in  neurasthenia.  In  hysteria  they  are  more  focal  in  character,  a 
choice  location  seeming  to  be  between  the  shoulder-blades.  When 
tested  by  percussion  or  by  the  passing  of  a  hot  or  cold  sponge  up  and 
down  the  spine  the  patient  winces  or  at  least  indicates  suffering  when 
certain  spots  are  passed  over.  In  this  the  trouble  resembles  the  focal 
meningitis  of  the  spine,  from  which  it  must  be  differentiated  of  course 
by  other  symptoms. 

Pains  are  frequently  complained  of  in  the  region  of  the  ovaries 
and  mammary  glands.  In  all  cases  of  genuine  hysteria  these  areas,  the 
hysterogenic  zones,  are  highly  sensitive  and  may  be  painful  upon  pres- 
sure. I  have  seen  hysterical  men  v/ho  suffered  from  sharp  pain  in  the 
testicles,  usually  the  left.  Trunk  pains,  resembling  intercostal  neural- 
gia, gastralgia,  cardialgia  and  even  the  cincture  phenomenon  of  organic 
spinal  disease,  may  be  present. 

Pains  are  not  frequently  complained  of  in  the  extremities.  Here 
the  altered  sensation  more  often  assum.es  the  character  of  numbness  or 
"pins  and  needles."  Once  I  saw  in  a  yoimg  wonsan  a  pamful  toe  that 
simulated  gout.  Under  treatment  it  soon  felt  like  a  ricedle  which  the 
patient  declared  she  had  accidentally  swallowed  when  an  infant.  Here, 
under  suggestion,  hyperalgesia  was  replaced  by  parsesthesia.  Cure 
followed  further  suggestion  and  the  skiagraphic  proof  that  there  was 
no  needle  present.  Mobius  has  described  under  the  name  akinesia 
algera  a  form  of  hysterical  immobility  caused  by  the  pain  produced  in 
every  form  of  movement,  voluntary  or  forced.  The  pain  is  purely 
psychic  in  origin.  It  may  involve  every  movement  of  the  body  and  at 
times  prove  a  most  serious  obstacle  to  treatment. 

Sensations  of  heat  and  cold,  of  formication,  of  alterations  in  size 
and  strength,  are  much  more  common,  in  my  experience,  as  hysterical 
symptoms  in  the  extremities  than  are  pains.  This  dift'erence  between 
the  sensory  phenomena  of  the  trunk  and  the  extremities  is  probably 
due  to  the  psychic  character  of  hysteria,  the  finer  and  more  com.plicated 
physiology  of  the  extremities  having  a  more  varied  psychic  representa- 
tion. The  sensation  of  pain  is  more  primitive  and  elemental  than  are 
the  hallucinatory  sensations  like  formication,  worms,  pins  and  needles. 

All  of  these  sensory  disturbances  are  of  central  or  psychic  origin. 
They  may  occasionally  be  avv^akened  or  localized  by  some  form  of 
peripheral  irritation,  but  they  are  mental  hallucinations.  They  are  the 
expression  of  the  direct  excitation  of  the  pain-perceptive  centers  of  the 
brain. 

Next  to  pains,  so  important  are  the  parjesthesias,  hypergesthesias 
and  anaesthesias  in  the  symptomatology  of  hysteria  that  they  must  be 
considered  a  little  more  in  detail. 


112  THE    NEURONIC    DISEASES 

Formication,  the  feeling  of  ants  and  worms  crawling  over  the 
body,  and  numbness  are  probably  the  most  frequent  parcusthesias.  It  is 
a  question  whether  some  of  the  strange  delusions  of  the  hysterical 
may  not  be  due  in  part  at  least  to  internal  as  well  as  external  forms 
of  paraesthesia.  A  patient  who  was  a  typical  hysteric  had  the  delusion 
that  there  was  a  fish  in  her  head  which  swam  about  there  and  came 
forward  to  drink  whenever  she  swallowed  liquid.  Hysterics  not  unfre- 
quently  complain  of  toads  in  their  stomach  and  of  worms  in  their 
bowels,  which  delusions  may  well  be  due  to  visceral  paraesthesia. 

Perverted  sensation  is  in  the  very  nature  of  things  psychic  and  is 
therefore  almost  pathognomonic  of  hysterical  or  other  forms  of  psycho- 
sis. It  may  be  provoked  by  various  peripheral  stimuli,  but  the  per- 
version can  only  be  the  result  of  central  trouble.  In  this  it  differs  from 
hyperaesthesia  and  anesthesia  w^hich  may  depend  upon  peripheral 
nervous  disturbance  as  well  as  central,  and  are  not  so  necessarily  indica- 
tive of  a  psychosis. 

Hypercesthesia  and  ancesthesia,  being  merely  degrees  of  sensory 
disturbance  and  not  perversions,  are  not  pathognomonic  of  a  psychosis 
and  therefore  are  less  valuable  as  symptoms  of  pure  hysteria.  They 
may  both  be  due  to  actual  peripheral  ner\^e  disease  and  thereby  be  asso- 
ciated with  probable  hysteria.  On  the  other  hand,  they  may  not  repre- 
sent any  actual  organic  disease  at  all,  but  may  be  entirely  central  in 
origin  and  therefore  indicative  of  a  pure  psychosis.  In  the  latter  case 
their  distribution,  their  favorite  location,  their  variability  and  change- 
ability and  their  modification  under  the  patient's  ever-varying  mental 
state  indicate  their  purely  hysterical  origin. 

It  is  rare  for  hypercustliesia  ever  to  be  complete.  It  is  more  fre- 
quently seen  in  spots  and  circumscribed  areas  or  in  conjunction  with 
certain  viscera  and  deep  structures  like  the  muscles  and  fascia.  The 
hypersesthesia  frequently  coincides  with  the  hysterogenic  zones,  a  fact 
which  is  made  use  of  to  initiate  or  check  an  attack  of  hysteria,  by 
making  pressure  upon  them.  These  hysterogenic  zones  on  the  anterior 
part  of  the  body  are  the  areas  just  under  the  mammary  glands,  just 
above  the  ovaries,  along  the  sternum,  at  the  outer  end  of  the  clavicle, 
at  the  lower,  lateral  edge  of  the  thorax  and  at  the  vertex  of  the  head. 
The  spinous  processes  of  the  back  are  often  hypersesthetic  as  well  as  the 
tip  of  the  coccyx.  The  left  side  of  the  body  being  the  sensitive  side, 
hyperaesthesia  as  well  as  anaesthesia  selects  it  most  frequently  when 
they  are  of  psychical  origin. 

The  special  senses  also  frequently  submit  to  an  hysterical  ex- 
aggeration of  their  function.  Flashes  of  light,  flickerings  and  other 
visual  phenomena  are  among  the  common  signs  of  hysteria.  An  in- 
crease of  the  visual  field  (Freund)  in  all  directions  is  much  rarer  than 
a  diminution.  The  "tubular  field  of  vision"  is  a  condition  in  which 
there  is  a  constriction  and  the  absolute  area  is  the  same,  no  matter  at 
what  distance  it  is  measured.  I  have  seen  it  once.  Partial  increase, 
however,  with  partial  diminution  and  the  increase  of  some  of  the 
color  fields,  which  virtually  amoimts  at  times  to  crossing  or  reversal  of 
the  color  fields,  is  a  form  of  partial  hyperaesthesia  that  I  have  not  un- 


THE    NEURONIC    DISEASES 


113 


FIGURE  26. 


Hysterical  aridesthesia.      (After  Thomsen.) 


114  i'^E    XEUROXIC    DISEASES 

frequently  seen.  Double  sight  with  one  eye,  not  otherwise  accounted 
for  by  optical  conditions,  is  hysterical. 

Taste  and  smell  and  hearing  may  all  be  exaggerated.  The  hyper- 
sensitiveness  of  these  nerves,  however,  is  clearly  psychic.  The  per- 
version of  their  function  is  probably  more  common  in  hysteria  than 
is  hyperassthesia. 

The  aiuesthesia  of  hysteria  is  clinically  the  most  valuable  of  the 
sensory  symptoms.  It  is  the  most  frequent,  is  less  intensely  subjective 
than  the  others  and  can  be  examined  with  a  higher  degree  of  objec- 
tivity. Like  the  other  sensory  symptoms,  it  is  purely  psychic,  as  shown 
in  its  distribution  and  variability.  As  Bernheim  well  points  out,  all 
psychic  anaesthesia,  however,  is  not  hysteria.  Hemianaesthesia  may  be 
directly  added  to  hemiplegia  by  pure  psychic  dynamism.  It  may  occur 
from  various  causes  in  patients  who  are  not  the  least  hysterical.  Hys- 
terical anaesthesia  is  observed  in  connection  with  all  forms  of  sensation, 
special  as  well  as  general. 

The  most  common  form  of  cutaneous  anaesthesia  is  that  Vv'hich 
involves  one  entire  half  of  the  body,  hemianaesthesia.  Next  in  fre- 
quency is  that  which  is  limited  to  the  conscious  segments  of  the  body, 
the  liand,  the  forearm,  the  arm,  the  leg,  the  top  of  the  head.  This  is 
the  glove-type  or  drawers-leg  type  of  anaesthesia.  Its  boundaries  usu- 
ally correspond  with  the  transverse  folds  and  joints  of  the  body  or  with 
the  so-called  transverse  amputation  lines. 

Both  the  hemianaesthesia  and  the  glove-type  reveal  the  psychic 
nature  of  hysteria,  for  they  correspond  to  the  mental  conceptions  of  the 
parts  of  the  body  and  not  with  the  anatomical  distribution  of  the  sen- 
sory nerves. 

The  least  frequent  of  all  the  forms  of  anaesthesia  is  that  in  w^hich 
the  insensibility  is  scattered  in  patches  or  circumscribed  areas  about  the 
body.  And  yet  even  this  form  is  not  in  correspondence  with  the  strict 
arrangement  of  the  sensory  nerves.  It  is  bizarre  and  irregular.  Its 
areas  are  located  in  and  about  the  hysterogenic  zones.  It  is  deter- 
mined by  such  numerous  local  influences  upon  the  patient's  mind  as 
pressure  from  the  clothing,  exposure,  ph3'Siological  function.  Its  bor- 
der lines  are  sharper  than  are  the  border  lines  of  organic  anaesthesia. 
This  diffuse  form  of  anaesthesia  should  be  always  most  guardedly  pro- 
nounced upon,  for  it  is  the  type  that  is  most  liable  to  cause  hysteria 
to  be  erroneously  diagnosed  for  such  organic  troubles  as  multiple 
sclerosis,  polyneuritis,  etc.     It  may  even  occur  with  these  diseases. 

This  cutaneous  anaesthesia  is  chiefl}'  a  pain  anaesthesia,  the  tactile 
sense  being  normal  or  only  slightly  blunted.  It  closely  resembles  in  this 
respect  the  dissociated  sensory  phenomena  of  syringomyelia.  It  is  fre- 
quently tactile,  however,  and  then  the  pain  sense  is  also  usually  entirely 
absent.  Occasionally  the  touch  sense  is  merely  blunted,  liypcesthesia. 
It  is  never  merely  delayed  as  in  certain  organic  troubles. 

Loss  of,  or  diminution  of,  the  temperature  sense,  thermanaesthesia, 
may  be  observed. 

All  these  superficial  forms  of  sensory  disturbance  are  met  with 
in  the  mucous  membranes  as  well  as  in  the  skin.  The  mouth,  the 
vagina,  the  rectum  may  all  be  involved.     The  superficial  reflexes  will 


THE    NEURONIC    DISEASES 


Its 


FIGURE  27. 


Hysterical  hemianjesthesia.     (After  Charcot.) 


ii6 


THIi    NEURONIC    DISEASES 


FIGURE  28. 


H>';\terical  anjesthesia.      (After   Charcot.) 


THE    NEURONIC    DISEASES 


117 


be  correspondingly  involved,  though  at  times  a  reflex  response  may  be 
obtained  in  spite  of  anaesthesia,  if  the  test  is  made  suddenly  and  when 
the  patient  is  not  expecting  it.  The  deep  sensations,  as  those  of  the 
viscera,  the  joints,  the  fascia,  are  also  subject  to  anaesthesia.  Hysterical 
astereognosis  and  loss  of  the  sense  of  position  may  be  present  from 
implication  of  the  muscular  sense  and  other  deep  senses. 

The  special  senses  undergo  hyperassthesia  and  anccsthesia.  Upon 
this  many  of  the  curious  phenomena  of  hysteria  depend.  The  visual 
disturbances  are  the  most  common  and  important  among  the  special 
senses.     Complete  amaurosis  is  very  rare  and   loss  of  central  visual 


FIGURE  29. 


ro 


Hysterical  contraction  of  the  visual   fields.     Private   case.     Charts   drawn  by 
Nance. 

acuity  almost  never  occurs.  Usually  there  is  a  more  or  less  concentric 
narrowing  or  contraction  of  the  field  of  vision,  which  of  course  must 
be  determined  by  a  perimetric  examination.  The  perception  of  colors 
may  be  lost  or  diminished,  or  the  limitations  of  the  color  fields  may  be 
reversed  so  that  they  will  overlap.  These  phenomena  are  usually  more 
marked  on  one  side  than  on  the  other.  When  unilateral  the  eye  affected 
is  usually  the  one  on  the  same  side  as  the  cutaneous  anaesthesia,  which 
is  mostly  the  left.  Whenever  the  order  and  extent  of  the  fields  for 
white  and  colors  are  reversed,  the  evidence  is  positive  of  the  existence 
of  hysteria.  It  cannot  be  simulated.  It  does  not  occur  in  any  other 
ocular  disorder.  Ring  scotomata  are  particularly  suggestive  of  a 
psychoneurosis.  That  the  loss  of  vision  is  mental  and  not  organic  is 
shown  by  the  fact  that,  unlike  organically  blind  people,  these  patients 
avoid  obstacles  placed  in  their  way.  It  can  also  be  proved  to  be  mental 
by  the  use  of  the  stereoiscope,  by  prisms  ingeniously  arranged  and  by  a 
box  in  which  the  lines  of  vision  from  the  eyes  are  made  to  decussate  by 
means  of  small  mirrors.  The  preservation  of  the  pupillary  reflexes  in- 
dicates its  non-organic  character,  and  even  though  the  pupils  are  af- 


Hi 


Tin;    NEURONIC    DISEASES 


fected,  as  they  sometimes  are  by  hysterical  spasm,  their  appearance 
and  mode  of  action  is  not  at  all  in  correspondence  \\ath  an  org-anic  loss 
of  the  visual  sense.  All  forms  of  anaesthesia  may  attack  the  retina,  so 
that  there  may  be  hemiansesthesia  or  quadrant  anaesthesia  or  focal  and 
diffuse  spots  of  anzesthesia.  The  same  may  be  said  of  the  achromatop- 
sia or  dyschromatopsia  that  may  exist,  it  is  to  be  remembered  that 
ocular  hysteria  is  common  in  children  and  men.  Organic  disease  of 
the  eye  may  accompany  the  functional  disturbance. 

The  fasfc  and  hearing  are  sometimes  lost  on  one  or  both  sides. 
The  alterations  of  taste  explain  the  readiness  with  which  these  patients 
will  resort  to  such  filthy  habits  as  swallowing  urine  and  eating  dirt. 
Moreover  it  accounts  for  their  hallucinations  and  absurd  declarations 
in  regard  to  the  articles  of  food  that  are  given  them  to  eat.    Hysterically 


FIGURE  30. 

LEFT 


FIGURE  31. 

RIGHT 


Ring    scotoma    in    a    hysteropic    boy.      (After    Wood.) 

deaf  patients  do  not  as  a  rule  incline  their  head  in  an  effort  to  hear  like 
those  affected  with  organic  deafness.  Osseous  conduction  is  usually 
absent.  There  is  often  cutaneous  anaesthesia  in  and  about  the  meatus 
of  the  deaf  ear. 

When  the  olfactory  sense  is  involved,  the  patients  do  not  com- 
plain oi  disgusting  odors  and  they  may  even  reverse  normal  opinion 
and  seem  to  enjoy  that  which  nauseates  the  attendants.  Hallucina- 
tions and  illusions  are  common  enough  here. 

It  is  a  curious  fact  that  sometimes  the  patient  himself  is  not 
aware  of  his  various  anaesthesias  and  only  realizes  them  when  they  are 
demonstrated  by  the  examining  physician.  Their  instability,  peculiar 
distribution,  sudden  transference  and  general  bizarre  character  make 
them  important,  almost  pathognomonic  symptoms  of  hysteria.  Janet 
thinks  they  are  but  the  objective  manifestations  of  the  contraction  of 
the  field  of  consciousness. 

All  forms  of  motor  disturbance  mav  be  observed  in  hysteria. 
Spasms,  both  tonic  and  clonic,  are  more  frequent  than  are  the  con- 
tractures, pareses  and  paralyses.    These  disturbances  are  never  as  com- 


THE    NEURONIC    DISEASES  II9 

plete  as,  nor  do  they  simulate  identically,  the  organic  motor  disturb- 
ances. Their  psychic  origin  is  noticeable  in  their  peculiar  fimctional 
character,  their  incompleteness,  their  localization  and  distribution,  their 
duration  and  their  instability  and  abrupt  changeability.  The  absence 
of  other  distinguishing  symptoms  that  accompany  organic  motor  dis- 
turbances indicates  the  psychic  or  hysterical  nature  of  these.  For  ex- 
ample, respiratory  spasm  of  hysterical  origin  is.  not  accompanied  by  the 
usual  signs  of  the  need  of  air ;  hysterical  paralyses  do  not  exhibit  the 
typical  flaccidity  or  spasticity,  the  atrophy,  the  reflex  and  electrical 
changes  which  are  associated  with  the  organic  paralyses.  The  motor 
disturbances  of  hysteria  are  due  to^  an  alteration  in  the  patient's  con- 
cepts of  motion.  Just  as  a  hysteric  really  feels  and  sees  and  hears  but 
does  not  know  that  she  does,  so  she  really  can  move  her  limbs  but  fails 
to  do  so  because  she  does  not  know  that  she  can.  For  this  reason  it 
has  often  been  erroneously  taught  that  aboulia.  or  paralysis  of  the  will, 
was  the  underlying  factor  in  hysteria.  In  the  words  of  Paget  the  hys- 
teric says  'T  cannot"  ;  it  looks  as  if  she  "will  not" ;  in  reality,  she  cannot 
will.  Such  a  view  of  hysteria  is,  however,  not  correct.  There  is  plenty 
of  volitional  power,  as  is  so  often  shown  by  the  persistence  and  deter- 
mination with  which  the  patient  carries  out  her  special  plans  and  de- 
sires. The  aboulia  of  hysteria  is  only  an  apparent  loss  of  will  power 
due  to  a  perversion  of  the  appropriate  concept  of  motion.  Suddenly 
restore  this  lost  concept  by  suggestion,  or  mental  shock,  and  the  aboulia 
will  vanish. 

Chief  among  the  hysterical  spasms,  if  indeed  it  is  to  be  regarded  as 
the  result  of  a  spasm  and  not  a  form  of  parsesthesia,  is  the  well-known 
globus  hystericvis.  The  patient  complains  of  a  lump  in  the  throat,  a 
ball  which  may  or  may  not  seem  to  have  risen  from  the  stomach  and 
which  feels  as  if  it  were  held  in  the  grip  of  the  pharyngeal  muscles. 
This  sometimes  produces  great  distress  and  together  with  spasm  of  the 
glottis  may  cause  so  severe  a  spell  of  chokmg  as  to  call  for  the  opera- 
tion of  tracheotomy.  The  muscles  of  respiration  are  frequently  in- 
volved. In  fact  the  emotional  and  respiratory  spasms  are  among  the 
most  common  motor  disturbances  of  hysteria.  The  crying  and  laugh- 
ing, often  so  meaningless,  are  of  this  nature,  as  likewise  are  the  attacks 
of  singultus  (sometimes  epidemic  according  to  Oppenheim,  Abeles  and 
others),  eructation,  of  yawnings  and  of  sneezing.  Instead  of  tachypnoea 
there  ma}^  be  aphonia  from  implication  of  the  vocal  cords.  Hysterical 
aphonia  and  aphasia  are  both  common,  especially  the  former.  Cough 
(tussis  hysterica),  when  present,  is  peculiar.  It  is  dry,  short  and  sharp 
like  a  dog's  yelp  and  is  absent  during  the  night.  Twitching  of  the  eye- 
lids, blepharoclonus  and  blepharospasm,  with  photophobia  and  water- 
ing of  the  eyes  may  be  present,  but  is  more  common  in  neurasthenia, 
a  disease  which  often  complicates  hysteria. 

Any  of  the  voluntary  muscles  of  the  body  may  be  subject  to  hys- 
terical spasm.  Twitching  and  convulsive  movements,  all  forms  of  vio- 
lent motion,  tonic  as  well  as  clonic,  may  attack  the  limbs  and  hurl  them 
about  or  hold  them  in  a  rigid  attitude.  When  the  back  muscles  are  in- 
volved there  will  be  opisthotonos  or  rhythmical  arching  ol  the  body. 
All  degrees  of  muscular  spasm  are  possible,  and  this,   taken  in  con- 


I20 


THE    NEURONIC    DISEASES 


junction  with  the  fact  that  the  movements  are  the  same,  only  more 
vigorously  performed,  as  normal  voluntary  movements,  has  formed 
the  basis  of  an  attempt  to  classify  them.  Even  with  the  most  violent 
spasms,  consciousness  is  never  entirely  lost ;  usually  it  is  entirely 
present,  thoug-h  in  the  more  severe  cases  it  is  clouded  and  disturbed 
with  hallucinations.  A  curious  hysterical  phenomenon  is  the  Saltatoric 
spasm,  first  described  by  Bamberger  in  1859.  It  is  rather  more  fre- 
quent in  males  than  females.  The  symptom  appears  usually  suddenly 
and  consists  of  very  rapid  alternating  contractions  in  the  flexors  and 
extensors  of  the  legs,  causing  the  patient  to  jump  entirely  off  of  the 
floor.  It  occurs  only  on  attempts  to  stand  and  ceases  when  the  patient 
sits  or  lies  down.  Scarcely  ever  does  it  attack  the  arms,  and  then  only 
slightly.    Hopping,  jumping  and  running  around,  whenever  he  touches 

FIGURE  32. 


Major  hysteria.      (After  Hamilton.) 

the  floor,  is  the  predicament  of  the  patient.  The  spasm  is  clonic  and 
involves  ehiefly  the  calf  muscles.  Gowers,  Kast  and  Eilenmeyer  be- 
lieve it  is  a  form  of  reflex.    I  am  inclined  to  regard  it  as  hysterical. 

A  consideration  of  the  various  periods  of  a  grand  attack  of  hys- 
teria, as  outlined  by  Charcot,  forms  an  interesting  commentary  upon 
the  psychic  nature  of  the  disease  and  upon  the  manner  of  the  action 
of  the  mind.  In  the  first  stage,  the  consciousness  being  fully  awake 
and  realizing  that  something  dreadful  is  impending,  there  are  charac- 
teristic prodromes.  There  is  irritability  of  temperament,  fear,  depres- 
sion of  spirits,  palpitation  of  the  heart,  restlessness,  anxiety,  aurge  from 
the  ovaries  or  stomach,  paraethesiae  of  various  sorts  (tinnitus)  eructa- 
tions, globus,  visual  mistiness  and  partial  clouding  of  the  mental  facul- 
ties. After  this  premonitory  stage  follows  in  a  short  time  the  second 
or  epileptoid  stage.  The  consciousness  becomes  still  more  obscure  and 
perceiving,  as  it  were,  its  gradual  loss  of  inhibitory  control  over  the 
lower  or  subconscious  faculties,  it  becomes  involved  in  a  struggle  in 
which  it  is  more  or  less  conquered.  In  almost  every  particular,  except 
the  suddenness  of  onset  and  the  completeness  of  unconsciousness,  this 
second  stage  of  grand  hysteria  resembles  an  epileptic  attack.  It  has 
been  called  hystero-epilepsy.  It  is  pure  hysteria  and  has  nothing  in 
common  with  epilepsy  but  the  resemblance.     The  patient  falls  to  the 


THE    NEURONIC    DISEASES 


121 


ground,  the  eyes  are  closed,  the  head  is  rigidly  drawn  backward  or  to 
one  side,  the  muscles  of  the  jaw  are  clenched,  the  tongue  is  protruded 
and  bitten,  the  face  is  red  and  then  cyanotic,  asphyxia  seems  imminent, 
arms  and  legs  are  strongly  extended  and  adducted,  the  hands  are 
tightly  closed,  the  back  is  arched  and  the  whole  body  is  rigid  and  stiff. 
In  a  few  minutes  this  rigidity  passes  off  and  a  stage  of  clonic  spasm 
follows.  The  face  assumes  horrible  grimaces,  the  limbs  and  body  un- 
dergo rapid  alternations  of  rigidity  and  relaxation,  the  patient  rolls 
from  side  to  side  or  makes  salaams  or  throws  her  legs  into  the  air  and 
does  all  kinds  of  absurd  and  purposeless  things.  She  cries,  screams, 
laughs,  bellows,  barks,  scolds,  yells  and  seems  to  be  in  a  perfect  de- 
lirium of  mind  and  muscle. 

There  is  in  all  this  a  slight  return  of  the  mental  faculties,  but  the 
consciousness  is  far  from  being  awake,  only  realizing  as  it  were  its 

FIGURE  33. 


Hystero-epilepsy.     Arc  de  Cercle.     (After  Richer.) 

powerlessness  and  want  of  control  over  the  subconsciousness.  It 
struggles  to  regain  its  normal  ascendency,  but  failing  to  do  so,  the 
patient  passes  into  the  third  stage  in  which  the  subconscious  dominates 
and  controls  the  physical  movements,  not  in  the  delirious  and  spasmodic 
way  of  the  unconscious  epilptoid  stage  nor  in  the  rational,  purposive 
way  of  the  fully  awakened  higher  consciousness  but  in  a  hazy,  semi- 
rational,  dream-like  manner  that  harmonizes  perfectly  in  all  probability 
with  the  ill-defined,  ill-regulated,  evanescent,  incongruous  multitude 
of  hazy  ideas  floating  en  masse  here  and  there  through  the  patient's  sub- 
consciousness. This  is  the  period  of  the  passionate  (plastic)  attitudes. 
The  hallucinations  of  which  the  patient  is  the  victim,  ma}-  almost  be 
positively  suspected  by  the  attitudes  she  assumes.  Fear,  anger,  ecstasy, 
eroticism,  meditation,  religious  em.otion,  jealousy,  love,  hate,  are  all 
marvelously  depicted.  The  ecstatic  and  divine  possessions  of  the 
mediseval  saints,  nuns  and  monks,  the  enraptured  attitudes  often  painted 
by  the  great  artists  in  their  pictures  of  the  early  fathers  of  the  church, 
and  all  that  class  of  tales,  biographies,  legends  and  art  in  which  high 
and  ecstatic  emiOtionalism  is  represented,  is  now  explained  upon  a 
hvsterical  basis. 


122  THE    NEURONIC    DISEASES 

The  hallucinations  of  the  patient  in  this  third  stage  of  grand  hys- 
teria may  be  modified  by  external  stimulation  through  any  one  of  the 
senses.  She  is  in  a  sort  of  hypnotic  state,  much  as  a  normal  person  is 
when  half  asleep.  Inpouring  impressions  are  received  and  acted  upon 
as  if  they  were  original. 

Finally,  as  a  last  stage,  there  follows  a  quiet  delirium  as  the  pa- 
tient is  emerging  from  her  subconscious  condition  into  one  of  full 
consciousness.  In  this  terminal  delirium  certain  animal  hallucinations 
play  the  most  important  role.  When  the  entire  attack  has  passed  off 
there  may  remain  some  disturbance  of  sensation,  movement,  etc.,  for  a 
time.  These  attacks  may  last  altogether  from  ten  to  thirty  minutes. 
When  they  follow  one  another  with  great  rapidity  for  several  days, 
the  condition  is  known  as  statiis  hystericus. 

Comparatively  few  cases  of  grand  hysteria,  as  described  above, 
are  seen  in  this  country,  or  outside  of  France  and  the  Latin  countries. 

FIGURE  34. 


Hystero-epilepsy.     (After  Mi'Is.l 

Here  the  attacks  are  more  apt  to  be  mild  and  the  symptoms  more  or- 
ganic-like and  localized.  There  may  be  slight  premonitory  feelings 
of  depression  and  exaltation,  irritability,  restlessness  and  gastric  sensa- 
tions, which,  however,  are  hardly  ever  obtrusive  enough  to  deserve 
the  name  of  aurae  as  it  is  used  in  epilepsy.  Then  follows  the  emotional- 
ism shown  by  crying,  laughing,  screaming,  attitudinizing.  Pains  and 
hypersesthesia  are  loudly  complained  of.  Tremor  and  vibratory  move- 
ments involve  the  whole  or  parts  of  the  body.  Even  local  paralysis  and 
contractures  may  appear. 

All  of  these  manifestations  occur  under  complete  consciousness, 
with  more  or  less  volitional  preservation  and  with  great  changeability. 
A  sudden  change  in  the  patient's  mental  state  may  cause  them  to  change 
suddenly  or  disappear  entirely  and  the  attack  iDe  thus  brought  to  an 
end.  On  account  of  this,  willfulness  and  obstinacy  seem  to  be  at  the 
bottom  of  the  patient's  doings,  and  the  attendants  becoming  thereby 
angry  and  impatient,  she  is  treated  with  some  form  of  punishment. 
This  is  a  serious  error  and  shows  that  the  attendants  have  no  real  con- 
ception of  the  nature  of  the  disease.  The  harsh  and  painful  methods  so 
often  adopted  in  the  management  of  these  cases  produce  their  results 


THE    NEURONIC    DISEASES 


123 


not  by  reason  of  their  punitive  characteristics,  but  by  reason  of  their 
influence  upon  the  diseased  mentality. 

The  tremor  of  hysteria  is  pecuharly  frequent  and  characteristic. 
It  may  involve  the  whole  body  or  only  the  extremities.  In  the  more 
common  forms  the  oscillations  (five  to  seven  a  second)  are  rapid, 
rhythmical  and  of  large  amplitude.  The  tremor  may  vary  so  as  to 
simulate  paralysis  agitans,  or  it  may  assume  the  appearance  of  the 
jerking  movements  of  multiple  sclerosis,  chorea  or  myoclonus.  Hys- 
terical chorea  is  pure  hysteria  that  is  sometimes  supposed  to  be  chorea. 

A'arious  forms  of  local  paralysis  or  limited  paresis  are  met  with  in 
hysteria.  A  close  stud}'  of  the  paralysis  reveals  its  psychic  origin, 
for  it  seems  to  be  clearly  due  to  a  sort  of  aboulia,  the  loss  of  will  power, 

FIGURE  35. 


Hystero -epilepsy.      (After  Mills.) 


however,  being  itself  due  to  the  loss  of  mental  conception  of  motion. 
It  disappears  under  ether  narcosis  and  electrical  stimulation.  It  is 
changeable  and  is  never  accompanied  by  atrophy  or  other  trophic  symp- 
toms. Instead  of  being  a  complete  paralysis  it  is  more  often  a  kind  of 
loss  of  energ3^  The  grasp  of  the  hand  is  feeble,  but  changes  even  while 
the  attendant  is  holding  the  hand.  The  weakness  is  volitional  in  origin, 
as  shown  by  the  fact  that  automatic  movements  are  often  retained. 

All  forms  of  organic  paralysis,  monoplegia,  hemiplegia  and  para- 
plegia may  be  simulated  in  hysteria.  The  monoplegias  are  probably 
the  most  frequent,  the  hemiplegias  the  least.  Organic  paralysis  is  best 
differentiated  by  exclusion,  though  as  a  rule  there  will  be  slight  varia- 
tions in  hysterical  paralysis  that  upon  very  careful  examination  will 


124 


THE    NEURONIC    DISEASES 


render  its  diag-nosis  usually  easy.  For  example,  hysterical  hemiplegia 
scarcely  ever  includes  the  face  and  tongue,  as  organic  hemiplegia  usu- 
ally does ;  and  the  contracture  upon  the  hemiplegic  side  may  be  in  the 
reverse  direction  from  what  it  would  be  in  organic  disease.^  In  the 
consideration  of  the  various  organic  paralyses,  further  details_  in  regard 
to  their  differentiation  from  the  hysterical  form  will  be  mentioned.  In 
all  these  paralytic  conditions  the  knee-jerks  are  never  lost;  as  a  rule 
they  are  increased. 

'  Hysterical  aphonia  is  a  paralytic  symptom  so  common  as  to  de- 
serve special  consideration.  The  voice  being  so  closely  involved  in  the 
mentalization  of  the  patient,  its  loss  is  one  of  the  most  frequent  forms 

FIGURE  36. 


Hystero-epilepsy.      (After    Mills.) 

of  hysterical  paralysis.  The  paralysis  is  usually  sudden  in  onset,  com- 
plete, and  involves  both  vocal  cords.  It  is  volitional  in  origin,  as  shown, 
by  the  fact  that  in  singing,  counting  or  in  any  other  form  of  automatic 
vocalization,  as  well  as  in  coughing  and  hawking,  it  is  sometimes  mo- 
mentarily restored.  Usually  the  patient  can  only  whisper.  At  other 
times  the  paralysis  is  not  so  complete,  the  voice  being  altered  and 
rendered  harsh  and  unnatural.  In  rare  cases  even  the  power  of  whis- 
pering is  lost.  This  is  known  as  hysterical  dumbness  or  mutism.  Un- 
like aphasics,  a  hysterical  mute  preserves  more  naturally  her  panto- 
mimic actions  and  cannot  even  articulate  a  single  word.  Close  to 
hysterical  mutism,  either  preceding  or  following  it,  is  hysterical  stutter- 
ing.   Hysterical  deafness  has  also  been  observed  with  the  mutism. 

The  ocular  paralyses  of  hysteria  are  the  subject  of  much  dis- 
cussion. Ptosis,  or  pseudoptosis,  due  to  a  spasm  of  the  orbicularis 
palpebrarum  is  not  uncommon.  Sometimes  the  eyelid  is  kept  widely 
open  by  a  spasm  of  the  levator  palpebrse.  The  diagnosis  of  these  con- 
ditions from  organic  paralysis  is  difficult,  but  powerful  psychic  sug- 
gestion, with  the  aid  of  electricity,  will  often  diagnose  correctly  and 
cure  the  paralysis.  The  muscles  of  the  eyeball  are  rarely  paralyzed. 
Oppenheim  says  they  are  generally  simulated  by  contracture  of  the 
antagonists,  as,  for  example,  spasm  of  the  internal  rectus,  causing  an 


THE    NEUROXIC    DISEASES 


125 


appearance  of  paralysis  of  the  externus.  He  further  declares  that  in 
his  experience  a  true  h3-sterical  paralysis  of  the  ocular  muscles  never 
occurs.  It  is  admitted  by  others,  however,  that  a  myosis,  paralysis  of 
the  muscles  of  accommodation,  and  pupillary  rigidity  may  occur. 
Monocular  diplopia  or  polyopia  may  result  from  closure  of  one  eye,  or 
defective  accommodation.  It  may  be  associated  with  micropsia  or 
macropsia.  As  in  all  hysterical  paralyses,  these  of  the  eye  are  char- 
acterized by  their  lack  of  permanency,  their  alteration  under  psychic 
influence  and  their  association  with  other  hysterical  manifestations. 
Dvsphagia,  with  or  without  disturbance  of  articulation,  is  an  oc- 
casional  symptom  of  hysteria.     It   is  due  to  paralysis  of  the  velum 

FIGURE  Z7. 


Hysterie  flexion  contracture  of 
one  leg.  (After  Richer,  taken  from 
Tourette's  work.) 

palati  and  deglutitory  muscles.  It  is  generally  complete  and  must 
therefore  be  most  carefully  distinguished  from  organic  paralysis. 

Diaphragmatic  paralysis  is  rare  in  hysteria,  though  it  is  often 
simulated  by  malingerers.  Cases  have  been  reported  by  Gilles  de  la 
Tourette,  Petrazzini  and  others.  It  is  very  alarmung  sometimes.  Ac- 
cording to  A\'ernicke,  there  is  an  insufficiency  of  the  diaphragm,  which 
is  common  in  both  hysteria  and  neurasthenia.  In  my  opinion  it  belongs 
to  the  latter  neurosis,  which,  as  is  well  known,  sometimes  complicates 
hysteria.  Paralysis  of  the  bladder  is  very  rare.  The  retention  of  the 
urine  and  the  occasional  dysuria  are  due  to  hysterical  spasm  of  the 
sphincter  vesicae. 

Disturbances  of  the  Alimentary  Canal. — Loss  of  appetite,  anorexia 
hysterica,  is  sometimes  a  serious  condition,  for  if  not  overcome  after 
a  time,  it  will  lead  to  inanition  and  even  death.  It  sometimes  alternates 
with  excess  of  appetite  or  bulimia.     Eructations  of  gas  from  the  stom- 


126  THE    NEURONIC    DISEASES 

ach  are  not  uncommon,  especially  in  cases  of  hystero-neurasthenia. 
X'omiting  is  more  frequently  a  purely  hysterical  manifestation  than  are 
the  eructations.  ]\Iucus  and  saliva  are  expelled,  usually  with  the  food 
that  has  just  been  swallowed.  In  spite  of  this  the  appetite  and  general 
physique  do  not  fail.  Stercoraceous  vomiting  may  occur  and  according 
to  Fazio  may  be  spasmodic  or  paralytic  in  origin,  but  is  not  due  to  sim- 
ple antiperistalsis.  The  vomiting  may  not  be  so  purely  a  hysterical 
svmptom  in  some  cases  as  it  is  the  result  of  the  ingestion  of  nauseous 
substances,  like  urine,  taken  purposely  to  provoke  sympathy.  As  a 
rule  vomiting  is  not  a  particularly  dangerous  symptom  in  hysteria, 
whatever  may  be  its  origin. 

Both  constipation  and  diarrhoea  are  observed  in  hysteria.  The 
former  is  so  common  as  to  have  been  considered  a  predisposing  cause, 
chiefly  through  autointoxication.  A  temporary  diarrhcea,  after  some 
violent  emotion,  may  occur  in  hysteria  as  well  as  in  som.e  normal  states. 

Abdominal  distension,  known  as  meteorism  and  tympanites,  with 
intestinal  gurgling  and  borborygmus,  occur  in  nervous  people  and  may 
be  very  annoying  in  hysteria.  The  distension  often  subsides  without 
the  evacuation  of  the  gas  that  caused  it. 

Disturbances  of  the  Circulatory  and  Vasomotor  Systons. — In  the 
paroxysm  the  pulse  is  apt  to  be  accelerated.  \X'hen  there  is  syncope  it 
is  retarded.  Cardiac  palpitation  is  usually  a  mere  subjective  sensation 
and  may  be  associated  with  difficulty  of  respiration.  Under  high  emo- 
tion the  palpitation  may  be  real.  The  pulse  often  remains  normal. 
Spontaneous  haemorrhages  from  various  parts  of  the  body  of  a  hys- 
terical patient  should  be  looked  upon  with  suspicion.  As  a  rule  it  is 
brought  on  by  secret  means  to  provoke  attention.  This  is  confirmed 
by  the  fact  that  such  hsemorrhages  rarely  occur  from  the  internal  organs 
which  are  beyond  the  reach  of  the  patient's  machinations.  It  is  de- 
clared, however,  upon  good  authority,  that  spontaneous  bleeding  from 
the  forehead,  breast,  foot  and  other  superficial  parts  of  the  body  does 
occasionally  occur.  [Metrorrhagia  may  be  very  profuse,  but  curiously 
the  general  health  is  but  little  affected. 

]vluch  more  common,  reasonable  and  objectively  demonstrable  is 
the  occasional  local  asphyxia  sometimes  associated  with  hysterical 
anaesthesia.  Oppenheim  once  excised  a  piece  of  muscular  tissue  from 
a  hysteric  without  any  bleeding.  A'asomotor  spasm  is  the  explanation 
of  this  phenomenon.  Pallor,  flushing,  cyanosis  may  all  be  observed, 
often  in  rapid  alternation  in  the  same  patient.  Souques  has  reported 
a  case  of  hysterical  Raynaud's  syndrome,  in  which  mere  suggestion 
with  a  placebo  caused  the  paroxysms  of  local  asphyxia,  which  up  to 
that  time  had  averaged  eight  a  day.  to  disappear  entirely.  Of  course, 
in  this  hysterical  type  of  Raynaud's  disease,  or  syndrome,  gangrene 
does  not  occur.  CEdematous-like  swellings,  non-pitting,  with  decreased 
local  temperature,  are  sometimes  seen.  On  account  of  the  oedema, 
pain  on  movement,  etc.,  a  hysterical  joint  may  closely  simulate  joint- 
disease.  The  vasomotor  disturbances  may  be  responsible  largely  for 
the  associated  hyperidrosis,  polyuria  and  even  diabetes  insipidus  that 
occasionally  take  place.  Hysterical  skin  aitections  are  vasomotor  in 
character.     Gangrene  has  thus  been  seen  to  follow  an  urticaria,  an  erv- 


THE    NEURONIC    DISEASES  I27 

thema  or  more  frequently  pemphigoid  blebs.  Occasionally  a  gasteri- 
form  eruption  was  the  first  symptom  (Van  Harlingen). 

The  very  nature  of  the  disease,  \vith  its  exalted  emotions  and 
imagination,  would  presuppose  frequent  disturbances  iii  the  sexual 
sphere.  Doubtless  this  is  the  reason  why  the  disease  was  so  long  re- 
garded as  primarily  due  to  sexual  aberrations.  The  effect  was  mis- 
taken for  the  cause.  Impotence  and  loss  of  sexual  desire  may  Jae  due 
to  local  anaesthesia.  With  a  local  hyper^sthetic  condition,  or  without, 
there  may  be  abnormal  desire  amounting  almost  to  nymphomania  or 
satyriasis.  Perversions  and  semi-hypnotic  delusions  in  this  sphere  are 
not  only  possible,  but  are  so  common  that  no  physician  who  regards 
his  own  comfort  and  reputation  would  think  of  examining  a  hysteric 
without  the  presence  of  a  third  party. 

Hysterical  fever  has  been  reported.  As  a  rule  it  is  the  product 
of  some  form  of  deception.  If  it  does  occur  it  must  be  exceedingly 
rare.  Hysterical  attacks  as  a  rule  do  not  occur  during  the  rise  of  the 
temperature.  If  changes  in  the  pulse,  respiration  and  renal  secretion 
accompany  the  elevation  of  temperature,  there  is  probably  some  obscure 
inflammatory  condition  present.  However,  pure  hysterical  tempera- 
tures of  108  and  113  degrees  F.  have  been  recorded.  A  large  question 
mark  is  to  be  put  after  the  statement  that  Teale  once  found  the  tem- 
perature in  a  hysterical  patient  122  degrees  F.  They  are  said  to  be 
characterized  by  large  daily  curves,  to  be  but  little  hitluenced  by  the 
usual  antipyretics,  and  to  vary  considerably  when  taken  in  different 
parts  of  the  body. 

Pathology  and  Pathogenesis. — Much  confusion  surrounds  the 
pathology  and  pathogenesis  of  hysteria.  This  is  not  because  we  have 
not  complete  data  upon  the  disease,  but  because  there  is  so  much  differ- 
ence of  opinion  as  to  the  nature  of  psychic  processes,  both  normal  and 
abnormal.  It  is  practically  universally  admitted  nowadays  that  hysteria 
is  a  psychic  manifestation  with  secondary  neuro-muscular  phenomena. 
It  is  primarily  and  essentially  a  psychosis.  This  psychosis  is  dependent 
of  course  upon  the  nature  and  course  of  the  patient's  individual  ex- 
periences as  brought  to  her  through  and  by  way  of  her  five  senses. 
Hence  the  role  played  by  these  senses  in  the  causation  of  the  disease 
and  the  long  list  of  physical  etiological  factors  that  have  hithertO'  been 
assigned  at  various  times  as  the  cause  of  hysteria.  Up  to  the  present 
time  the  pathology  of  hysteria  has  been  made  to  include  almost  every 
possible  alteration  in  about  every  possible  organ  and  tissue  of  the  body. 
One  thing  is  certain,  namely,  that  there  are  no  constant  pathological 
findings  of  any  sort,  and  in  all  of  the  cases  there  are  no  changes  in  the 
central  nervous  system  upon  which  a  pathology  can  be  erected. 

For  this  reason  some  deny  that  hysteria  should  be  considered  as 
a  disease  at  all,  looking  upon  it  as  a  mere  mental  and  nervous  disturb- 
ance caused  by  the  changes  and  diseases  in  any  or  all  of  the  tissues  of 
the  body. 

On  the  other  hand,  some  authorities  regard  it  as  the  result  of  some 
hypothetical  changes  in  the  molecular  substance  of  the  nerve  cells, 
causing  them  to  manifest  an  abnormal  functional  activity,  which  classi- 
fies hysteria  as  a  dynamic  disease  without  discoverable  lesions. 


128  THE    NEURONIC    DISEASES 

In  both  of  these  explanations  it  will  be  noted  that  a  physical  basis, 
a  pathology  in  the  general  sense  of  the  word,  is  assumed  for  the  dis- 
ease. It  is  a  strange  fact  that  the  great  variability,  instability  and  sud- 
den changeability  of  the  clinical  manifestations  of  hysteria  have  not 
long  since  led  the  authorities  to  relinquish  the  idea  of  a  physical  basis 
for  these  changes.  So  materialistic  is  the  average  trend  of  thought 
that  nien  find  it  hard  to  conceive  of  a  disturbance  of  mentality  without 
an  underlying  change  of  physical  structure.  This  is  scarcely  to  be  won- 
dered at,  for  logically  it  would  seem  to  be  a  necessity  that  every  change 
of  action  presupposes  a  change  of  some  sort  in  the  acting  substance. 
And  yet  there  are  ways  by  which  activities  may  be  changed  and  the 
underlying  substance  remain  both  physically  and  functionally  undis- 
turbed. This  is  true  not  only  in  certain  abnormal  states,  but  is  open 
to  daily  obser\"ation  in  perfectly  normal  states.  Mental  activities  are 
complex  in  character  and  depend  upon  the  play  of  their  elementary 
constituents  upon  one  another.  These  constituents  may  be  acting  in- 
dividually in  the  way  that  they  should  in  all  their  normal  perfection,  but 
by  means  of  an  exaltation  of  some  and  a  diminution  of  others  or  even 
by  a  simple  rearrangement  among  them,  the  resulting  complex  and 
final  activity  may  be  very  different  from  what  was  expected,  or  be  sud- 
denly changed  from  what  was  at  that  moment  in  performance. 

A  rough  illustration  may  make  this  clearer.  Suppose  in  a  great 
railroad  office  all  the  employes  are  doing  their  usual  duties  in  their 
usual  way ;  the  great  complex  system  will  move  in  the  usual  way.  The 
elements  of  the  system,  the  individuals,  will  be  working  normally,  and 
so  the  sum  total  of  activities,  the  working  of  the  entire  railroad  from 
end  to  end,  will  be  normal.  Suppose,  however,  some  unusual  factor  is 
introduced  among  the  activities  of  the  individual  employes :  suppose 
the  president  of  the  company  or  the  manager,  with  all  his  authority 
to  command,  should  give  to  oile  of  these  individual  employes  an  erratic 
order  to  pass  on  over  the  system.  The  employe  takes  the  order  and 
does  with  it  in  his  usual  way  what  his  chief  told  him  to  do;  so  does 
the  next  employe  and  the  next;  until  finally  the  whole  system  is  sud- 
denly disturbed  in  its  usual  routine  of  activity.  The  individuals,  even 
the  chief,  were  normal  in  structure,  were  well  within  the  limits  of  their 
functional  activity,  and  yet  by  an  unusual  play  of  these  activities  as 
individuals  upon  one  another,  there  has  resulted  a  most  unusual  work- 
ing of  the  entire  complex  activity  of  the  whole  system. 

Hysteria  is  a  psychosis  primarily  and  essentially.  It  involves  in 
its  last  analysis  a  disturbance  of  the  mental  faculties — namely,  the 
memory,  the  imagination,  the  will  and  the  intellect.  These  so-called 
faculties,  as  well  shown  by  that  great  teacher  of  modern  physiological 
psychology.  Wilhelm  Wundt,  are  not  actual  entities  or  things  with  a 
physical  habitat  in  the  brain  or  elsewhere.  They  represent  merely 
processes  or  forms  of  activity.  They  are  merely  convenient  names 
for  particular  kinds  of  complex  and  compound  movements.  Accord- 
ing to  Wundt,  sensations  and  feelings  are  the  primary  and  only  ele- 
ments of  all  psychic  manifestation.  These  sensations  and  feelings  are 
dependent,  of  course,  upon  the  physical  changes  in  the  nerve  cells  and 
fibres.     These  sensory  and  sesthetic  phenomena  combine  or  separate 


THE    NEURONIC    DISEASES 


129 


among  themselves  in  such  a  wa}'  as  to  produce  that  complex  activity 
which  we  denominate  the  mind.  The  feelings,  by  becoming  stronger, 
develop  into  emotions ;  emotions  overflow  into  muscular  action  if  they 
are  strong  enough,  and  we  call  the  process  volition.  Percepts  are 
awakened  by  sensory  stimulation  and  being  brought  into  juxtaposition 
or  combined  with  other  percepts  form  concepts.  The  comparing  and 
contrasting  of  concepts  is  the  process  that  underlies  imagination,  un- 
derstanding and  judgment. 

Thus  the  whole  mind  is  formed  by  the  interplay  of  certain  ^ele- 
mentary processes  based  upon  sensation  and  feeling.  These  sensations 
and  feelings  may,  of  course,  be  disturbed  by  physical  lesions  in  or 
about  the  nerve  elements  and  the  processes  which  underlie  psychic 
action  will  be  disturbed. 

This  is  the  explanation  of  the  wav  in  which  physical  causes  often 
give  rise  to  hysteria,  as  well  as  to  many  other  forms  of  mental  trouble, 
such  as  polyneuritic  psychosis,  the  psychoses  of  the  infectious  diseases, 
etc.  But  it  is  evident  from  Wundt's  point  of  view  or  from  the  stand- 
point of  modern  voluntaristic  psycholog}-,  that  the  mental  faculties, 
so-called,  may  be  disturbed  by  a  disturbance  in  the  miere  interplay  of 
the  elementar}-,  constituent  processes  that  make  up  these  faculties. 
These  elementary  constituents  may  not  necessarily  be  abnormal  indi- 
vidually, but  if  some  of  them  be  thrown  into  a  state  of  unusual  activity, 
the  routine  balance  between  them  all  is  so  far  disturbed  as  to  cause  a 
marked  disturbance  in  the  sum  total  of  all  their  activities — namely,  the 
mind.  This  explanation  makes  of  hysteria  a  psychic  disturbance  de- 
pendent upon  either  physical  or  functional  causes.  The  physical  causes 
may  lie  in  disease  of  the  ultimate  nerve  elements,  thus  changing  the 
elementary  sensations  and  feelings  that  form  the  ultimate  substrata  of 
mind.  On  the  other  hand,  the  functional  causes  may  reside  in  an 
unwonted  disturbance  in  the  usual  interplay  of  what  may  be  quite 
normal  sensations  and  feelings. 

Among  the  physical  causes  there  may  be  found  all  sorts  of  lesions 
giving  rise  to  hysteria.  For  this  reason  physical  diseases  of  all  kinds 
may  provoke  among  those  neurotically  unstable  an  outbreak  of  hysteria. 
On  the  other  hand,  fright,  sorrow,  excess  of  joy,  mental  strain,  may 
develop  into  hysteria  in  those  neurotically  unstalDle,  not  because  these 
mental  states  are  abnormal,  but  because  they  are  so  unusual  as  to  dis- 
turb or  at  least  represent  a  disturbance  in  the  usual  form  of  mentaliza- 
tion.  No  explanation  of  hysteria,  in  which  disease  there  is  admittedly 
no  pathological  findings,  so  harmonizes  all  the  clinical  phenomena  and 
shows  the  half-truth  contained  m  most  of  the  explanations  hitherto 
offered.  For  example,  the  old  view  that  it  was  due  to  a  paralysis  of 
the  will  is  true  in  part  only.  In  some  cases  aboulia  is  present  because 
the  psychic  process  which  we  call  the  will  and  which  is  a  product  O'f 
the  emotions,  which  emotions  in  turn  are  dependent  upon  the  elemental 
feelings,  is  disturbed  by  the  disturbance  in  these  underlying  processes. 
Certain  feelings  are  too  weak  or  too  strong;  the  corresponding  emo- 
tions have  caused  the  rise  of  weak  or  altered  motives ;  the  resultant 
motor  activity  fails  entirely  or  is  entirely  perverted.  Janet  speaks  of 
a  "contracted  consciousness"  underlving  hysteria.     In  some  cases  this 


130  THE    NEURONIC    DISEASES 

may  be  true,  just  as  the  volition  process  may  be  rendered  paretic. 
Others  have  thought  that  hysteria  was  due  to  an  excess  of  mental 
inhibition.  It  is,  in  some  cases.  Still  ethers  find  that  emotionalism  and 
an  excess  of  imagination  enter  most  largely  into  its  pathogenesis.  In 
some  cases  they  undoubtedly  do.  And  finally,  not  a  few  believe  that  it 
is  merely  the  result  of  a  vicious  education  and  discipline  in  a  neu- 
ropathic and  unstable  individual.  In  a  large  percentage  of  cases  this 
also  is  most  emphatically  true. 

In  all  of  these  views,  ho^^•ever,  it  will  be  remarked  that  the  trouble 
is  primarily  a  pure  psychosis.  The  explanation  which  we  have  given, 
based  upon  a  rational  and  physiological  explanation  of  mind,  affords 
the  best  generalization  for  the  harmonizing  and  clarifying  of  all  these 
apparently  diverse  but  really  disjointed  parts  of  one  and  the  same 
view^ 

Diagnosis. — In  an  ordinary,  uncomplicated  case,  hysteria  is  not 
difficult  to  detect.  The  large  majority  of  the  cases,  however,  are  not  of 
the  ordinary  type  or  uncomplicated ;  hence  the  diagnosis  of  hysteria 
is  nearly  always  a  matter  demanding  caution,  thoroughness  and  experi- 
ence. It  should  ahvays  be  diagnosed  by  the  exclusion  of  all  other  pos- 
sible functional  and  organic  diseases ;  and  in  arriving  at  the  diagnosis 
the  psychic  origin  of  hysteria  should  never  be  lost  sight  of.  Even 
though  the  most  careful  and  experienced  physicians  may  be  at  times 
entirely  at  sea,  the  remembrance  of  the  two  facts  just  stated  will  go 
a  long  way  tow^ard  making  a  diagnosis  accurate. 

The  mental  origin  of  the  motor,  sensory  and  other  symptoms  of 
hysteria  can  nearly  always  be  determined  by  the  character  and  loca- 
tion of  these  symptoms  and  their  alteration  when  the  patient's  attention 
is  distracted,  or  his  mind  is  put  out  of  action,  as  it  were,  by  chloroform 
or  ether  narcosis  or  hypnotism.  An  experienced  examiner  sometimes 
learns  to  detect  hysteria  almost  intuitively,  and  this  is  not  altogether 
surprising.  Psychic  manifestations  of  all  sorts,  or  rather  symptom.s 
of  all  sorts  that  ow^e  their  origin  to  the  mind  of  the  patient,  when 
collected  and  presented  en  masse,  present  a  more  or  less  characteristic 
picture  differing  from  a  collection  of  symptoms  that  owe  their  origin  to 
simple  organic  changes  in  the  nervous  structures.  The  voluntaristic 
explanation  of  mind — namely,  that  it  is  merely  a  term  to  cover  certain 
interdependent  and  interrelated  processes  among  the  elementary  sensa- 
tions and  feelings — accounts  for  the  variability,  distribution,  change- 
ability and  other  peculiar  characteristics  of  the  symptom-complex  of 
this  psychic  disease,  hysteria,  and  emphasizes,  on  the  other  hand,  the 
fixity,  the  anatomical  distribution  and  the  greater  permanency  and 
continuity  of  the  symptoms  of  the  organic  diseases  with  which  it  is 
liable  to  be  confounded. 

The  psychic  nature  of  hysteria  makes  plain  why  it  is  so  often 
associated  with  organic  diseases.  For  its  activity,  mind  is  dependent 
upon  the  activity  of  its  primary  elements,  the  sensations  and  feelings, 
and  these  in  turn  are  dependent  upon  the  action  of  the  histological 
nerve  and  other  tissues  of  the  body.  Given  an  organic  disease  or  dis- 
turbance of  any  kind  anywhere  in  the  body,  and  it  is  onl}'  a  question  of 
temperament,  time  and  severity  of  this  disease  before  a  psychic  dis- 


THE    NEURONIC    DISEASES  I3I 

turbance  will  be  provoked  that  may  eventuate  in  a  more  or  less  severe 
attack  of  hysteria.  One  must  not  get  the  idea  from  this  that  hysteria 
is  only  a  mental  disturbance  symptomatic  of  some  organic  disease, 
for  such  a  notion  would  only  represent  a  half  truth.  The  mind  is  the 
result  of  two  sets  of  underlying  factors.  On  the  one  hand  it  is  de- 
pendent upon  nerve  integrity  and  their  normal  sensations  and  feelings ; 
but  on  the  other  hand  it  is  a  process,  a  mere  form  of  activity,  dependent 
upon  the  normal  interplay  of  the  elementary  processes  of  sensation  and 
feeling.  Hence,  not  all  cases  of  hysteria  are  the  product  of  gross 
organic  diseases  or  are  even  associated  with  them.  The  association  of 
the  two  diseases  m„ay  obtain  even  without  any  relationship  other  than 
the  mere  association.  All  these  facts  must  be  taken  well  into  account 
when  differentiating  hysteria  fro'm  organic  diseases  and  emphasize  the 
importance  of  diagnosing  the  hysteria  by  the  exclusion  of  every  other 
possible  disease.  It  is  safer  to  overlook  a  hysteria  than  it  is  to  pass 
organic  symptoms  as  being  hysterical.  The  condition  of  certain  organs 
that  are  entirely  beyond  the  control  of  the  mind,  as,  for  instance,  the 
pupils,  the  heart  and  respiration,  etc.,  may  all  be  invoked  to  exclude 
hysteria. 

Probably  the  disease  that  is  most  frequently  mistaken  for  hysteria 
is  multiple  sclerosis.  Indeed,  Westphal  described  a  general  neurosis, 
classified  by  Charcot  and  his  school  as  a  form  of  true  hysteria,  which 
could  not  be  distinguished  from  multiple  sclerosis  either  in  its  course  or 
its  symptoms,  and  which  he  called  pseudo-sclerosis.  True  multiple 
sclerosis,  however,  may  be  distinguished  from  either  hysteria  or  West- 
phal's  pseudo-sclerosis  by  the  presence  of  nystagmus,  the  condition  of 
the  optic  nerve,  the  voluntary  intentional  tremor  and  the  absence  of 
psychic  influences.  The  scanning  speech  of  multiple  sclerosis  is  more 
uniform  and  consistent  than  is  the  irregular  speech  sometimes  observed 
in  hysteria.  In  the  latter  disease  some  words  are  scanned  and  others 
are  merely  jerked  out  irregularly,  quickly  or  slowly.  The  paraplegia 
of  multiple  sclerosis  usually  reveals  a  suggestion  of  spasticity,  and 
clonus  when  present  is  absolutely  involuntary,  regular  and  intense. 
Remember,  however,  that  hysteria  and  multiple  sclerosis  are  often 
associated,  and  one  must  be  careful  to  determine  the  symptoms  that 
belong  to  either  of  the  respective  diseases. 

In  hrain  tumor  and  cerebral  syphilis  there  are  symptoms  that 
hysteria  at  times  closely  simulates.  Moreover,  both  conditions  may 
develop  or  at  least  be  associated  with  hysterical  phenomena.  An  error 
in  diagnosis  is  therefore  not  uncommon.  When  there  are  the  usual 
ophthalmoscopic  signs  of  tumor  or  syphilis  present,  there  can  be  no 
possibility  of  mistake.  The  headache  of  the  organic  troubles  is  differ- 
ent from  that  of  hysteria  in  being  m^ore  continuous,  less  sharp,  more 
definitel}''  localized  and  more  prominent  in  the  early  hours  of  the  morn- 
ing. With  the  cephalalgia  of  the  organic  diseases  the  mind  is  heavy, 
dull  and  apathetic,  the  countenance  is  expressionless  and  the  pulse  is 
retarded.  There  may  be  vomiting.  Usually  the  other  symptoms  of 
hysteria  are  sufffciently  pronounced  to  render  a  differential  diagnosis 
clear. 

'  Hysterical    paraplegia    may    be    mistaken    for   the    paraplegia    of 


132  TJJE    NEURONIC    DISEASES 

myelitis.  In  the  latter  disease,  however,  the  character  and  distribution 
of  the  sensory  disturbance,  as  well  as  the  bladder  and  rectal  troubles, 
are  sufficient  to  differentiate  the  two  diseases.  In  myelitis  the  absence 
of  all  psychosis  and  the  non-implication  of  the  special  senses  are  to  be 
carefully  noted.  In  the  same  way  vertebral  caries  may  be  distinguished 
from  hysteria,  the  sensitiveness  of  the  former  disease  being  more  cir- 
cumscribed and  less  like  a  cutaneous  hyperjesthesia. 

Hysterical  joints  are  often  mistaken  for  arthritic  disease.  A 
careful  examination  of  the  joint  for  organic  disease  and  of  the  patient 
for  other  hysterical  stigmata  wall  make  the  distinction  clear. 

Hysterical  pains  ought  not  as  a  rule  to  be  hard  to  dift'erentiate 
from  neuralgic  pains  or  pains  due  to  organic  disease.  One  has  but  to 
remember  that  hysterical  pain  is  a  psychic  phenomenon  and  therefore 
has  no  definite,  fixed,  anatomical  location  as  have  the  pains  of  organic 
disease.  On  the  other  hand,  the  latter  pains  are  not  so  susceptible  to 
suggestion  and  diversion  of  the  attention  as  are  the  psychic  pains  of 
hysteria.  The  other  symptoms,  both  of  hysteria  and  organic  disease, 
are  usually  sufficiently  in  evidence  to  give  very  material  assistance  in 
the  diagnosis.  The  pains  of  angina  pectoris,  cephalalgia,  etc.,  may  thus 
give  rise  to  some  confusion,  but  a  careful  application  of  the  above 
principles  in  making  the  differential  diagnosis  will  render  the  latter 
less  difficult. 

The  same  may  be  said  of  the  differential  diagnosis  between  hys- 
terical and  other  forms  of  spasm,  such  as  chorea,  tetany,  hystero- 
epilepsy,  etc.  The  psychic  complexion  of  the  hysterical  spasm  is  want- 
ing in  the  muscular  phenomena  of  these  diseases. 

Hysterical  chorea,  so-called,  is  a  rhythmical  movement,  slower  and 
more  regular  and  not  so  incoordinated  as  are  the  jerkings  of  true 
chorea.  Chorea  magna,  as  I  have  explained  elsewhere,  is  nothing  but 
hysteria. 

Likewise,  hystero-epilepsy  is  merely  a  severe  form  of  hysteria  in 
which  the  state  of  consciousness  and  convulsions  resembles  somewhat 
that  of  epilepsy.  As  there  is  no  connection  between  hysteria  and 
epilepsy  but  this  superficial  resemblance  in  a  few  cases,  it  would  be 
w^ell  to  drop  entirely  the  use  of  the  term  hystero-epilepsy.  It  is  as 
misleading  and  unwarranted  as  the  term  typho-malaria. 

Hysterical  patients  often  become  neurasthenic  and  z'ice  versa. 
(  )ccasionally  both  troubles  coexist  in  the  same  individual  without  any 
other  connection.  They  both  have  their  distinctive  signs,  which  should 
always  be  carefully  separated,  as  I  have  pointed  out  under  the  head  of 
neurasthenia. 

Hysterical  vomiting  has  not  infrequently  given  rise  to  the  errone- 
ous diagnosis  of  gastric  ulcer,  peritonitis,  perforation  and  appendicitis. 
As  a  rule  hysterical  vomiting  takes  place  so  soon  after  the  swallowing 
of  food  that  the  latter  comes  up  quite  unchanged.  The  absence  of 
characteristic  pains,  elevated  temperature,  local  tenderness  and  the 
general  history  and  psychic  nature  of  the  trouble,  vrill  help  to  deter- 
mine easily  the  hysterical  origin  of  the  vomiting. 

Oppenheim  points  out  that  there  are  persons  wixh  a  congenital 
(perhaps  due  to  a  developmental  inhibition)  or  early  developed  weak- 


THE    NEURONIC    DISEASES  I33 

ness  in  some  particular  part  of  the  central  nervous  system,  say  the 
cerebellum,  the  medulla  or  particular  cortical  centers.  Later  in  life 
these  fail  to  functionate  normally  and  disorders  arise  that  are  not 
strictly  organic  nor  yet  are  purely  hysterical.  They  may  cause  con- 
fusion in  diagnosis,  however,  and  should  be  guarded  against. 

It  is  undoubtedly  true  that  there  is  a  strong  inclination  in  hys- 
terical patients  to  practice  deception.  The  exaggeration  of  the  egotism 
with  its  necessary  tendency  to  selfishness,  the  diminution  in  the  inhibi- 
tory influence  of  the  intellect  and  higher  faculties  and  the  consequent 
overactivity  of  the  emotions,  imagination  and  more  elementary  facul- 
ties, lead  to  the  adoption  of  means  and  measures  to  accomplish  ends 
that  are  not  on  a  very  high  plane  of  justice  and  morality.  A  moment's 
consideration  will  convince  one,  however,  that  such  deceptions  are  not 
criminal,  as  they  would  be  if  resorted  to  b\-  a  normal  or  non-hysterical 
person.  Psychically  the  hysteric  individual  is  a  child  ;  mentally  she  has 
fallen  back  to  an  almost  ape-like  condition.  To  punish  her  in  a  vin- 
dictive spirit  is  both  cruel  and  unjust;  to  administer  corporal  pain 
with  the  hope  of  reforming  her  is  useless  and  unscientific.  Her  mind 
is  at  fault.  It  is  diseased.  It  works  differently  from  the  normal  mind. 
It  is  under  the  control  and  influence  of  abnormal,  strange  and  bizarre 
percepts  and  concepts.  On  accomit  of  this  it  may  be  acrmg  most 
logically  though  the  outward  manifestations  appear  so  extraordniary 
and  provoking.  The  partial  consciousness,  the  emotionalism,  tiie 
screaming,  the  dramatic  attitudes,  the  pugnacity  may  all  be  due  to 
hallucinations  and  illusions  of  a  frightful  character,  or  to  unusually 
active  memory  and  imagination  processes  rather  than  tO'  any  nerve 
influences.  The  deceptions  of  true  hysteria  may  be  identical  with  the 
deceptions  of  malingerers.  The  difiference  between  the  two,  however, 
lies  in  the  underlying  motive,  and  the  cause  and  origin  of  that  motive. 
In  both  it  is  a  strong  desire  for  some  form  of  self-gratification.  In  the 
hysteric,  however,  it  is  usually  a  desire  to  gratify  the  mere  personal 
ego,  the  love  of  self,  sympathy,  praise  or  some  other  form  of  spiritual 
self-aggrandizement.  In  the  malingerer  it  is  a  desire  for  the  acquisi- 
tion of  soime  physical  enjoyment,  money,  physical  comfort,  presents, 
etc.  In  this  sense  "hysterics"  due  to  mere  bad  discipline,  is  a  sort  of 
mild  form  of  malingering  and  being  not  the  same  as  true  hysteria 
may,  unlike  the  latter,  be  treated  at  times  advantageously  by  severe 
punitive  measures. 

True  malingering  may  be  distinguished  from  true  hysteria  by 
various  symptoms  and  measures,  one  of  the  best  of  which  is  chloroform 
or  ether  narcosis.  Spasms  of  hysterical  origin  disappear  and  the 
sensory  reflexes  undergo  change  as  the  narcosis  deepens.  The  paraly- 
sis may  be  tested  by  electricity.  Hysteria  being  a  psychosis,  its  mani- 
festations are  so  largely  subjective  in  character  that  the  examiner  has 
but  few  objective  signs  by  which  to  determine  whether  the  patient  is 
feigning  or  not.  Nevertheless,  it  takes  an  exceptionally  shrewd  in- 
dividual to  imitate  all  of  the  symptoms  of  hysteria  or  even  a  part  of 
-them,  and  to  portray  them  with  all  their  variability,  changeableness, 
peculiar  distribution  so  that  they  will  continuously  and  constantly  depict 
the  picture  O'f  true  hysteria.     It  is  much  easier  to  simulate  organic 


134  'fHE    NEURONIC    DISEASES 

disease  than  it  is  hysteria ;  so  that  if  the  simulator  of  hysteria  be  closely 
watched  he  will  portray  some  of  his  symptoms,  such  as  the  paralysis, 
contracture,  etc.,  in  a  way  that  will  resemble  organic  disease  rather 
than  hysteria.  The  moment  he  does  that  his  game  is  lost,  for  the 
symptoms  which  simulate  organic  disease,  as,  for  instance,  fixity  of 
the  paralysis,  anatomical  distribution  of  the  anaesthesia,  the  vomiting, 
etc.,  do  not  fit  in  well  with  the  other  symptoms  that  he  is  feigning,  and 
therefore  it  is  evident  that  he  is  afflicted  with  no  disease,  either  organic 
or  functional.  As  I  have  before  intimated,  hysteria  is  always  diagnosed 
best  by  the  exclusion  of  all  other  possible  diseases,  because  it  is  possi- 
ble for  it  to  imitate  all  other  diseases  so  closely ;  and  by  a  careful 
study  of  its  general  complextis  rather  than  of  its  individual  symptoms 
alone,  because  it  is  a  disease  of  the  personality,  a  psychosis,  and  not 
a  disease  of  special  anatomical  structures. 

Prognosis. — The  prognosis  of  hysteria  in  regard  to  life  is  good. 
In  regard  to  recovery  it  is  favorable  for  the  attack,  unfavorable  for 
the  general  constitutional  trouble.  Hysterical  conditions  secondary 
to  organic  disease  depend  upon  the  removal  of  these  organic  lesions. 
The  patient's  congenital,  physical  and  mental  constitution,  her  age, 
her  environment,  all  must  be  taken  into  account  in  determining  the 
possibility  of  recovery.  ]\Iedicine  cannot  hope  to  alter  natural  traits 
and  inherited  defects.  It  can  do  much,  however,  to  mitigate  their 
eftects.  Exciting  causes  it  can  often  remove  and  consequent  bad 
habits  it  can  change.  While  a  physician  may  offer  a  generally  favorable 
prognosis  in  regard  to  particular  factors  of  hysteria,  as,  for  instance, 
the  recovery  from  a  sudden  acute  outbreak,  he  should  frankly  admit 
the  probability  of  relapses  and  he  must  be  very  guarded  in  holding  out 
hope  of  a  complete  and  permanent  disappearance  of  the  disease.  In  a 
small  number  of  cases,  complete  and  permanent  cure  has  been  ob- 
tained. 

Treatment. — In  the  treatment  of  hysteria  the  guiding  thought 
should  always  be  its  psychic  nature.  It  is  primarily  a  disease  of  the 
mind ;  in  a  large  number  of  cases  it  is  the  result  of  a  vicious  habit  of 
mentalization.  This  must  be  modified  in  some  way  before  any  real 
benefit  from  treatment  can  be  hoped  for.  All  forms  of  mental  disci- 
pline are,  of  course,  most  effective  in  the  impressionable  period 'of 
childhood  and  their  most  brilliant  results  are  secured  in  hysteria  when 
adopted  as  prophylactic  measures.  Xevertheless,  mental  discipline  and 
psychic  treatment  are  imperativeh'  called  for  by  an  hysteric  at  all 
times,  whether  young  or  old,  whether  during  the  convulsive  attacks  or 
during  the  intervals  between  them.  In  other  words,  first,  last  and  all 
the  time  the  sheet  anchor  in  the  management  of  hysteria  is  the  psychic 
treatment. 

Typical  hysteria  occurs  at  all  ages  and  in  general  exhibits  itself  in 
the  same  way  in  children  as  it  does  in  adults.  The  treatment  of  the 
hysteria  of  childhood  differs  in  no  special  respect  from  the  treatment 
of  hysteria  in  the  adult. 

The  hysteria  of  the  adult  is,  as  a  rule,  the  expression  of  a  peculiar 
form  of  constitution,  and  usually  is  preceded  by  certain  premonitory 
indications  in  childhood  that  should  put  the  physician  on  his  guard  and 


THE    NEURONIC    DISEASES  I35 

urge  him  to  give  some  advice  to  the  parents  as  to  the  education  and 
training  of  the  child.    Of  course,  the  science  of  medicine  cannot  change 
the  pecuHar,  inherited  temperament  v/hich  forms  the  background  for 
the  later  hysterical  outbreaks,  but  if  its  teachings  are  listened  to  and 
followed   it   can   do   wonders   in   forestalling  these  outbreaks   and    in 
keeping  latent  the  ever- threatening  tendency  towards  them.    The  whole 
field  of  child  training,  including  a  knowledge  of  psychology  and  mental 
development,    of    pedagogy    and     educational   discipline,   and    of   the 
psychological  laws  of  growth  and  evolution,  is  an  exceedinglv  broad 
one.     Either  because  parents,  and  alas,  too  often  the  family  physician, 
are  unwilling  or  unable  to  prepare  themselves  for  so  extensive  a  sphere 
of  thought  and  activity,  they  fail  to  manage  hysteria  either  from  the 
prophylactic  or  the  therapeutic  standpoint.     Unfortunately,  much  of 
the  advice  given  under  the  head  of  the  treatment  of  hysteria  in  text- 
books of  even  very  recent  issue  is  erroneous,  because  of  the  erroneous 
conception  of  the  true  nature  of  hysterical  physical  phenomena  and  the 
peculiar  aberration  those  phenomena   undergo   in  hysteria.      Without 
occupying  too  much  space  here,  let  one  illustration  suffice.     Xearly  all 
the  text-books  suggest  that  hysteria,  whether  in  the  child  or  in  the 
adult,  is  largely  an  aboulia  and  that  therefore  the  patient's  will  should 
be  strengthened  in  every  possible  way.      As  a  matter  of  fact,  the  voli- 
tion of  the  patient  is  not  paralyzed  so  much  as  it  is  perverted.     Hys- 
terical patients  only  too  often  show  a  most  vigorous  av ill-power  in  the 
line  of  their  perverted  motives.     Even  vvdien  they  are  paralyzed  or  in 
a  cataleptoid  state,  the  will  is  not  so  much  in  abeyance  as  that  it  is 
working,  perchance,   too  vigorously,  in   a  direction  entirely  different 
from  the   ordinary  channels.     An     overwrought     imagination     with 
reminiscences  of  intense  fear,  or  of  religious  ecstasy  or  of  sexual  exalta- 
tion, may  so  absorb  the  patient's  inner  consciousness  that  the  ordinary 
channels  of  mental  activity  are  quite  neglected  and  the  patient  is  there- 
fore the  apparent  victim  of  such  outward  negative  manifestations  as 
anaesthesia,  paralysis,  etc.    In  the  light  of  modern  physiological  psychol- 
ogy, so  ably  taught  by  Wundt,  in  which  all  mental  phenomena  are  but 
composite  ps3xhical  experiences  resulting  from  the  interplay  and  inter- 
connection of  the  tvro  elementary  processes,  sensation  and  feeling,  hys- 
teria like  all  other  forms  of  psychosis,  is  the  expression  of  an  unusual, 
and  so  far  unnatural,  balance  and  harmony  between  these  elementary 
processes.     Its  cure  is  the  restoration  and  preservation  of  this  balance, 
the  establishment  of  the  normal,  or  what  is  universally  accepted  as  the 
normal,  interplay  of  the  primary  processes  or  occurrences  that  go  to 
make  up  the  so-called  memory,  will,  imagination  and  intellect,  by  the 
regulation  and  discipline  of  the  physical  elements,  sensation  and  feel- 
ing.    This  conception  of  the  nature  of  hysteria  on  the  basis  of  modern 
physiological  psychology,  while  it  does  not  lessen  the  magnitude  of  the 
task  involved  in  its  prevention  and  treatment,  gives  to  the  task  a  more 
hopeful  and  rational  ground  whereon  to  work,  than  any  explanation 
hitherto  afforded. 

To  ward  off  hysteria  in  one  who  has  been  born  of  neurotic  parents, 
who  shows  in  herself  early  in  life  a  congenital  neuropathic  tempera- 
ment, or  who  has  begun  to  reveal  hvsterical  manifestations  as  the  re- 


136  THE    NEURONIC    DISEASES 

suit  of  a  too  close  association  with  a  hysterical  mother  or  of  a  too 
close  confinement  to  a  predisposing  environment,  the  indications  are 
clear  and  involve  the  making  of  all  such  changes  in  the  child's  life  as 
will  change  her  psychic  elements  of  sensation  and  feeling.  Removal 
from  home,  the  avoidance  of  too  much  sympathy,  the  regulation  of 
studies  and  reading,  the  adoption  of  system  in  all  life's  activities,  and, 
in  fact,  the  employment  of  all  measures,  persuasive,  punitive,  educa- 
tional, social,  disciplinary  and  of  ev^ery  other  kind  that  will  tend  toward 
a  regular,  even,  systematic,  well-balanced  mental  and  physical  existence, 
in  which  no  set  of  sensations,  no  set  of  feelings,  no  special  faculty  or 
organ  of  the  mind  or  body  is  exercised  at  the  expense  of  or  more  than 
any  other.  As  most  of  these  children,  for  example,  are  of  the  so-called 
artistic  temperament  with  its  preponderance  of  the  imaginative  and 
emotional  faculties,  they  should  be  given  games,  studies  and  a  general 
regimen  that  involve  little  or  no  exercise  of  imagination  and  feeling, 
but  rather  the  intellect  and  reasoning  faculty.  The  exercise  of  the 
imagination  and  emotions  should  not  be  prohibited  entirely,  as  is  too 
often  done,  for  that  merely  reverses  the  unbalanced  state  of  mental 
activity ;  but  they  should  be  kept  in  partial  abeyance  by  the  giving  of 
more  work  to  the  other  faculties. 

Passing  on  to  the  consideration  of  the  treatment  of  hysteria  in 
the  adult,  the  subject  may  be  looked  at  from  various  standpoints.  In 
the  first  place,  the  same  sort  of  prophylactic  treatment  and  discipline 
for  the  suppression  of  the  disease  is  as  applicable  as  it  is  xn  the  child : 
its  results,  however,  will  not  prove  so  happy  because  the  adult  cannot 
be  controlled  as  a  child  can,  and  too  often  will  not  submit  to  proper 
self-discipline,  and  because  in  the  adult  the  hysterical  habit  has  usually 
become  fixed  more  and  more  firmly  m  the  course  of  the  preceding  years. 
Nevertheless,  given  a  willing  patient,  prophylactic  discipline  along  the 
lines  suggested  for  neurotic  children  will  do  a  very  great  deal  in  pre- 
venting the  hysterical  outbursts  or  in  mitigating  their  severity  when 
they  have  once  broken  forth.  A  volume  might  be  written  alm.ost  upon 
the  details  of  such  prophylactic  treatment,  for  it  v/ould  involve  the 
consideration  of  all  kinds  of  cultured  and  uncultured  individuals  and 
all  forms  of  mental  and  physical  activity  known  to  the  human  race. 
The  whole  matter  may  be  axiomatically  stated  in  the  one  sentence, 
restorfe  as  far  as  possible  the  balance  in  the  mental,  moral  and  physical 
activities  of  the  individual  patient  to  whom  the  advice  is  being  given. 

Physical  diseases  with  which  hysteria  is  so  often  associated  must, 
of  course,  be  removed.  Ill  health  must  be  corrected  with  tonics,  exer- 
cise, massage,  baths,  electricity,  proper  diet,  sleep,  etc.  The  mind  must 
be  appropriately  ministered  to  as  well  as  the  body.  All  of  which  can 
be  only  suggested  here  on  account  of  the  vastness  of  the  subject. 

In  the  second  place,  the  treatment  of  the  hysterical  outbreaks, 
the  paralytic  and  convulsive  periods  and  their  special  symptoms,  needs 
some  consideration.  The  means  at  our  disposal  for  combating  this 
manifestation  of  hysteria  are  psychic,  mechanical,  medicinal.  I  am  so 
convinced  that  hysteria  is  entirely  a  psychosis  that  I  believe  what 
benefit  we  obtain  from  such  measures  as  are  involved  in  all  the 
hydropathic,   climatologic,  medico-mechanical  and  electric  procedures 


THE    NEURONIC    DISEASES  I37 

that  have  been  recommended  and -are  legitimately  employed,  is  due  to 
the  effect  upon  the  patient's  mind.  Of  course,  I  do  not  mean  by  this 
that  remedies  applied  to  organic  troubles  with  which  the  hysteria  may 
be  associated  do  not  help  to  remove  the  psychosis,  but  they  do  it  indi- 
rectly by  removing  the  organic  disease  which  may  be  aggravating  the 
hysteria.  In  a  word,  if  a  case  is  one  of  pure  hysteria,  free  from  all 
forms  of  organic  trouble,  the  remedial  measures  that  so  often  seem  to 
banish  the  hysterical  symptoms  do  so  by  directly  influencing  the  pa- 
tient's mind.  I  take  it  that  the  entire  treatment  of  pure  hysteria  is 
in  its  last  analysis  psychotherapy,  whatever  the  means  employed  to 
influence  the  patient's  mind. 

Even  in  an  hysterical  attack,  therefore,  the  nrst  thing  to  do  is  to 
win  the  patient's  mind  so  far  as  possible.  To  do  this  the  physician 
must  first  of  all  impress  his  personaHty,  his  mastery  over  the  patient  and 
the  situation  and  his  ability  to  handle  the  case,  not  only  on  the  patient, 
but  upon  all  those  in  her  presence.  He  may  have  to  be  harsh  or  gentle, 
comnaanding  or  persuasive,  indifferent  or  sympathetic ;  each  case  will 
require  its  own  method  and  the  physician  himself  must  alone  decide 
what  course  of  action  to  take.  The  patient's  confidence  must  be  ob- 
tained and  after  that  there  must  be  no  temporizing  with  her.  Ofttimes 
this  can  only  be  accomplished  when  the  patient  is  away  from  her  home 
and  among  strange  surroundings.  The  hospital  is  the  only  place  and 
the  Weir-Mitchell  method  of  seclusion,  with  a  daily  systematic  pro- 
gram, modified,  of  course,  for  each  individual  case,  is  often  the  only 
means  of  obtaining  the  desired  influence  over  the  patient.  The  physi- 
cian must  frequently  impress  the  patient  with  not  only  his  mastery, 
but  also  with  the  superiority  ,of  his  mind  and  metital  attainments. 
He  dare  not  be  boastful,  but  he  nmst  command  the  patient's  respect, 
admiration  and  even  awe.  To  do  this  he  must  often  be  a  highly  cul- 
tured man,  for  these  patients  are  themselves  frequently  highly  cul- 
tured. If  the  physician's  mental  endowments  are  such  as  to  cause  an 
accomplished  hysteric  to  hold  small  respect  for  him,  it  is  obvious  that 
he  will  have  but  little  of  her  confidence  and  so  much  the  less  mental 
control  over  her.  It  is  well,  therefore,  to  be  able  to  meet  the  various 
tastes  and  mental  endowments  of  these  patients  by  a  broad  knowledge 
of  science,  literature  and  art.  Moreover,  out  of  such  a  broad  knowl- 
edge, suggestions  can  judiciously  be  made  in  regard  to  the  patient's 
reading,  studies  and  artistic  occupations.  I  make  it  a  rule  to  include 
in  the  written  program  for  the  use  of  the  nurse,  the  books  to  be_  read, 
the  amusements  to  be  indulged  in,  the  general  lines  of  couA^ersation  to 
be  prohibited,  and  deem  them  quite  as  important  as  the  directions  which 
I  give  in  regard  to  the  medicines,  food,  baths,  electricity,  etc. 

Psychotherapy  involves  the  question  of  the  employment  of  hypno- 
tism and  suggestion.  What  has  just  been  said  about  the  relationship 
of  the  physician  to  his  patient  is  of  the  nature  largely  of  suggestion. 
As  to  the  use  of  artificial  hypnosis  there  is  some  question.  Hypnosis 
itself  is  a  hysterical  condition,  and  the  substitution  of  one  hysterical 
state  for  another  may  be  inadvisable.  Hence,  hypnotism  had  better 
never  be  resorted  to  except  as  a  final  measure  after  all  other  means 
have  been  tried  and  have  failed.    And  yet  it  must  be  frankly  admitted 


138  THE    XEUROXIC    DISEASES 

that  for  the  removal  of  paralyses,  anaesthesias  and  contractures,  it  is 
not  only  to  be  recommended  iDut  sometimes  proves  highly  efficacious. 
One  must  be  careful  always  to  make  appropriate  post-hypnotic  sug- 
gestions, so  that  the  patient  does  not  come  out  of  her  sleep  in  a  worse 
hysterical  state,  with  other  and  more  serious  stigmata,  than  those  with 
which  she  entered  it. 

I  believe  it  makes  very  little  difference  in  the  treatment  of  hysteria 
as  to  the  character,  mode  of  application  or  time  of  employment  of  such 
excellent  measures  as  baths,  massage,  electricity  and  gymnastics.  The 
essential  point  is  to  insist  upon  their  being  taken  with  regularity  and  sys- 
tem, and  not  to  allow  the  patient's  mere  whims  and  changeableness  to  in- 
fluence the  use  of  them.  To  overcome  her  egotism  and  self-regard,  to 
strengthen  her  higher  mental  inhibition,  and  to  direct  her  thoughts  into 
channels  that  lead  away  from  herself  and  her  own  elementary  sensa- 
tions and  feelings,  it  is  wholesome  to  render  the  taking  of  the  baths, 
massage  and  electricity  somewhat  of  a  slight  task,  possibly  unenjoyable 
but  absolutely  necessary.  In  this  way  cold  baths,  electric  shocks,  tire- 
some exercises,  apart  from  their  tonic  and  stimulating  effect  upon  the 
physiological  processes  of  the  body,  accomplish  their  happy  eft'ects 
when  adopted  as  a  part  of  the  treatment  of  hysteria. 

In  regard  to  the  use  of  medicines  in  hysteria,  it  may  be  generally 
stated  that  they  are  of  little  avail.  Hysteria  is  a  psychosis  which  re- 
veals itself  most  prom.inently  at  times  through  the  nervous  apparatus ; 
hence  it  is  sometimes  called  a  psychoneurosis.  This  neurosis  is  seen 
in  such  symptoms  as  the  muscular  spasms,  vasomotor  disturbances,  con- 
tractures and  such  automatic  acts  as  laughing,  crying,  etc.  To  reach 
such  conditions  the  antispasmodics  are  sometimes  useful.  Valerian  and 
zinc  are  the  best  in  the  list.  Asafoetida,  the  bromides,  quinine,  sumbul, 
methylene  blue,  may  all  be  tried,  bvtt  without  psychotherapy  will  usu- 
ally be  found  wanting.  Narcotics,  such  as  opium  and  choral,  must  be 
rigidly  avoided ;  when  once  administered  to  the  patient,  the  comfort 
of  the  attendant  is  at  an  end.  Chloroform  inhalations  may  be  used  to 
relieve  certain  cases  of  convulsion  and  contracture. 

Means  of  combating  special  symptoms  are  innumerable  and  will 
readily  suggest  themselves  to  the  physician  who  is  fully  cognizant  of 
the  purely  psychic  nature  of  the  disease. 

As  soon  as  possible  hysterically  paralyzed  patients  should  be  en- 
couraged to  walk. 

The  disappearance  of  special  symptoms  does  not  mean  that  the 
disease  itself  is  cured.  Remissions  and  relapses  are  to  be  expected  in 
such  a  constitutional  disorder.  The  means  of  avoiding  these  were  in- 
dicated under  the  discussion  of  the  prophylaxis  of  the  disease. 

PSYCHONEUROSES  THAT  ARE  RELATED  TO  SLEEP  AND 
TO  THE  HYSTERICAL  STATE. 

There  are  certain  psychoneurotic  states  about  which  there  is  a 
great  deal  of  confusion  and  much  honest  difference  of  opinion.  I 
refer  to  all  that  class  of  phenomena  which  is  variously  spoken  of 
under  the  head  of  hypnosis  and  hypnotism,  dreams,  somnarnbidism, 


THE    XEUKOXIC    DISEASES  I39 

■catalepsv,  ecstasy,  lethargy,  etc.  Some  authors  speak  of  these  as  dis- 
orders of  sleep ;  others  rank  them  as  manifestations  of  hysteria  and 
mental  aberration.  They  are  not  exactly  normal  phenomena,  of  course, 
and  yet  many  regard  them,  as  merely  disturbances  of  a  normal  function. 
sleep.  Others  look  upon  them  as  absolutely  abnormal  and  in  that 
sense  not  to  be  spoken  of  as  related  to  sleep  at  all.  According  to  the 
latter  they  are  phases  of  hysteria,  possibly  evidences  of  a  severe,  or  at 
least  positive,  psychosis  of  fundamental  origin. 

In  my  own  opinion  much  of  this  confusion  is  quite  unnecessary 
and  is  the  direct  outgrowth  of  certain  old-time  misconceptions  in  re- 
:gard  to  the  nature  of  mind  and  in  regard  to  the  limitations  or  exact 
raeaning  of  the  words  normal  and  abnormal.  I  presume  there  is  no 
dispute  in  regard  to  the  fact  that  both  sleep  and  hysteria  represent  a 
mental  change  associated  with  and  founded  upon  some  physical  or 
physiological  change  in  the  nervous  mechanism.  If  we  start  from  the 
standpoint  of  the  state  of  wakefulness  as  we  observe  it  in  the  average 
man,  then  sleep  and  hysteria  are  both  anything  but  a  state  of  normal 
wakefulness.  The  mind,  the  consciousness,  if  you  please,  is  more  or 
less  in  abeyance  in  both  states.  We  speak  of  sleep,  hoAvever,  as  normal 
and  of  hysteria  as  abnormal.  Justly  so,  for  though  the  terms  normal 
and  abnormal  are  very  elastic,  they  are  used  not  in  the  sense  of  repre- 
senting absolutely  what  is  right  and  what  is  wrong,  for  human  knowl- 
edge is  not  definite  enough  }-et  for  us  to  assume  that  critical  standpoint, 
but  in  the  sense  of  representing  what  occurs  in  the  average  or  majority 
of  people.  All  animals  sleep,  therefore  that  is  normal;  only  a  few 
animals  have  hysteria,  therefore  that  is  abnormal.  Such  is  the  logical 
method  adopted  by  both  the  scientific  and  unscientific  world.  Up  to 
a  certain  point  it  is  a  correct  and  safe  method. 

There  is  a  glaring  weakness,  however,  in  such  reasoning  when  we 
strive  to  arrive  at  exact  knowledge.  Averages  and  mere  numerical  pre- 
dominence  do  not  confirm  facts.  There  must  be  other  features  to 
establish  them  as  absolutely  undeniable.  They  must  be  fixed  and 
unalterable :  they  must  always  be  identical  in  ever}-  detail ;  they  must 
appear  absolutely  always  the  same  under  the  same  circumstances ;  and 
we  must  know^  absolutely  everything  about  those  circumstances  before 
we  can  pronounce  the  law  that  they  are  normal  or  abnormal. 

As  so  few  of  these  conditions  are  made  to  surround  many  of  the 
phenomena  which  we  now  call  facts,  our  assertions  in  regard  to  the 
normality  or  abnormality  of  the  latter  are  only  approximately  and  pre- 
sumptively correct.  By  striking  the  average  we  come  as  near  as  we 
can  in  fulfilling  the  above  conditions  and  that  which  seems  to  approxi- 
mate most  nearly  to  abiding  by  them  we  call  facts  and  declare  them  to 
be  normal  or  abnormal. 

Sleep  is  such  a  normal  fact :  hysteria  is  such  an  abnormal  fact. 
When  we  begin  to  verge  away,  ever  so  little,  from  the  average,  we  at 
once  find  that  our  normal  and  abnormal  facts  are  a  little  shaky  and  are 
at  once  seen  to  be  open  to  variation  and  exception.  All  men  sleep, 
but  how  ?  Some  longer,  some  shorter  ;  some  profoundly,  some  lightly. 
There  are  degrees  of  sleep  then,  and  perhaps  other  characteristics  about 
it  that  are  not  necessarily  exhibited  in  the  average.     At  once  they  be- 


140  THE    NEURONIC    DISEASES 

come  abnormal,  these  exceptional  sleep  variations.  A  man  who  sleeps- 
a  whole  month  or  one  who  does  not  sleep  at  all  for  a  month  are  both 
abnormal  because  the  average  man  does  not  do  either.  But  how  about 
the  sleeping  itself,  the  prolonged  abeyance  of  consciousness — is  that 
abnormal  ?  The  prolongation  of  it,  of  course,  is  exceptional  and 
abnormal,  but  so  far  as  we  can  determine  the  sleep,  the  mere  abeyance 
of  the  consciousness,  is  not  abnormal.  Again,  few  men  have  hysteria,, 
but  those  that  do  have  it  exhibit  also  variations  and  exceptions  in  their 
manner  of  revealing  it.  There  may  be  such  a  profound  yet  partial 
abeyance  of  the  mental  faculties  that  the  patient  for  the  time  being- 
seems  to  be  in  another  world  entirely ;  on  the  other  hand,  the  condition 
mav  amount  to  only  a  high  degree  of  egotism  or  emotionalism,  such  as 
even  so-called  normal  men  exhibit  in  periods  of  unwonted  excitement. 

There  are  degrees  of  hysteria  or  psychosis,  then,  and  variations 
from  the  extremes  of  madness  down  to  the  normal  manifestations 
of  mere  excitement. 

Now  it  begins  to  be  clear  why  opinions  differ  as  to  the  normality 
or  abnormality  of  certain  mental  exhibitions.  There  is  a  midground 
which  shifts  from  normal  to  abnormal  according  to  the  reasoning,  the- 
predilections  and  the  personal  equation  of  the  investig&tor. 

All  of  these  psychoneurotic  phenomena  then  we  will  grant  are 
forms  of  mentalization,  extending  from  the  complete  abeyance  of  it  on. 
the  one  hand  (temporarily  in  sleep,  permanently  in  death),  to  the  ex- 
treme riotous  and  decidedly  exceptional  exhibition  of  it  temporarily  in 
hysteroid  conditions,  permanently  in  certain  forms  of  insanity  on  the 
other  hand. 

To  avoid  all  confusion  in  regard  to  the  middle-ground  of  the 
psychoses,  the  terms  normal  and  abnormal  had  better  be  dropped. 

These  troubles,  then,  of  mentalization,  falling  between  sleep  at 
one.  end  of  the  line  and  extreme  idiocy,  dementia  and  insanity  at  the 
other,  involve  the  mind  and  its  anatomico-physiological  basis  as  well 
as  all  its  variations  and  their  particular  anatomico-physiological  bases. 

A  definition  of  mind  has  been  the  goal  of  philosophers  of  all  time. 
Physiological  psychology  defines  it  as  a  function,  a  compound  of  the 
interplay  of  certain  well-recognized  sensory-motor  functions  or  im- 
pulses. It  is  therefore  not  an  entity  itself,  but  a  m.ere  phenomenon,  a 
process,  representing  the  complicated  action  and  interaction  of  certain 
anatomico-physiological  functions   upon  one  another,   or  all  together. 

That  is  the  physio-psychological  definition  and  conception  of  mind. 
It  does  not  oppose  the  discussion  of  any  other  conception  or  object  in 
the  least  to  metaphysical  debates  in  regard  to  dualism,  in  regard  to  the " 
mind  being  a  separate  entity  apart  from  brain,  or  in  regard  to  the 
existenoe  of  immateriality  or  any  other  such  knotty  problem.  It  simply 
doesn't  enter  that  sphere  of  research,  but  merely  declares  that  so  far 
as  it  is  concerned,  cessation  of  brain  function  means  cessation  of  mind, 
partial  cessation  of  brain  function  or  disturbance  of  it  means  partial 
cessation  or  disturbance  of  mentalization,  an  abnormal  psychosis. 

With  this  brief  attempt  at  clearing  away  the  confusing  factors  in 
regard  to  the  physiological  meaning  of  the  terms  mind  and  normal,. 


THE    NEURONIC    DISEASES  I4I 

we  are  in  a  better  position  to  analyze  and  understand  the  psychoneu- 
Toses  mentioned  at  the  head  of  the  section. 

Sleep  is  a  function  which,  when  performed  under  what  are  called 
normal  conditions,  represents  a  complete  abeyance  of  all  mentalization, 
with  complete  absence  of  consciousness.  There  is  no  proof  for  the 
belief  held  by  some  that  mentalization  never  ceases,  even  during  sleep, 
and  that  we  merely  are  unable  to  remember  when  awake  what  our 
thoughts  were  doing  when  we  were  asleep.  The  most  reliable  evidence 
all  points  to  the  fact  that  in  healthful  sleep  the  mentalization  is  abso- 
lutelv  at  a  standstill.  The  mere  nutritive  and  vegetative  functions  that' 
underlie  it  go  on. 

Healthful  sleep  being  a  physiological  phenomenon,  it  hardly  calls 
for  further  description  here.  Like  all  physiological  functions,  how- 
ever, it  is  sometimes  disarranged. 

The  disturbances  of  sleep  are  many  and  varied.  Dreaming  is 
probably  the  commonest  disturbance.  In  fact,  so  common,  so  near 
to  the  experience  of  the  average,  is  dreaming,  that  the  world  looks  upon 
it  as  a  normal  condition,  another  evidence  of  the  fallacious  method 
of  arriving  at  knowledge  by  identifying  that  merely  which  can  be 
predicated  of  the  average  with  normality. 

Dreaming  represents  an  incomplete  sleep,  a  partial  cessation  of  cer- 
tain high  neuro-physiological  functions,  a  partial  awaicening  of  mind. 
Dreams,  of  course,  are  innumerable  and  in  their  partial  character  repre- 
sent all  phases  of  mentalization.  In  a  broad  way,  however,  it  may  be 
said  that  the  imaginative,  creative  faculties  and  the  memory  are  active, 
whereas  the  volitional  and  reasoning  functions  are  in  a  state  of  in- 
activity. The  inhibitory  control  of  the  latter  over  the  former  is  with- 
drawn and  thus  is  accounted  for  the  rapidity,  the  strangeness  and  the 
incongruity  of  the  actions  in  our  dreams.  Most  wonderful  combina- 
tions and  thoughts  and  doings  arise  in  this  state.  They  remain  uncon- 
nected bv  the  higher  psychic  forces.  They  are  so  m.arvelous  that 
primitive,  ignorant  and  superstitious  people  look  upon  them  as  super- 
natural visitations,  as  flights  of  the  soul  into  space,  and  as  telepathic, 
clairvoyant,  spiritualistic  and  prophetic  agencies.  They  are  purely 
psychic  phenomena,  of  course,  and  doubtless  depend  upon  an  abnormal 
interplay  for  the  time  between  the  basal  anatomico-physiological  func- 
tions of  the  brain.  They  have  their  counterpart  metaphorically  in  the 
physical  sphere  in  the  spastico-ataxic  manifestations  of  certain  diseases 
of  the  upper  motor  neurones,  which  withdraw  the  inhibitory  control  of 
these  neurones  from  those  seated  in  the  cord  below. 

Pavor  nocturmis,  the  night  terrors,  seen  in  both  adults  and  children, 
but  more  especially  in  the  latter,  is  usually  a  psychopathic  manifesta- 
tion that  occurs  when  sleep  is  passing,  according  to  the  experiments  of 
Kohlschiitter,  from  its  maximum  intensity  to  a  lesser  degree  of  depth. 
It  is  thus  a  sort  of  a  dream,  but  occurring  in  an  individual  with  a  neu- 
rasthenic or  hysteric  tendency  it  assumes  the  depressed,  distressing, 
psychalgic  form  which  eventuates  in  fright  and  terror. 

Xightmare,  so-called,  is  a  dream  state  in  which  the  fancy  revels  in 
the  creation  of  parahtic  conditions  or  in  which  the  volition  especially 
is  suppressed  while  the  other  faculties  are  partially  awake,  especially 


142  THE    NEURONIC    DISEASES 

the  apperceptive  faculties.  Sometimes  in  these  dream  states  the  apper- 
ceptive functions  are  so  far  awake  that  ideas  and  questions  may  be 
presented  and  be  taken  in  by  the  sleeper.  There  is  not  a  complete  closure 
here  of  the  pathways  for  afiterent  impulses.  The  whole  dream  and  its 
direction  may  thus  be  guided  by  a  touch  on  the  body  or  a  sound  in  the 
room,  or  a  sudden  flash  of  light.  The  stimulus  may  be  an  auto- 
stimulus  and  come  from  the  body  within.  Thus  are  accounted  for  the 
dreams  that  are  provoked  and  directed  sometimes  by  an  over-loaded 
stomach  or  a  full  bowel. 

In  all  of  these  states  the  sleep  is  abnormal ;  the  dreaming  is  an 
abnormality  and  rests  on  an  abnormal  anatomico-physiological  basis.  It 
is  the  result  of  an  abnormal  interplay  betv/een  the  inpouring  and  in- 
poured  afferent  impulses.  Some  of  the  mental  functions  are  active, 
some  are  inactive.    Thus  a  strange  and  abnormal  mentalization  obtains. 

Sometimes  these  partial  mental  activities  include  the  emissive  or 
motor  centers.  A  psychoneurotic  reflex,  a  sort  of  low  volition,  or  rather 
ideo- volition,  with  a  reflex,  is  set  up  and  the  individual  does  things  in  his 
sleep.     Thus  we  have  the  somnambulistic  phenomena  accounted  for. 

Hypnotism  is  nothing  but  a  form  of  artificial  somnambulism. 
Partial  abeyance  of  the  mental  faculties  is  the  basis  of  all  these  exhibi- 
tions. An  automatism  characterizes  them  and  just  as  the  withdrawal  of 
certain  mental  forces,  and  the  concentration  of  certain  others,  causes 
the  wonderful  ideas  that  are  enacted  in  the  simple  dreaming  state,  so 
the  same  disproportion  between  them  enables  the  somnambulist  to  do 
the  remarkable  feats  that  he  sometimes  does.  A  sleeper,  for  instance, 
can  walk  on  the  perilous  edge  of  a  roof  because,  unlike  one  who  is 
awake,  he  is  not  embarrassed  by  any  observations  or  thoughts  of  the 
dangers  of  his  situation.  In  regard  to  them  and  other  attendant  circum- 
stances his  mind  is  asleep.  All  that  it  is  taking  in  are  the  impulses 
pouring  up  from  his  feet  or  his  hands,  his  ears  or  his  eyes.  In  a  reflex 
way  these  impulses  pass  through  the  subconscious  or  lower  coordinat- 
ing apparatus  and  out  again  to  the  appropriate  muscles.  The  sleep 
walker  is  thus  a  veritable  automatic  mechanism ;  a  most  delicate  one, 
to  be  sure,  but  a  completely  unembarrassed  mechanism. 

Automatism  is  a  trait  of  all  animals  and  is  seen  in  many  common 
acts  of  life.  The  developmental  stage  in  regard  to  the  intelligence,  the 
habits  and  the  mental  capacity  all  determine  a  man's  degree  of  automa- 
tism. Automatism  sometimes  gives  one  credit  for  heroism.  A  man 
rushes  into  danger  often  because  he  is  a  stupid  automaton.  The  old 
adage  that  fools  rush  in  where  angels  fear  to  tread  is  another  way  of 
defining  automatism  in  men.  What  is  vulgarly  called  "nerve"  is  a  semi- 
automatic performance  which  a  higher  degree  of  intelligence  would 
forego. 

Habits  establish  automatism.  Most  of  the  common  acts  of  life, 
like  walking,  speaking,  writing,  many  of  the  rarer  accomplishments, 
like  piano  playing,  tight  rope  dancing,  trapeze  swinging,  are  perform- 
ances practiced  as  habits  until  they  have  become  automatic.  They  are 
the  result  of  a  subconscious  reflex  and  during  their  performance  the 
mind,  so  far  as  they  are  concerned,  is  partially  asleep  or  wholly  diverted. 

That  somnambulism  is  but  the  same  sort  of  automatism  is  shown 


THE    XEUROXIC    DISEASES  I43 

in  the  fact  that  the  habits  of  the  individual  often  determine  the  char- 
acter of  the  sleep  performances.  A  writer  gets  up  in  his  sleep  and 
writes ;  a  singer  sings ;  a  mechanic  goes  to  his  tools. 

In  ordinary  somnambulism  the  stimulus  to  the  mind  comes  from 
within.  It  is  an  auto-automatism.  In  hypnotism,  on  the  other  hand, 
the  stimulus  comes  from  without.  The  suggestions  of  the  hypnotizer 
enter  into  the  partial  mentalization  of  the  patient  and  their  origin  not 
being  recognized  by  the  higher  reasoning  faculties  whicn  are  asleep, 
they  enter  into  the  mental  reflex,  give  it  its  direction  and  so  cause  the 
subject  to  do  what  the  hypnotizer  suggests. 

This  is  mere  artificial  somnambulism.  It  is  an  abnormal  sleep 
phenomenon,  an  automatism  given  directly  by  an  external  ideo-motor 
suggestion.  It  is  certainly  not  a  normal  condition  in  the  sense  of  being 
an  average  experience.  It  is  a  pure  functional  disturbance  in  the 
psychic  sphere  and  so  far  as  it  is  allowable  to  speak  of  functional  dis- 
turbances or  of  the  underlying  inherited  or  acquired  nervous  defect 
upon  which  such  disturbances  are  usually  based,  as  conditions  of  dis- 
ease, hypnotism  and  all  its  allied  phenomena  are  disease  manifestations. 
They  resemble  hysteria  and  other  psychoses  in  being  abnormal  or  ex- 
ceptional forms  of  mentalization. 

Hypnotism  is  a  subject  that  has  been  much  written  upon,  and  about 
which  many  divergent  views  have  been  expressed.  The  history  of  the 
development  of  the  subject  is  interesting  in  the  extreme,  but  would  not 
be  especially  pertinent  here  and  would  take  up  too  much  space.  Suffice 
it  to  say  that  at  the  present  time  it  is  founded  upon  suggestion  and  all 
of  its  phenomena  are  the  result  of  the  influence  of  the  suggestions  of 
the  hypnotizer  made  to  the  hypnotized.  There  is  no  transference  of  any 
physical  force  or  influence.  The  subject  acts  in  response  solely  to  his 
own  mental  mechanism,  but  that  mental  mechanism  is  given  its  direc- 
tion of  activity  by  the  suggestions  offered  to  the  susceptible  subject. 

To-day  there  are  two  schools  whose  opinions  upon  some  features 
of  hypnosis  and  hypnotism  are  somewhat  dissimilar.  The  Nancy 
school,  at  the  head  of  which  is  Bernheim,  and  the  founder  of  which  was 
Liebault,  does  not  regard  hypnosis  as  an  abnormal  state  in  the  strict 
sense  of  the  word,  for  it  argues  that  all  men  are  more  or  less  influenced 
by  suggestion  and  it  is  only  a  question  of  degree  as  to  the  susceptibility 
of  the  individual.  It  declares,  therefore,  that  taking  human  beings  just 
as  they  come,  eighty  per  cent,  of  them  at  least  are  hypnotizable. 

The  Paris  school,  at  the  head  of  which  stood  Charcot,  insists  that 
hypnosis  is  a  decidedly  pathological  phenomenon  and  that  it  is  allied 
to  genuine  hysteria.  It  maintains  that  only  the  weak-minded  and  un- 
balanced, those  who  tend  toward  the  hysteroi  ]  state,  can  be  hypnotized 
in  the  legitimate  sense  of  the  word.  Ah  men,  of  course,  they  admit, 
are  open  to  suggestion,  but  hypnotism  is  something  more  than  mere 
suggestion.  It  needs  a  defective  organism  on  the  part  of  the  subject 
for  its  proper  revelation. 

It  seems  to  me  that  the  dift'erence  between  the  opinions  of  these 
two  great  schools  rests  upon  some  fundamentally  dift'erent  ideas  apart 
from  the  subiect  of  which  they  are  the  prominent  exponents.     Their 


144  THE    NEURONIC    DISEASES 

debate  is  really  around  the  word  disease,  or  that  which  may  be  con- 
sidered normal  or  abnormal. 

That  all  men  are  open  to  suggestion  is.  a  truism  insisted  upon  by 
the  Nancy  school ;  few  men  have  hysteria  is  the  truism  uttered  by  the 
Paris  school.  Is  all  suggestion  in  its  influence  hysterical,  or,  on  the 
other  hand,  is  hysteria  nothing  but  a  form  of  suggestion?  If  the  two 
schools  can  be  brought  to  a  point  where  they  can  answer  these  ques- 
tions in  exactly  the  same  way,  their  difference,  it  seems  to  me,  will  have 
vanished  into  thin  air. 

The  mind  is  a  mobile  phenomenon  evolved  by  a  very  mobile 
anatomico-physiological  basis.  It  is  never  the  same  for  obvious  reasons 
at  different  times  in  the  same  man,  and,  still  more  especially,  never 
the  same  in  two  different  individuals.  Its  mobility  and  changeability 
vary  according  to  the  stimuli  that  provoke  it  into  existence,  and  the 
condition  of  the  physical  basis  upon  which  those  stimuli  act.  It  is 
therefore  always  more  or  less  susceptible  to  change  under  these  condi- 
tions. If  the  stimuli  are  strong  or  if  the  physical  basis  is  unstable, 
just  in  the  same  proportion  will  the  susceptibility  of  the  mind  be  to 
change.  This  may  occur  and  yet  the  condition  not  be  regarded  as  being 
abnormal.  There  is  an  indeterminate  point,  however,  beyond  which  the 
susceptibility  does  deserve  the  name  of  disease.  When  the  instability  is 
so  great  that  every  form  of  stimulus,  whether  froni  within  or  from 
without,  controls  and  directs  the  mental  operations,  wholly  or  partially, 
so  that  the  individual  seems  to  have  no  self-control  whatever,  the  state 
becomes  hysteroid,  may  even  become  an  actual  hysteria,  may  pass  into 
a  profound  form  of  pure  insanity. 

x*\s  I  have  pointed  out  in  the  section  upon  hysteria,  this  disease  is 
one  of  mental  unbalance,  a  true  psychosis,  in  which  a  certain  form  of 
suggestion,  egoistic  auto-suggestion,  plays  a  prominent  role.  In  hys- 
teria the  patient's  mental  state  is  a  sort  of  waking  somnambulism,  if 
I  may  use  the  apparent  contradiction.  One  part  of  the  mental  mechan- 
ism is  out  of  balance  with  another  part.  The  inactive  part  may  not 
be  asleep  or  below  the  normal  waking  state,  but  the  active  part  is  too 
vigorously  awake  and  in  excess  of  the  normal  waking  state.  To  use 
metaphors,  it  is  not  that  one  part  of  the  mind  is  so  much  paralyzed  as  it 
is  that  another  part  is  in  a  state  of  spasm. 

This  unbalance  is  so  pronounced  and  so  intense  that  it  affects  the 
ingoing  and  outgoing  impulses  even,  and  we  call  the  condition  a  psycho- 
neurosis  on  account  of  the  marked  physical  and  mental  clinical  mani- 
festations. If  hysteria  be  thus  a  psychosis,  a  mental  unbalance  of  a 
particular  sort,  it  simulates  the  condition  of  the  unbalanced  individual 
who  is  swayed  by  every  suggestion  that  is  poured  in  upon  him. 

If  hysteria  be  a  disease,  as  it  undoubtedly  is,  then  the  mental 
unbalance  is  a  sort  of  disease,  for  it  is  but  a  mild  degree  of  the  same 
thing. 

Psychosis  thus  admits  of  degrees  and  variations,  but  we  have  not 
decided  as  yet  upon  the  exact  line  where  the  normal  condition  ends  and 
the  abnormal  begins.  No  man's  mind  is  absolutely  impermeable  to 
changes  of  stimuH,  or  in  other  words  suggestion,  for  it  is  itself  the  very 
representative  result  of  those  multiple  stimuli.     When  does  the  vield- 


THE    NEURONIC   DISEASES  I45 

ing  to  these  stimuli  become  so  great  that  there  is  no  longer  self  in  the 
process ;  or  when  do  the  stimuli  set  up  such  a  powerful,  overwhelming 
activity  in  one  direction  that  there  is  apparent  inactivity  in  another 
direction  ?  Who  can  answer  ?  He  that  can  will  point  out  to  us  exactly 
the  line  between  what  should  be  called  normal  and  what  should  be  called 
abnormal.  Near  that  line,  extending  on  either  side  of  it,  in  the  one 
direction  toward  perfect  mentalization  and  in  the  other  direction  toward 
insanity,  will  be  found  the  weak  and  the  susceptible  individuals  who 
are  hypnotizable.  On  the  one  side  they  will  be  regarded  as  normal 
and  possibly  number  seventy  or  eighty  per  cent,  oi  the  community; 
on  the  other  they  will  be  considered  abnormal  and  will  constitute  a 
much  smaller  percentage.  At  either  end  of  the  line  will  be  found  the 
individuals  who  cannot  be  hypnotized  at  all,  for  either  they  will  have 
too  stable  or  too  unstable  minds. 

The  conditions  for  producing  hypnosis  are  clear  enough.  There 
must  be  susceptibility  in  the  subject  and  there  must  be  forceful  self- 
confidence  in  the  hypnotizer.  Infants  and  insane  people  cannot  obvious- 
ly be  well  influenced.  Weak,  neuropathic,  rather  neurasthenic  and  hys- 
teroid  people  make  the  best  subjects.  Marked  hysteria,  like  insanity 
and  dementia,  is  not  readily  amenable  to  hypnotism.  The  hysterical 
state  between  the  paroxysms  is,  however,  capable  of  hypnosis. 

Two  things  are  aimed  at  in  hypnotism.  First  the  patient  must 
be  put  to  sleep.  This  is  done  by  getting  him  to  gaze  at  a  brig-ht  object, 
a  little  above  his  eyes,  thus  wearying  his  eye  muscles ;  by  gently  stroking 
the  hrow  outwards  with  the  two  hands ;  and  by  urging  him  to.  keep  his 
attention  fixed  on  the  thought  of  going  to  sleep  while  the  operator,  in  a 
soft,  monotonous  tone  of  voice,  keeps  commanding  "go  to  sleep,  go  to 
sleep ;  now  you  are  asleep,  sleep,  sleep,  sleep,"  etc.,  repeating  this,  or 
some  similar  phrase,  over  and  over  until  the  patient  is  asleep  or  rather 
in  a  state  of  hypnosis.  Ofttimes  many  trials  have  to  be  made  before 
success  is  attained. 

If  hypnosis  is  accomplished,  suggestions  may  then  be  made  to  the 
patient  to  do  this  or  that ;  or  he  may  be  told  that  this  ill  or  that  ache 
is  gone,  etc.  Be  sure  always  to  make  the  suggestion  that  it  will  not 
return  when  he  awakes. 

A  quick  pufif  of  breath  or  a  command  to  "awake"'  will  be  enough 
usually  to  revive  the  subject. 

Of  course,  it  goes  v/ithout  saying  that  only  mental  symptoms  can 
be  thus  influenced  and  not  very  many  of  them.  Imaginary  and  self- 
suggested  ills  are  the  most  successfully  managed  thus  . 

Hypnosis  may  in  a  particularly  weak  individual  be  set  up  by  inter- 
nal stimuli.  This  is  what  is  called  autohypnosis.  It  is  capable  of  devel-' 
ing  from  habit.  Hence  since  hypnosis  is  itself  an  abnormal  condition, 
oping  from  habit.  Hence  since  hypnosis  is  itself  an  abnormal  condition, 
bypnotic  state,  the  practice  of  hypnotism  should  be  interdicted  by  law 
except  when  in  the  bands  of  physicians,  and  by  them  it  should  be  re- 
sorted to  only  when  other  means  have  failed. 

In  certain  conditions  it  is  a  powerful  and  legitimate  therapeutic 
agent,  but  it  has  been  very  much  overvaunted. 

Another  manifestation  of  the  somnambulic  state  is  the  condition 


146  THE    XEUROXIC    DISEASES 

known  as  catalcf'sy.  It  is  closely  related  to  hysteria  and  is  dependent 
upon  the  overaction  of  certain  mental  activities,  to  the  detriment  of 
others.  It  can  be  sometimes  produced  artificially  by  a  loud  noise,  a 
sudden  flash  of  bright  light  or  a  fixation  of  the  eyes  upon  some  bril- 
liant object.  The  patients  become  statuesque  in  appearance.  Their 
limbs  are  waxy-Lke  so  that  they  can  be  placed  in  any  position,  and  they 
will  remain  there,  without  signs  of  exhaustion.  All  sensation  seems 
to  be  lost,  but  the  special  senses  are  but  little  affected.  The  eyes  remain 
open  and  staring.  At  times  the  rigidity  of  the  muscles  is  so  great  that 
the  patient  may  be  placed  with  only  his  head  and  feet  resting  on  chairs 
and  considerable  weights  laid  upon  his  body. 

In  lethargy  a  still  higher  degree  of  abnormal  abstraction  occurs, 
all  the  senses,  general  and  special,  being  abolished.  These  patients 
cannot  be  reached  by  suggestion.  The  eyes  are  half  closed  and  the 
muscles  are  relaxed.  Percussion  of  the  nerves  may  still  cause  some 
muscular  contraction,  showing  that  the  neuromuscular  excitability  is 
still  present.  It  is  said  that  this  state  can  also  be  produced  artificially 
bv  exerting  pressure  on  the  eyeballs  in  particular  individuals,  or  by 
closing  the  eyes  of  one  already  in  a  state  of  catalepsy. 

All  of  these  mental  states  are  hysteroid  in  character  and  indicate  a 
profound  psvchic  unbalance  with  enormous  overaction  in  some  direc- 
tions and  corresponding  underaction  in  others. 

What  are  the  physical  changes  underlying  the  phenomena  we  do 
not  know,  and  probably  never  will  know  until  we  are  more  familiar 
\vith  the  normal  mechanism  of  the  mind. 

We  have  now  seen  that  complete,  profound  sleep,  involving  all  of 
the  mental  processes,  is  a  normal  condition  periodically  undergone  by 
the  nervous  system.  We  have  also  seen  that  partial  sleep,  involving 
only  a  part  of  the  faculties,  may  occur  in  such  a  mild  form,  dreams,  as 
to  be  regarded  as  normal,  and  yet  vary  up  through  the  many  stages  of 
somnambulism,  natural  or  artificial,  catalepsy  and  lethargy  to  apparent 
death. 

We  have  noted  the  similarity  of  all  these  conditions,  especially  the 
latter,  with  the  psychospastic  and  psychoparalytic  phenomena  of 
hysteria. 

The  last  disorder  of  sleep  is  its  entire  absence.  This  is  known  as 
iiisojinia.  It  is  a  rare  condition  and  is  indicative  almost  of  a  form  of 
insanity. 

Life  cannot  be  maintained  longer  than  about  three  weeks  in  the 
absence  of  all  sleep.  What  is  often  called  insomnia  is  merely  a  mild 
and  relative  form  of  the  trouble.  Drowsiness,  short  naps  and  mo- 
mentar}'  lapses  that  practically  amount  to  light  sleep,  are  experienced 
by  those  who  from  various  diseases  declare  they  are  the  victims  of 
insomnia. 

The  treatment  of  these  relative  forms  of  the  trouble  consists  of  the 
removal  of  the  cause  and  the  management  of  the  underlying  habits  and 
disease.  In  some  insane  states  a  prolonged  insomnia  sometimes  oc- 
curs until  the  patient  dies  of  sheer  exhaustion. 

As  I  have  said,  it  is  impossible  to  live  without  sleep:  it  follows 
that  everv  form  of  unnatural  wakefulness,  therefore,  has  some  under- 


THE    NEURONIC    DISEASES  I47 

lying,  continuous  cause.  Absolute  insomnia  does  not  exist  except  for  a 
few  weeks  in  certain  mental  and  fatal  cases  of  disease.  Relative  in- 
somnia, which  is  the  common  form  complained  of,  is  not  a  causeless 
trouble.  In  most  cases  the  cause  is  obvious ;  in  a  few  it  may  be  very 
obscure.  Every  case  of  insomnia,  therefore,  should  be  most  exhaustive- 
ly examined  for  the  cause  of  it  before  a  moment's  thought  is  given  to 
its  treatment.  There  is  no  mere  symptom  in  neurology  that  has  been 
more  often  managed  as  a  disease  per  se,  and  that  as  a  consequence 
has  led  to  more  disastrous  habits  with  drugs  and  other  agents  than 
sleeplessness.  Even  physicians  themselves  have  been  their  own  victims 
in  this  stupendous  piece  of  folly.  Chloral  taking  and  the  steady  use  of 
hypnotics  shows  on  the  face  of  it  that  a  symptom  is  being  wrestled  with 
while  the  hidden  cause  is  still  going  on  exercising  its  deleterious  in- 
fluence. It  shows  also  in  too  many  cases  that  the  adviser  is  too  lazy 
or  too  ignorant  to  find  out  and  to  combat  the  cause.  And,  alas !  it 
sometimes  terminates  in  mania  and  death. 

The  common  causes  of  insomnia  are  easily  grouped  under  certain 
general  heads.  In  the  first  place,  many  people  inherit  an  irritable,  weak 
and  neuropathic  constitution  which  refuses  to  functionate  normally, 
or  as  the  average,  healthy  constitution  functionates.  It  is  prone,  there- 
fore, to  be  wakeful,  with  or  without  adequate  provocation.  These 
cases  are  the  inherited  and  habit  insomnias.  They  are  purely  nervous 
in  origin.  Some  of  them  may  show  the  nervous  insufficiency  in  vaso- 
motor disturbance  which  is  the  cause  of  the  cerebral  activity  and 
wakefulness.  Certain  heart  and  vascular  troubles  can  obviously  disturb 
the  intracranial  circulation.  Lithasmia,  gout,  uraemia  and  other  auto- 
toxic  and  diathetic  conditions  can  irritate  and  interfere  with  normal 
functional  activity.  Fever  is  a  disturber.  Simple  exhaustion  sometimes 
produces  irritability  that  prevents  the  much-needed  sleep.  Various 
substances  that  are  ingested  are  sleep-destroA'ers  at  times,  such  as  cof- 
fee, tea,  alcohol,  etc.  One  must  also  think  of  the  intoxications  with 
lead  and  tobacco,  the  infections  like  syphilis,  malaria,  etc.  All  of  these 
conditions  must  be  earnestly  searched  for  in  every  case.  Only  as  a 
dernier  ressort  should  drugs  ever  be  employed. 

Before  turning  in  hopelessness  to  drugs,  all  sorts  of  dietetic, 
hygienic,  hydrotherapeutic,  electrotherapeutic  and  other  mechanical 
measures  should  be  tried  first.  I  always  urge  that  after  a  light  supper 
all  earnest  mental  exertion  should  be  stopped.  The  evening  should 
be  passed  in  as  indifferent  a  manner  as  possible.  Quietude  on  the 
couch,  with  a  minimum  of  excitement,  such  as  reading,  games,  conver- 
sation, should  be  attempted.  Occasionally  a  slow,  short  walk  in  the 
open  air  for  a  few  minutes  in  the  middle  of  the  evening  will  be  helpful. 
Never  take  a  brisk  walk  just  before  going  to  bed.  Some  cases  do 
well  to  retire  in  half  an  hour  after  coming  in  from  outdoors.  Others 
prefer  a  slight  tepid  bath  and  a  little  light  lunch,  such  as  crackers  and 
warm  milk.  One  must  experiment  here.  The  great  desideratum  is  to 
quiet  the  nervous  apparatus  and  to  avoid  every  possible  vasomotor  dis- 
turbance. Music  has  a  quieting  effect  on  some,  irritating  on  others.  A 
monotonous  noise,  such  as  dripping  water  in  a  neighboring  room,  has 
sent  an  insomniac  sometimes  to  sleep.     Monotony  of  thought,  such  as 


148  THE    NEURONIC    DISEASES 

counting,  humming,  listening  to  dull  reading  and  repeating  senseless 
rhymes,  may  be  helpful  to  some,  but  to  man}-  others  I  have  found  such 
measures  to  be  simply  exasperating.  There  are  a  hundred  ways  of 
fostering  monotony  and  quiet  and  sedation.  Each  one  must  learn  them 
by  experimentation. 

If  medicines  must  be  resorted  to,  I  give  the  preference  to  trional, 
sulphonal  and  the  bromides.  Chloral  I  consider  a  dangerous  drug. 
More  habitues  are  probably  produced  by  chloral  than  by  any  other 
remedy.  Hyoscyamus,  usually  in  combination  with  the  bromides,  has 
often  served  well. 

Other  hypnotics  that  may  be  useful  to  fall  back  upon  are  camphor, 
paraldehyde,  methane,  amylene  hydrate,  lupulin,  chloralamide,  small 
quantity  of  alcohol,  cannabis  indica,  chloralose,  ethylene  bromide, 
gelsemium,  hypnone,  scopalamine  hydrobromate.  sumbul,  tetronal, 
musk,  asafoetida  and  valerian. 

The  very  length  of  this  list  suggests  that  the  drug  treatment  of 
insomnia  is  at  best  only  a  makeshift.  In  intractable  cases,  few  as  they 
are,  and  where  the  cause  cannot  possibly  be  discovered,  the  symptom 
must  at  times  be  temporarily  looked  upon  as  being  the  disease  itself. 

Never  use  opium  or  chloral  in  these  cases  except  in  extremity. 
They  will  surely  become  habitues.  I  have  more  than  once  heard  a 
physician's  reputation  torn  to  pieces  by  one  of  these  drug  takers  when 
perchance  all  he  did  was  to  write  a  single  prescription  for  chloral  or 
an  opiate.  Though  the  emergency  may  have  demanded  it  at  the  time, 
the  weak-minded  patient  seized  upon  the  opportunity  to  begin  a  drug 
habit  which  had  finally  driven  him  to  seek  a  neurologist. 

The  treatment  of  insonmia  is  not  an  easy  matter.  It  is  one  of  the 
most  difBcult  tasks  in  medicine.  Its  general  principles  only  have  I  here 
indicated.  Firmness,  tact  and  a  careful  study  of  the  trouble  as  a  mere 
symptom  and  not  as  a  disease  will  accomplish  the  best  results  in  the 
end.  Temporary  measures,  such  as  the  quick,  injudicious  use  of 
hypnotics,  will  be  sure  to  lead  to  more  or  less  misfortune. 

Cases  of  prolonged  sleep,  lasting  froin  a  day  even  to  several  years, 
belong  to  the  condition  of  lethargy,  or  cases  in  which  a  facile  habit 
has  developed  of  undergoing  autohypnosis. 

Probablv  the  longest  so-called  sleep  on  record  is  the  instance  re- 
ported bv  Herbst,  of  Bremen,  of  a  woman  who  was  in  a  state  of 
lethargy  seventeen  years.  Ingestion  of  food  was  normal  except  that 
it  had  to  be  specially  prepared  for  her.  There  was  a  semi-conscious 
state,  as  she  moaned  and  otherwise  indicated  when  she  wanted  atten- 
tion. 

The  "sleeping"  and  "fasting  girls"  of  the  dime  museums  are 
lethargic  hysterics. 

The  so-called  sleeping  sickness,  sleeping  dropsy,  maladie  du  som- 
meil,  negro  lethargy  is  a  parasitic  trouble  found  occurring  endemically 
in  Africa,  chiefly  along  the  West  coast,  and  limited  entirely  to  the 
negro.  The  trypanosoma  gambiense,  recovered  from  the  cerebrospinal 
fluid  of  the  victims,  with  a  species  of  tsetse  fly,  Glossina  palpalis,  as 
the  intermediate  host,  is  probably  the  cause  of  the  trouble. 

No  distinctive  pathological  changes  have  been  found,  though  in 


THE    NEUKOMC    DISEASES  I49 

one  instance  there  were  evidences  of  a  subacute  leptomeningitis, 
chromatolysis  of  various  degrees  in  the  cells  of  the  ventral  cornua  of 
the  cord  and  a  slight  falling  out  of  the  nerve  fibres  (Warrington). 

The  prominent  symptom  of  the  disease  is  the  prolonged  sleep  or 
lethargy,  more  accurately  coma,  in  which  the  patients  waste  away 
and  die  after  several  weeks  or  months,  always  within  a  year. 

They  rarely  recover.     Treatment  seems  to  be  ineffective. 

VERTIGO. 

Vertigo  is  a  symptom  and  accompanies  many  diseased  conditions. 
It  is  only  worthy  of  special  consideration  because  it  is  such  a  frequent 
symptom  and  because  it  occurs  sometimes  by  itself. 

The  imperfection  of  neurological  science  is  glaringly  exposed  in  the 
way  we  still  have  to  regard  in  sonie  instances  such  mere  symptoms  as 
vertigo,  chorea  and  hydrocephalus,  as  though  they  were  special  disease 
entities. 

Vertigo  is  a  loss  of  the  sense  of  equilibrium.  It  may  be  sub- 
jective or  objective.  The  victim  may  imagine  his  environment  to  be 
stationary  while  he  himself  is  in  a  whirling  state,  or  it  may  seem  to  him 
that  he  is  stationary  wliile  his  surroundings  are  in  a  condition  of 
unnatural  movement.  Vertiginous  sensations  involve  incoordination 
as  well  as  a  loss  of  equilibrium. 

Some  have  thought,  from  the  classical  experiments  of  Flourens  and 
the  phenomena  observed  in  aural  vertigo,  that  the  semicircular  canals 
were  the  special  and  sole  organs  that  subserved  the  maintenance  of 
equilibrium. 

As  stated  by  Edinger,  J.  Richard  Ewald  removed  the  labyrinth 
from  both  sides  of  a  dog.  The  result,  of  course,  was  a  loss  of  muscular 
tone  and  of  the  power  to  m.aintain  vertical  equilibrium.  Walking  and 
standing  were  impossible.  Note,  however,  that  these  troubles  were  re- 
covered from,  "the  tracts  for  tactile  and  other  impressions  making  up 
for  the  loss."  The  ablation  of  the  cortical  motor  areas  was  next  made, 
with  a  resulting  incoordination  and  the  loss  of  the  power  for  making 
any  regular  movements.  But  even  this  was  slowly  recovered  from. 
Suspicion  being  awakened  that  all  movements  were  dependent  now 
solely  upon  visual  control,  the  mutilated  dog  was  placed  in  a  dark 
room.     He  immediately  fell  helpless  to  the  floor. 

If  this  experiment  means  anything,  it  means  that  coordination  and 
the  maintenance  of  equilibrium  depend  upon  several  factors,  each  one 
of  which  is  capable,  up  to  a  certain  point,  of  assuming  the  whole  func- 
tion. The  motor  areas  of  the  brain,  the  visual  organs  and  the  semi- 
circular canals  all  play  an  equally  important  part.  If  the  semicircular 
canals  alone  were  the  organs  of  equilibrium  it  is  difficult  to  understand 
how  the  maintenance  of  equilibrium  could  even  in  the  slightest  degree 
be  reacquired  after  their  removal,  in  spite  of  the  preservation  of  the 
tactile  and  visual  senses. 

As  I  have  shown  elsewhere,  vertigo  and  the  loss  of  the  sense  of 
equilibrium  are  the  result  of  a  disturbance  in  a  more  extensive  sensory- 
motor  field  than  is  represented  by  the  semicircular  canals.     In  view  of 


150  THE    XEL'RO-XIC    DISEASES 

the  fact  that  in  certain  of  the  lowest  vertebrates  (fishes)  whose  move- 
ments require  the  nicest  sort  of  equihbrium  there  are  no  semicircular 
canals ;  in  view  of  the  fact  that  experimentation  has  shown,  as  in  the 
dog.  that  equilibrium  may  be  recovered  and  maintained  after  the  com- 
plete removal  of  the  labyrinth ;  in  view  of  the  fact  that  both  anatomy 
and  physiology  point  out  that  the  sense  of  equilibrium  is  essentially  a 
complicated  sensory-motor  phenomenon :  and  finally,  in  view  of  the 
fact  that  the  anatomy  of  the  apparatus  of  equilibration,  of  which  the 
semicircular  canals  form  only  a  part,  offers  a  more  rational  basis  for 
its  sensory-motor  character  than  does  so  limited  an  organ  as  the  semi- 
circular canals  alone :  I  think  that  we  are  still  justified  in  asserting 
that  the  semicircular  canals  are  not  alone  the  organs  of  equilibration, 
and  that  the  vertigo  of  ]\Ieniere's  disease  is  not  due  solely  to  injury  of 
the  canals,  but  to  the  injury  done  to  the  elaborate  and  complicated 
apparatus  of  equilibration  of  which  the  canals  constitute  a  part. 

One  object  in  presenting  all  this  is  to  show  that  vertigo,  if  our 
knowledge  of  the  anatomy  of  the  apparatus  of  equilibration  is  at  all 
correct,  may  be  produced  by  irritation  of  any  of  its  other  ramifications, 
as,  for  instance,  in  the  eye  and  in  the  stomach  as  well  as  in  the  ear. 
Hence,  it  seems  to  me  that  Gowers'  statement  referring  to  other  forms 
of  vertigo  than  aural  vertigo  is  too  much  of  a  pure  assumption  as  it 
stands:  "It  is  certain  that  in  the  majority  of  cases  in  which  such 
vertigo  has  been  ascribed  to  other  causes,  these  have  only  had  an 
exciting  influence  and  the  symptom  has  been  essentially  due  to  the  eflfeci 
of  unobtrusive  labyrinthine  disease,  bringing  the  center  into  an  unstable 
condition." 

The  study  of  vertigo  is  one  of  the  most  intricate  in  medicine,  and 
though  we  are  quite  familiar  with  its  subjective  and  objective  mani- 
festations, its  immediate  cause  remains  yet  a  profound  myster}-.  The 
maintenance  of  equilibrium  cannot  be  satisfactorily  assigned  to  any 
single  center,  though  its  disturbance  m.ay  easily  depend  upon  a  number 
of  distant  reflex  disturbances.  There  is  a  multiplicity  of  impressions 
constantly  pouring  in  upon  the  brain  through  the  various  avenues  of 
sense  which  must  necessarily  keep  the  mind  in  a  state  of  extreme  ten- 
sion, so  that  the  slightest  exaggeration  one  way  or  the  other  will  result 
in  mental  confusion  and  more  or  less  vertigo.  We  learn  instinctively 
how  to  control  and  marshal  these  ever-passing  sensations  before  the 
mind,  but  if  for  a  time  they  become  too  frequent,  rapid  or  sudden,  th-^ 
controlling  force  of  the  intellect  is  weakened  and  we  are  confused  and 
overcome  by  them.  Everybody  knows  how  quickly  vertigo  is  estab- 
lished by  rapidly  revolving  mirrors,  peculiar  whirring  sounds,  electrical 
sensations  upon  the  skin  and  such  distant  irritative  conditions  as  dys- 
pepsia and  constipation. 

Physiological  psychologists  are  agreed  now  that  our  knowledge  of 
the  relationship  of  things,  as  well  as  of  space  and  its  dimensions,  is  the 
result  of  experience  gained  from  the  use  of  our  muscles.  The  infant 
learns  these  dimensions  by  the  frequent  application  of  its  hands  to  the 
objects  which  it  sees ;  and  the  sight,  which  is  the  only  other  sense 
that  reveals  to  us  an  extended  object,  and  that  never  shows  us  more 


THE    XEUROXIC    DISEASES  I5T 

than  two  dimensions  at  one  and  the  same  time,  does  so  entirely  throusrii 
the  "muscular  sense"  exercised  in  the  use  of  the  muscles  of  the  eyeball. 

Now  when  we  study  the  nature  of  equilibrium.  Ave  discover  that 
it  is  dependent  upon  a  normal  consciousness  of  the  proper  relationship 
of  things  outside  of  the  centers  of  consciousness.  It  is  not  purely 
pyschic,  as  some  have  imagined.  There  is  the  sensation  of  a  motor 
process  in  it.  Dr.  Hughlings  Jackson  has  long  insisted  upon  the  im- 
portance of  this  fact,  while  Dr.  Reynolds  wrote  as  long  ago  as  1854 
that  "the  feeling  of  equilibrium  results  from  the  harmony  of  our  differ- 
ent sensations  among  themselves  and  with  the  motor  impulse  which  is 
their  combined  effect.  When  any  one  group  of  the  sensorial  impres- 
sions is  distorted  or  removed,  the  balance  is  disturbed,  and  as  these 
impressions  are  themselves  the  stimuli  of  muscular  action,  attempts  are 
made  for  its  restoration  .  .  .  producing  vertiginous  or  allied  move- 
ments." 

The  principal  factors  m  the  preservation  of  equilibrium  are  there- 
fore consciousness  and  normal  sense  impressions.  A  vertiginous  im- 
pression reflected  through  consciousness  may  end  in  a  complete  or  in- 
complete motor  act.  In  the  latter  case  there  is  merely  a  residual  dis- 
turbance of  past  impressions  without  a  fulfillment  of  the  present 
impulse  in  complete  motion,  while  in  the  former  the  patient  is  uncon- 
trollably moved  in  one  direction  or  another. 

If  the  views  of  Spitzka  and  Starr  in  regard  to  the  sensory  paths 
in  the  medulla  be  correct,  they  bear  strongly  in  favor  of  this  sensory- 
motor  theory  of  vertigo.  Thus  Spitzka  concludes  that  impressions  from 
the  cochlea  reach  the  cortical  centers  in  the  superior  temporal  gyrus 
by  way  of  the  posterior  division  of  the  eighth  pair  of  nerves,  the 
trapezium  of  the  same  side,  part  of  the  lemniscus,  posterior  pair  of  the 
corpora  quadrigemina,  external  geniculate  body  and  the  corona.  Ac- 
cording to  some  observations  of  Starr,  which  prove  the  correctness  of 
the  views  of  Flechsig  and  Von  Monakow,  the  lemniscus  tract  is  asso- 
ciated with  the  so-called  "muscular  sense"'  and  is  chiefly  distributed  to 
the  inferior  quadrigeminal  body.  Some  physiologists  think  that  it  is 
even  continued  up  as  far  as  the  corona.  It  is  believed  that  this  tract  is 
associated  with  the  sense  of  sight,  as  well  as  with  the  coordination  of 
movements.  Flourens  found  that  injuries  to  the  corpora  quadrigemina 
of  one  side  caused  "forced  movements,"  and  that  their  complete  removal 
resulted  in  incoordination  of  movement. 

The  point  which  I  desire  to  insist  upon  is  the  close  relationship 
of  all  these  tracts  for  sight,  hearing  and  the  "muscular  sense"  in  the 
corpora  quadrigemina  and  their  more  distinct  termination  in  the 
cerebral  cortex  than  in  the  cerebellum.  If  vertigo  were  a  kind  of  en- 
cephalic ataxia,  and  due  simply  to  disturbed  coordination,  it  might 
readily  be  attributed  to  the  cerebellum. 

\\'hile  the  function  of  the  cerebellum  may  be  that  of  coordination 
and  the  maintenance  of  "continuous  tonic  muscular  contractions,"  and 
while  as  Spitzka  tersely  remarks,  it  may  be  the  center  where  "impres- 
sions of  touch  and  position  are  associated  with  those  of  time  and 
space,"  I  find  no  authority  for  assuming  that  it  is  in  any  way  the  cen- 
ter for  the  institution  of  movements  or  the  maintenance  of  these  move- 


152  THE    NEURONIC    DISEASES 

ments  in  a  regular,  methodical  manner,  which,  to  my  mind,  is  the  un- 
derlying phenomenon,  objectively  or  subjectively,  of  true  vertigo. 

Vertigo  is  something  more  than  simple  incoordination,  though 
incoordination  may  enter  as  one  of  its  principal  elements.  In  vertigo 
there  is  a  disturbance,  not  merely  of  the  reflex  functions,  but  of  the 
higher  powers  as  well.  The  motor  and  sensory  phenomena  of  vertigo, 
in  typical  cases  at  least,  are  not  mere  sequences  of  abnormal  motor  and 
sensory  impulses,  but  they  are  the  impulses  themselves. 

Simple  incoordination  manifests  itself  in  irregular  unmethodical 
movements  and  thus  shows  that  it  is  due  to  an  affection  of  some  slib- 
ordinate  regulating  center  of  the  brain ;  true  vertigo  manifests  itself 
in  regular  methodical  movements  and  thus  reveals  disease  of  a  higher 
independent  center. 

It  is  a  significant  fact,  when  considered  in  this  connection,  that  the 
vertigo  which  is  so  characteristic  of  cerebellar  disease  and  which  is 
identical  with  the  vertigo  of  Meniere's  disea,se,  is  caused  only  by  lesions 
in  the  middle  lobe,  or  that  part  of  the  cerebellum  which  is  most  liable 
to  involve  the  sensory-motor  tracts  of  the  medulla;  and  furthermore, 
that  lesions  of  the  lateral  lobes  not  pressing  upon  or  involving  the 
middle  lobe  do  not  give  rise  to  any  known  symptoms. 

And  it  is  still  more  significant  that  vertigo  is  not  pathognomonic 
of  cerebellar  disease,  for  it  may  be  caused  by  lesions  in  other  parts  of 
the  brain  as  well.  Even  in  its  coodinating  function,  it  is  more  than 
probable  that  the  cerebellum,  instead  of  sending  out  direct  coordinating" 
impulses  to  the  muscles,  merely  coordinates  the  impulses  sent  down 
from  the  cerebral  centers  above.  Indeed,  as  Ranney  has  said,  "it  is  a 
curious  fact  that  most  of  the  effects  of  cerebellar  lesions  are  attributable, 
to  a  greater  or  less  extent,  to  irritation  of  the  crura." 

According  to  Goltz,  Serres,  Cayrade  and  others,  the  function  of 
equilibrium  is  profoundly  affected  by  destruction  of  the  corpora 
quadrigemina.  The  experiments  of  Ferrier  upon  monkeys,  fishes  and 
rabbits,  and  of  McKendrick  upon  pigeons,  revealed  the  same  effects. 
The  corpora  striata  have  also  been  shown  by  physiological  experiment 
to  preside  over  the  maintenance  of  equilibrium,  especially  after  the 
removal  of  the  hemispheres. 

Every  indication  points  to  the  fact,  then,  that  we  must  look  for 
the  center  of  equilibrium  not  in  one  particular  part  of  the  brain,  but 
in  the  harmonious  action  of  the  various  sensory  and  motor  centers  one 
upon  another. 

Vertigo  then  being  merely  a  symptom  no  systematic  discussion  of 
its  etiology  and  pathology  is  possible  for  we  would  have  to  discuss  all 
the  diseases  in  which  vertiginous  sensations  occur. 

I  have  already  shown  the  nature  and  general  causation  of  the  phe- 
nomenon and  now  will  mention  a  few  of  the  more  common  forms  of 
vertigo  and  their  probable  etiology.  I  do  this  with  the  special  desire 
of  forestalling  the  various  views  w^hich  some  promulgate  in  regard  to 
the  cause  of  all  vertigos. 

Ocular  Vertigo.  The  eyes  and  the  optic  nerves  constitute  a  most 
important  inlet  for  afferent  impulses.  Any  disorder  in  the  visual  ap- 
paratus must  necessarily  upset  the  orderly  procession  of  these  impulses 


THE    NEURONIC    DISEASES  I53 

both  in  relation  to  one  another  and  to  those  from  other  sources.  Hence 
we  find  in  nearly  all  diseases,  whether  functional  or  organic,  that  exer- 
cise the  slightest  influence  on  the  optic  apparatus  and  the  function  of 
sight,  more  or  less  vertiginous  sensation.  It  is  a  mere  repetition  then 
to  say  that  muscular  insufficiencies,  refractive  errors,  reflex  functional 
disturbances,  intoxications,  brain  lesions,  are  all  more  or  less  accom- 
panied by  vertigo. 

Aural  Vertigo.  The  same  may  be  said  of  diseases  of  the  ear  that 
was  said  of  those  of  the  eye.  One  variety  of  aural  vertigo  has  long 
been  dignified  with  the  special  name  of  Meniere's  disease.  The  latter 
term  is  employed  very  loosely  nowadays  and  many  writers  speak  of  all 
forms  of  vertigo  whether  due  to  internal,  middle  or  external  ear  abnor- 
malities as  types  of  Meniere's  disease.  In  true  Meniere's  disease  only 
the  semicircular  canals  are  affected.  At  least  that  is  what  Meniere 
himself  seems  to  have  believed.  His  second  and  fourth  propositions 
are  that  certain  functional  troubles,  having  their  seat  in  the  internal 
auditory  apparatus,  may  give  rise  to  cerebral  symptoms  such  as  in- 
tense vertigo,  uncertainty  of  gait,  turning  to  the  right  or  left  and  fall- 
ing, all  of  which  may  be  attended  with  nausea,  vomiting  and  syncope, 
and  that  all  this  tends  to  confirm  the  belief  that  the  lesion  which  is  the 
cause  of  these  functional  troubles  is  in  the  semicircular  canals.  In  his 
original  paper  he  describes  ten  cases,  in  only  one  of  which  was  there 
an  autopsy.  This  case,  the  tenth  of  the  series,  had  no  disease  of  the 
nervous  centers,  but  the  semicircular  canals  were  filled  with  a  "reddish, 
plastic  material."  It  was  on  the  strength  of  this  single  observation 
that  he  declared  the  canals  to  be  the  cause  of  the  cerebral  symptoms. 

Aside  from  the  unscientific  character  of  such  a  hasty  generaliza- 
tion, this  one  case,  as  Breniner  points  out,  will  hardly  explain  those  in 
which  the  cerebral  symptoms  come  and  disappear  rapidly.  And  if  the 
hemorrhage  into  the  semicircular  canals  were  the  cause  of  the  trouble 
here  and  in  the  majority  of  the  apoplectiform  cases,  as  Knapp  argues, 
it  remains  to  be  shown  why  the  hemorrhage  is  bilateral,  since  the  aural 
symptoms  are  so  frequently  bilateral. 

Both  Steiner  and  Sewall  carefully  removed  the  semicircular  canals 
from  the  shark,  whose  auditory  apparatus  is  practically  identical  with 
man's,  without  obtaining  any  disturbance  of  movement.  The  former 
experimenter  believes  that  the  loss  of  equilibrium  results  from  lesions 
of  the  brain  or  its  membrane,  causing  alterations  of  pressure,  for  he 
has  again  and  again  destroyed  the  canals  in  sharks,  frogs  and  lizards 
without  injuring  the  brain,  and  discovered  no  disturbance  in  the  power 
of  equilibration.  After  careful  investigation  Bottcher  and  Baginsky 
have  come  to  the  conclusion  that  the  cause  of  the  rotation  of  the  head 
in  Flourens'  and  Goltz's  experiments  was  the  injury  done  to  the  brain, 
and  not  merely  to  the  semicircular  canals.  Bottcher  marks  the  fact  that 
the  auditory  nerve  is  not  bound  down  at  any  point  between  the  brain 
and  the  labyrinth,  and  that  if  one  is  careful  not  to  pull  upon  this  nerve 
the  vertiginous  sensations  are  not  awakened  by  the  injury  of  the  semi- 
circular canals.  The  slightest  traction  upon  the  auditory  nerve  in- 
jures its  attachment  at  the  medulla,  and  so  gives  rise  to  the  symptoms 
described  by  Flourens,   Cyon,   and   Goltz.     In     the     experiments    of 


154  THE    XEUROXIC    DISEASES 

Bottcher  the  head,  furthermore,  did  not  always  rotate  in  accordance 
with  the  particular  canal  injured,  as  Goltz  had  formulated.  The  iden- 
tity of  these  canals  with  the  cochlea  in  the  embryo,  their  continuity  with 
the  epicerebral  space  through  the  aquaeductus  vestibuli,  and  their  ever- 
shifting  relations  amongst  themselves  in  the  quadrumana,  which  go 
about  sometimes  in  the  horizontal  and  sometimes  in  the  erect  position, 
argue  strongly  against  the  special  function  of  these  canals  being  the 
maintenance  of  equilibrium. 

In  the  discussion  of  my  paper  upon  the  same  subject  before  the 
Philadelphia  Neurological  Society,  Xov.  24,  1890,  Dr.  Dercum  re- 
ported some  observations  he  had  made  of  the  comparative  anatomy  of 
the  labyrinth  for  the  purpose  of  securing  new  light,  if  possible,  upon 
the  function  of  the  semicircular  canals.  He  said:  "They  bear  a  dis- 
tinct relation  to  the  lateral  line  organs  of  fishes,  the  nerve  hills  of  the 
latter  being  identical  in  structure  with  the  maculae  acousticse.  Just  as 
the  inclosure  of  these  nerve  hills  in  tubes  seems  to  have  for  its  object 
the  gaining  of  distinctness  and  detiniteness  of  impression  so  the  in- 
closure of  the  maculae  within  the  semicircular  canals  seems  to  have  the 
same  object.  It  is  significant  that  each  macula  is  situated  at  the  end 
of  a  canal,  and  this  suggests  that  the  canal  is  a  kind  of  conduit  to  carry 
ofT  vibrations  after  they  have  made  their  impression  on  the  macula ;  and 
further,  that  if  interference  of  vibration  occurs,  it  occurs  at  a  point 
distant  from  the  macula.  Confusion  of  sound  is  thus  avoided.  The  in- 
ference from  physiological  experiment  that  these  structures  have  for 
their  special  object  the  maintenance  of  equilibrium,  has  always  seemed 
to  me  open  to  most  serious  objection." 

It  is  a  well-known  fact  that  many  fishes  have  a  utricle  and  three 
semicircular  canals,  while  some  have  only  one  and  two  canals. 
Amongst  the  lowest  vertebrates  the  lamprey  has  a  saccule  with  audi- 
tory hairs  and  otoliths  in  communication  with  two  semicircular  canals, 
while  the  myxine  or  hag  has  only  one  canal.  Doubtless  there  are  im- 
portant sensory  impulses  of  a  special  character  which  pass  through 
these  organs,  but  equilibration,  due  as  we  ha^-e  seen  to  the  fusion  of  a 
vast  complex  mass  of  sensations  pouring  in  upon  the  brain  from  all 
sides,  cannot  possibly  be  the  result  of  merely  a  single  set  of  impulses 
from  such  an  end-organ  as  the  semicircular  canals.  The  very  nature  of 
vertigo  involves  the  idea  of  more  or  less  loss  of  consciousness,  and  this 
alone  would  seem  to  indicate  a  higher  cause  for  the  trouble  than  sim- 
ply these  canals. 

If  it  be  granted  that  the  pathological  cause  of  this  vertigo  is  to  be 
found  in  the  semicircular  canals,  it  is  hard  to  understand  how  in  all 
cases  the  cochlea  or  the  cochlea  branch  of  the  auditory  nerve  should 
necessarily  be  affected.  In  Flourens'  experiment,  the  entire  removal  of 
the  canals  did  not  impair  the  hearing.  So  striking  was  this  fact,  that 
Flourens,  as  well  as  others,  was  led  to  believe  that  the  branch  of  the 
auditory  nerve  which  supplies  the  semicircular  canals  subserves  motor 
purposes  only.  On  the  other  hand,  if  Gelle's  experiments  are  to  be 
trusted,  the  cochlea  is  in  no  way  the  source  of  vertiginous  impressions. 

Simple  continuity  of  structure  w-ill  not  accotmt  for  the  loss  of  hear- 
ing Avhen  the  lesion  is  a  hemorrhage  into  the  canals,  ^nd  pressure  alone 


THE    NEURONIC    DISEASES  I55 

will  not  answer  as  a  cause  in  all  cases  of  so-called  Meniere's  disease. 
In  the  first  place,  there  is  no  regular  correspondence  between  the 
amount  of  deafness  and  the  intensity  of  the  vertigo ;  secondly,  with 
total  loss  of  hearing  in  Meniere's  disease  all  known  methods  of  diag- 
nosis prove  that  the  nerve  itself,  and  not  merely  the  internal  ear,  is 
affected ;  thirdly,  physiological  experiment  shows  that  simple  pressure 
does  not  cause  total  loss  of  hearing  when  no  injury  is  done  to  the 
cochlea  or  cochlea  branch  of  the  auditory  nerve ;  and  finally,  no  case 
has  ever  been  reported  in  which  the  cochlea  was  primarily  affected 
with  consequent  involvement  of  the  canals  and  vertigo,  though  in  blood 
supply  and  anatomical  structure  the  cochlea  and  canals  are  similar. 
Hence,  in  Meniere's  disease,  I  conclude  that  the  lesion  must  concern  the 
whole  labyrinth  or  lie  entirely  outside  of  it. 

It  was  Dr.  Wilks,  of  England,  I  think,  who  held  that  Meniere's 
disease  was  a  neurosis  of  the  centers  of  audition  and  equilibrium,  and 
in  its  paroxysmal  form  at  least  was  much  like  migraine  with  its  eye 
complications. 

While  this  explanation  cannot  be  adopted  for  all  cases,  there  is 
little  doubt  about  the  central  nature  of  the  disease  in  many  of  its  as- 
pects. Burnett  declared  that  "the  neuropathic  diathesis  is  well  marked 
in  most  cases  of  aural  vertigo."  The  grouping  of  the  symptoms,  as 
well  as  the  proximity  of  the  tracts  and  centers  involved,  point  to  the 
encephalic  origin  of  the  affection.  Especially  is  this  indicated,  how- 
ever, by  the  sensory-motor  nature  of  the  vertigo,  whatever  be  the  peri- 
pheral source  of  the  disturbance,  and  its  association  with  the  state  of 
consciousness. 

Sudden  or  parox3'Smal  vertigo,  causing  the  patient  to  fall  some- 
times as  in  a  stroke  of  apoplexy,  followed  by  nausea  and  vomiting. 
headache,  difficulty  of  hearing,  stubborn  tinnitus  or  even  deafness,  bilat- 
eral or  unilateral,  with  various  other  possible  accompaniments  such 
as  facial  paresis,  nystagmus,  constitutes  the  clinical  picture  of  Meniere's 
disease. 

According  to  Meniere  himself  it  is  due  to  hemorrhage  into  the 
semicircular  canals.  As  the  syndrome  occurs  in  other  ear  troubles,  and 
in  cranial  injuries  and  brain  diseases,  the  semicircular  canals  may  be 
only  secondarily  and  functionally  disturbed. 

In  most  of  the  cases  the  nausea  and  vomiting  soon  cease,  the  ver- 
tigo passes  away  in  the  course  of  a  few  weeks  or  appears  only  at  re- 
mote intervals,  while  the  hearing  remains  more  or  less  permanently 
•damaged. 

The  zrrfigo  of  the  neuroses  bears  a  close  similarity  to  many  cases 
of  ^Meniere's  vertigo.  In  hysteria,  hystero-neurasthenia,  epilepsy,  un- 
usual and  unexpected  sounds,  sights  and  other  sensory  irritations 
arouse  a  vertiginous  condition.  The  feeling  of  distress  and  impulse  to 
leap  which  many  persons  iiave  upon  high  places  is  a  mild  form  of 
hystero-neurasthenic  vertigo. 

Many  irritating  and  destructive  diseases  of  the  nasal  cavities,  of 
the  larynx,  and  elsewhere  about  the  head  often  provoke  vertiginous 
sensations. 

Intoxications,   such   as   those   of   alcohol,   lead,   nicotine,   caffeine. 


156  THE    NEURONIC    DISEASES 

autointoxication  from  alimentary  disorders  and  intestinal  parasites,  in- 
fectious states  are  all  prone  to  manifest  among  their  most  prominent- 
symptoms  nausea  and  vertigo.  In  this  class  probably  falls  the  so- 
called  paralytic  vertigo  which  is  endemic  in  the  Geneva  canton,  Switz- 
erland, and  which  is  attributed  by  Geslier  to  misasmatic  influences^ 
The  Kubisagara  of  Japan  is  probably  the  same  sort  of  a  trouble. 

Aiicciiiia  produces  the  symptom.  Malnutrition  of  the  nervous  ele- 
ments may  provoke  the  same  functional  disorders  in  them  sometimes 
as  does  intoxication.  Atheromatous  conditions  of  the  arterial  walls- 
and  circulatory  disorders,  especially  sudden  changes  in  the  intracranial 
circulation  are  characterized  by  attacks  of  giddiness. 

The  climacteric  vertigo  is  probably  largely  circulator}-  ui  origin: 
though  other  factors  play  a  role  also. 

Disseminated  sclerosis  with  its  apoplectiform  seizures  is  notable 
for  its  vertigo.  A  moment's  reflection  upon  the  pathology  of  this  affec- 
tion makes  clear  the  raison-d'etre  of  the  vertiginous  phenomena. 

Vertigo  may  even  have  a  psychic  origin.  It  is  not  uncommon  in. 
hypochondriac  neurasthenia.  Oppenheim  even  goes  so  far  as  to  assert 
that  it  is  his  belief  that  every  one  may  produce  in  himself  a  feeling  of 
dizziness  by  thinking  of  incoordination  and  by  depicting  to  himself 
the  feeling. 

Prognosis.  The  hope  of  recovery  from  attacks  of  vertigo  is  en- 
tirely dependent  upon  the  curability  or  removal  of  the  pathological  state 
out  of  which  it  arises.  Intoxication  and  alimentary  vertigoes  are  prac- 
tically all  curable.  The  dizziness  that  accompanies  arteriosclerosis- 
very  often  disappears  as  the  disease  progresses.  Sometimes  that  oc- 
curs in  other  cerebral  troubles,  though  as  a  rule  these  vertigos  are  ex- 
ceedingly persistent.  Removable  conditions  in  the  nose,  eyes,  ears  or 
alimentary  tract  may  all  be  expected  to  carry  with  them  when  removed 
the  giddiness  which  forms  a  part  of  their  symptomatology. 

Meniere's  vertigo  is  very  resistant  to  treatment.  It  often  disap- 
pears leaving  behind  it  disturbance  of  hearing. 

Treatment.  This  should  always  be  toward  the  removal  or 
amelioration  of  the  cause  or  underlying  disease.  There  is  no  need 
to  say  that  intoxications,  infections,  reflex  irritants,  dyscrasize  and 
cachexias  of  all  kinds,  and  anatomical  and  functional  anomalies,  should 
all  be  corrected  and  removed  as  far  as  possible.  It  would  be  a  mere 
waste  of  space  to  recapitulate  here  all  of  the  measures  for  doing  this- 
when  reference  to  them  can  be  made  to  the  various  chapters  devoted 
to  the  diseases  with  which  vertigo  is  associated. 

The  symptomatic  treatment  of  vertigo  should  only  be  temporary 
and  when  all  efforts  to  remove  its  obvious  cause  have  signally  failed. 
Amyl  nitrite,  nitroglycerin,  the  bromides,  phenacetin,  hydrobromate 
of  quinine,  alkalies,  digitalis,  strychnia,  etc.,  may  be  employed  when 
the  appropriate  condition  is  present.  Glyerinophosphates,  gold,  the 
ferruginous  preparations,  bichloride  of  mercury  may  be  thought  of 
for  their  tonic,  and  alterative  effect  and  be  administered  for  some  time 
in  small  doses. 

The  bromides  and  belladonna  have  relieved  some  cases  of 
Meniere's  vertigo  under  my  care.     The  treatment  with  massive  doses 


THE    NEURONIC    DISEASES  15? 

of  quinine,  suggested  by  Charcot,  has  ignominiousl}^  failed  in  a  num- 
ber of  cases  in  which  I  tried  it.  To  be  sure  the  vertigo  left  after  the 
use  of  the  alkaloid  for  several  weeks  but  Meniere's  vertigo  not  infre- 
-quently  ceases  thus  without  any  medication.  Charcot  recommended 
that  the  quinine  be  given  up  to  the  point  of  cinchonism.  At  first  the 
trouble  may  be  made  temporarily  worse.  On  account  of  the  danger 
to  the  hearing,  aurists  urge  great  conservatism  in  the  use  of  quinine. 
If  the  patient  is  willing  to  exchange  deafness  for  the  vertigo,  Charcot's 
suggestion  to  puncture  the  membrana  tympani  may  be  put  into  prac- 
tice. 

Blood-letting  is  heroic  for  vertigo  but  it  has  done  good  in  some 
cases  when  intense  congestion  was  present.  In  other  cases  sodium 
salicylate  or  hypodermics  of  pilocarpine  every  other  day  have  relieved 
most  distressing  attacks. 

After  all  it  must  be  admitted  that  the  only  treatment  of  this  symp- 
tom is  the  treatment  of  the  malady  to  which  it  belongs.  All  other  at- 
temps  to  relieve  it  are  unscientific,  haphazard  and  usually  disappointing. 

NEURASTHENIA. 

If  the  term  disease  is  to  be  made  to  cover  all  forms  of  abnormal 
manifestation,  then  neurasthenia  is  entitled  to  be  regarded  as  a  dis- 
ease as  well  as  cancer  or  syphilis.  No  manifestation  has  been  more 
happily  named,  for  nerve-tire,  nerve-exhaustion,  nervous  inadequacy 
express  exactly  the  essential  condition.  It  is  a  nerve-tire,  however,  that 
is  abnormal  in  the  sense  that  it  is  not  immediately  recovered  from  as 
in  the  temporary  nerve-tire  that  results  from  a  slight  over-exhaustion. 
The  nerve-inadequacy  has  fallen  below  such  a  point,  either  by  the 
severity  of  the  cause,  the  prolongation  of  the  trouble,  or  the  peculiar 
susceptibility  of  the  patient,  that  certain  functions  within  the  neurones 
and  in  those  tissues  in  direct  relationship  with  those  neurones  are 
affected.  As  a  consequence  a  more  or  less  definite  symptomatology  is 
presented. 

The  exhaustion  is  characteristic  of  the  entire  nervous  system.  It  is 
a  disease  of  the  nervous  apparatus  in  toto.  Though  in  different  pa- 
tients it  may  manifest  itself  more  prominently  through  the  cerebral, 
spinal  or  peripheral  nervous  apparatus  according  to  the  peculiar  con- 
stitutional and  temperamental  predilection  of  the  patient,  there  is  no 
good  reason  for  subdividing  neurasthenia  into  cerebrasthenia,  myelas- 
thenia,  sexual  neurasthenia,  gastric  neurasthenia,  etc.  One  does  not 
divide  typhoid  fever  into  diarrhceal,  febrile  and  delirious  types  be- 
cause individual  patients  exhibit  more  prominently  enteric,  febrile  or 
neurotic  symptoms. 

The  only  logical  and  practical  subdivision  of  neurasthenia  is  into 
the  congenital  and  acquired  forms.  The  former  is  a  true  nervous  in- 
adequacy, a  defect  of  prenatal  origin,  a  failure  of  biological  develop- 
ment ;  the  latter  is  a  true  nervous  exhaustion,  a  postnatal  depreciation, 
a  failure  of  physiological  function  from  depressing  influences. 

Etiology.'  Heredity  plays  a  very  important  role  in  the  develop- 
ment of  neurasthenia.    In  the  congenital  types  of  the  disease  it  is  prac- 


158  THE    NEURONIC    DISEASES 

tically  the  sole  cause.  The  patient  is  born  with  an  unstable  and  inad- 
equate nervous  apparatus  which  later  on  reveals  its  symptoms  of  irri- 
table  w^eakness  not  as  a  result  of  the  trials  and  struggles  of  life  directly 
but  rather  because  it  cannot  meet  and  override,  by  reason  of  its  inher- 
ent weakness,  these  trials  and  struggles  which  to  a  normal  nervous  ap- 
paratus w^ould  be  as  nothing.  In  these  cases  the  environment  is  not 
the  cause  of  the  trouble  but  rather  the  patient's  inherited  nervous  ina- 
bility to  accommodate  himself  to  what  would  be  a  normal  environment. 
'These  cases  are  hard,  if  not  impossible,  to  treat,  because  every  sort 
of  social  condition  provokes  the  neurasthenic  phenomensP  in  tlieir  irri- 
table and  unaccommodating  nervous  organism. 

The  large  majority  of  the  cases  of  acquired  neurasthenia  are  en- 
dowed by  heredity  with  what  is  called  a  neuropathic  constitution.  They 
have  a  nervous  apparatus  which  under  proper  conditions  may  never 
reveal  any  neurasthenic  symptoms  but  which  under  other  conditions 
leads  it  to  break  down  rapidly  and  seriously.  Unlike  the  former  class- 
of  individuals,  these  are  merely  unstable.  With  some  of  them  even 
work  and  strain  that  would  be  unfavorable  to  perfectly  normal  indi- 
viduals do  not  produce  deleterious  effects. 

These  are  cases  that  are  always  neurasthenic  until  they  are  placed 
in  a  position  or  are  given  tasks  that  harmonize  with  their  tastes,  their 
training,  their  mental  calibre  and  their  feelings.  In  the  development  of 
these  neurasthenics  their  environment  is  a  most  important  element  but 
it  has  as  a  co-operating  factor  the  inherited,  unstable,  unresisting  nerv- 
ous organism  which  is  prone  to  topple  over  when  that  environment  be- 
comes particularly  inharmonious.  Many  artists  are  of  this  class  and 
it  is  among  them  that  the  so-called  artistic  temperament  is  mostly 
found.  Their  nervous  organization  is  not  exactly  abnormal  but  it  is 
so  mobile,  sensitive  and  responsive  that  very  slight  causes  provoke  it 
into  revealing  abnormal  symptoms,  which  if  long  continued  may  result 
in  a  complete  nervous  breakdown. 

These  cases  are  amenable  to  treatment  but  from  the  very  nature 
of  things,  their  management  is  difficult,  taxing  and  tedious. 

I  should  say  that  from  eighty  to  ninety  per  cent,  of  the  cases  of 
typical  neurasthenia  fall  into  one  or  other  of  the  above  classes  in 
which  heredity  plays  so  important  a  part. 

Among  the  antecedents  we  find  various  nervous  troubles,  such  as 
neurasthenia,  hysteria,  migraine,  epilepsy,  melancholia,  insanity  and 
other  neuroses  and  psychoses.  The  family  taint  runs  along  the  nerv- 
ous line.  Gout  and  rheumatism  are  not  infrequent  in  the  ancestry. 
Alcoholism  in  the  parents,  excessive  use  of  tobacco,  dissipation,  over- 
indulgence of  the  sexual  appetite,  are  all  frequently  observed  in  the 
heredity.  Severe  and  prolonged  mental  strain  wdthout  a  correspond- 
ing or  appropriate  attention  to  their  physical  vigor  and  functions  in 
the  parents  will  result  in  a  neuropathic  constitution  in  the  child.  The 
same  may  be  said  of  all  forms  of  monotonous,  one-sided  activity 
whether  mental  or  physical.  These  neurasthenics  occasionally  expose 
their  bad  inheritance  in  slight  physical  stigmata  of  degeneracy. 

In  a  word  all  factors  that  tend  to  lower  the  mental  and  physical 
health  of  the  parents,  tend  to  confer  on  the  children  a  nervous  consti- 


THE    NEURONIC    DISEASES  I59 

tution  that  is  neurasthenic  or  prone  to  become  neurasthenic  upon  the 
shghtest  occasion. 

The  purely  acquired  cases  of  neurasthenia,  cases  in  which  the  con- 
stitution was  originally  strong  and  the  heredity  excellent,  do  occur 
though  they  are  comparatively  rare.  In  such  cases  only  exciting  causes 
can  be  charged  with  the  disease. 

Among  the  exciting  causes  of  neurasthenia  we  recognize  both  the 
mental  and  the  physical. 

Mental  causes  include  continued  and  exalted  emotionalism,  exces- 
sive use  of  the  intellect,  and  all  forms  of  mental  strain,  especially  if 
associated  with  worry  and  anxiety.  It  is  a  fact,  general  opinion  to 
the  contrary  notwithstanding,  that  mere  overwork  or  hard  work  does 
not  result  in  mental  breakdown,  if  the  individual's  inheritance  is  good, 
the  work  is  not  disagreeable  and  his  habits  as  to  sleep,  rest,  nutrition 
and  systematic  physical  exercise  are  carefully  regulated.  If  properly 
guarded  in  this  way  and  if  properly  exercised  in  regard  to  all  of  its 
faculties  equally  so  as  to  avoid  an  unbalanced  activity,  the  human  brain 
is  capable  of  bearing  a  greater  strain  than  is  ever  put  upon  it  by  the 
average  work  of  man.  It  is  the  worry,  the  fret  and  the  one-sided 
strain  and  unsystematic,  unwholesome  use  of  the  brain ;  and  not  the 
mere  amount  of  the  work  imposed  upon  it,  that  enter  chiefly  into  the 
mental  causation  of  neurasthenia. 

Close  to  the  mental  causes  are  the  nervous  strains.  Usually  the 
two  go  together.  Thus  sexual  irregularities,  excessive  venery,  and 
masturbation  frequently  develop  neurasthenia  though  at  times  they  are 
but  the  expression  of  a  neurasthenic  irritability.  Cause  and  effect 
here  must  be  carefully  differentiated  in  each  individual  case. 

Many  of  the  causes  of  neurasthenia  are  kept  alive  by  the  neuras- 
thenic state,  so  that  a  "vicious  circle"  obtains  and  must  be  broken  some- 
where. 

Traumatic  neurasthenia  is  usually  due  to  a  psychoneurotic  shock. 
The  same  may  be  said  of  the  prolonged  irritation  superinduced  by  the 
many  reflex  causes  that  are  mentioned  in  the  books.  A  local  nidus 
of  disease,  a  physical  defect  which  disturbs  the  associated  functions, 
otr  a  physiological  abnormality  of  any  sort  may  well  be  conceived  of 
as  an  exciting  cause,  acting  m  a  reflex  way  upon  a  predisposed  neuro- 
pathic apparatus.  In  this  manner  eye-strain,  pelvic  disease,  gastro- 
intestinal trouble  with  associated  malnutrition  may  all  provoke  and 
prolong  an  attack  of  nervous  exhaustion. 

Infectious  diseases  and  all  forms  of  toxaemia  may  act  as  causes. 
The  toxin  may  act  directly  upon  the  neurones  so  as  to  diminish  their 
nutritive  and  specific  function,  or  it  may  act  indirectly  upon  the  pri- 
mary assimilation  of  the  alimentary  tract  and  circulatory  apparatus. 
Syphilis  for  instance  injures  both  the  functions  of  nutrition  and  the 
neurility  of  the  individual  neurones.  Any  of  the  infectious  diseases, 
as  well  as  intoxication  by  alcohol,  nicotine,  lead  and  arsenic,  may  thus 
cause  neurasthenia. 

Autointoxication  can  be  invoked  as  a  factor,  and  in  close  connec- 
tion with  it  is  the  enteroptosis  and  gastroptosis  referred  to  in  Glen- 
ard's  theory. 


l6o  THE    NEURONIC    DISEASES 

A  severe  loss  of  blood  may  very  obviously  produce  neurasthenia, 
the  blood  being  the  source  of  the  nutrition  of  the  nervous  elements. 
Some  careful  examinations  of  the  blood  of  neurasthenics  by 
Holdam,  Smith  Lodor  and  others  show  that  it  is  almost  constantly 
deficient  in  oxygen  carrying  capacity.  This  of  course  affects  the  in- 
ternal metabolism  and  suggests  some  form  of  toxaemia  as  an  underly- 
ing cause. 

Finally  it  must  not  be  forgotten  that  even  severe  and  prolonged 
physical  exercise  sometimes  terminates  in  neurasthenia.  Many  a  mild 
neurasthenic  is  made  worse  by  adopting,  under  a  mistaken  idea,  a  vig- 
orous regimen  of  outdoor  games  and  indoor  gymnastics.  The  one- 
sidedness  of  all  such  measures,  apart  from  the  fact  that  they  only  add 
more  strain  to  an  already  strained  nervous  apparatus,  would  seem  to 
be  enough  to  condemn  them  for  the  treatment  of  neurasthenia.  Euro- 
pean trips,  incessant  golf  and  tennis  playing,  long  constitutional  walks 
may  in  this  way,  when  undertaken  at  the  wrong  time  and  without  ad- 
vice, be  a  most  fruitful  cause  of  severe  nervous  prostration  instead  of 
a  remedy  as  was  hoped  for. 

Pathology  and  Pathogenesis.  As  long  ago-  as  1869  Beard 
stated  his  conviction  that  there  were  definite  structural  alterations  in 
the  nervous  system  in  neurasthenia  though  undetectable  with  our  pres- 
ent means  of  research.  To  call  the  trouble  a  functional  disturbance 
and  deny  all  possibility  of  change  in  the  functionating  structure  is  an 
illogical  contradiction. 

If  the  term  neurasthenia  is  to  include  all  forms  of  secondary  as 
well  as  primary  nervous  disturbance  we  will  have  to  admit  that  there 
is  more  or  less  truth  in  all  of  the  theories  of  the  disease  based  upon 
the  many  and  various  extraneural  pathological  findings.  The  etiolog- 
ical substrata  of  the  affection  will  in  many  cases  have  to  be  included 
in  its  catalogue  of  pathological  contents.  Some  consideration  will  have 
to  be  given  then  to  the  cellular  vibratory  theory  of  Beard,  the  spinal 
hyperaemia  and  anaemia  account  of  Hammond,  the  dyspeptic  malnu- 
trition of  Hayem  and  Winter,  the  faulty  cellular  metabolism  within 
the  sensory  tracts  of  Jewel,  the  vasomotor  irregularities  of  Dumas,  the 
gastrointestinal  disarrangements  of  Leven,  the  enteroptoses  of  Glenard. 
the  autointoxication  theory  of  Bouchard,  the  cerebrospinal  hypotonia 
of  Cheron,  and  the  altered  nutrition  in  nerve  elements  of  Erb  and 
others. 

None  of  these  theories  and  findings  are  universally  applicable  or 
sufficiently  constant  to  make  them  the  basis  of  a  true  pathology  or 
pathogenesis. 

In  simple  primary  neurasthenia  there  are  no  discoverable  perma- 
nent pathological  alterations  in  any  of  the  internal  organs  of  the  body. 
We  are  forced  to  conclude,  therefore,  that  the  entire  pathology  of  neu- 
rasthenia as  a  disease  is  to  be  found  in  the  molecular  and  chemical 
changes,  brought  about  by  various  causes,  within  the  nervous  elements, 
the  neurones  themselves. 

To  C.  F.  Hodge  is  due  much  credit  for  revealing  the  changes 
which  the  neurones  undergo  as  the  result  of  prolonged  exercise  and 
stimulation.    Basing  his  conclusions  upon  a  series  of  experiments  upon 


THE    NEURONIC    DISEASES  l6l 

the  lower  animals,  he  affirms  that  the  cell-nuclei  are  invariably  shrunk- 
en, displaced  within  the  cell  and  bounded  by  an  irregular,  jagged  edge. 
They  lose  their  open  and  reticulated  appearance  and  become  darker 
upon  staining.  There  was  observed  a  regular  quantitative  relation  be- 
tween the  strength  of  the  stimulus  and  the  amount  of  nuclear  shrink- 
age. The  nucleolus  in  some  instances  contamed  granules,  which 
moved  slowly  about  and  were  extruded  into  the  nucleus.  The  move- 
ments of  the  nucleoli  had  every  appearance  of  being  amoeboid.  After 
they  had  become  somewhat  broken  up  they  were  rapidly  dissolved. 
Under  the  same  conditions  the  size  of  the  entire  cell  was  diminished 
and  its  power  of  absorbing  stains  was  greatly  lessened.  Vacuolation 
appeared  within  the  cell  protoplasm,  a  proof  that  the  cell  substance 
was  used  up  in  the  action.  In  this  process  "the  cell  tires  rapidly  at 
first,  then  more  gradually  to  a  condition  of  fatigue.'"  Vas  observed 
that  mild  stimulation  caused  a  swelling  of  the  cell  body  while  the 
central  part  of  the  cell  was  rendered  more  or  less  clear  by  the  move- 
ment of  the  chromatin  bodies  toward  the  periphery.  Similar  observa- 
tions have  been  made  by  Mann  who  states  that  it  requires  prolonged 
and  adequate  rest  to  restore  these  exhausted  cells  back  to  their  original 
appearance. 

The  shrinking  of  the  cell  at  its  nucleus,  together  with  the  vacuo- 
lation of  its  substance,  may  be  made  to  take  place  also  by  the  injec- 
tion of  various  toxic  substances  into  the  blood,  as  has  been  done  with 
absinthe  in  guinea  pigs  (Starr).  Toxaemia  not  only  affects  the  cell 
body.  In  all  probability  the  earliest  changes  brought  about  in  this 
way  in  the  neurone  occur  in  the  delicate  protoplasmic  endings  (Thom- 
son). From  experiments  made  with  potassium  bromide  Wright  con- 
cludes that  the  inhibiting  power  of  this  medicament  upon  intellectual 
and  motor  processes  depends  upon  its  effects  upon  the  ends  of  the 
protoplasmic  processes,  while  the  cell  bodies  themselves  are  only  made 
to  suffer  after  prolonged  exposure  to  its  influence. 

If  the  blood  supply  to  the  nerve  cells  be  diminished  or  its  nutri- 
ent quality  be  impoverished,  changes  similar  to  those  just  described 
occur  with  singular  constancy  in  the  cells. 

It  is  a  fair  conclusion  that  the  same  causes,  overstimulation, 
toxcEmia  and  malnutrition  which  with  an  inherited  neuropathic  consti- 
tution we  see  play  so  important  a  part  in  the  etiology  of  neurasthenia, 
produce  the  same  or  similar  alterations  in  the  nerve  cells  of  the  victims 
of  this  latter  disease. 

Symptoms.  I  am  in  hearty  accord  with  Dana  when  he  says  that 
fifty  per  cent,  of  the  cases  of  neurasthenia  so-called,  may  be  classed 
under  other  heads  of  disease.    The  term^  is  much  abused. 

The  symptoms  of  neurasthenia  are  not  only  numerous  and  varied 
"but  they  never  group  themselves  exactly  in  the  same  way  in  all  pa- 
tients. This  is  not  to  be  wondered  at  when  it  is  remembered  that  the 
disease  is  one  involving  the  whole  nervous  organism  and  that  its  clin- 
ical presentation  is  modified  by  the  peculiar  constitution  and  tempera- 
ment of  the  victim.  In  spite  of  all  this,  however,  there  is  a  degree  of 
uniformity  in  the  clinical  picture  that  makes  it  worthy  of  a  special 
place  in  medical  nosology.     This  clinical  picture  is  sufficiently  distinct 


l62  TilE    NEURONIC    DISEASES 

even  to  render  possible  a  dilterential  diagnosis  of  neurasthenia  from 
the  many  other  troubles  which  it  often  resembles,  and  with  which  it 
is  frequently  associated,  though  at  times  it  is  extremely  difficult. 

In  a  general  way  it  may  in  the  first  place  be  stated  that  all  of  the 
symptoms  of  neurasthenia  reveal  and  depend  upon  a  condition  of  irri- 
table zveakncss.  Whether  in  the  mental  sphere  or  the  nervous,  whether 
in  the  field  of  sensation  or  motion,  whether  vasomotor,  secretory  or 
trophic,  the  symptoms  that  present  themselves  always  represent  ab- 
normal fatigue,  instability  from  Aveakness  and  diminished  power  of  re- 
sistance, and  an  utter  lack  of  sustaining  force. 

This  striking  characteristic  of  the  symptomatology  of  nervous  ex- 
haustion is  constant  and  uniform.  It  is  pathognomonic.  Analyze 
every  manifestation  of  neurasthenia  and  if  it  represents  a  fatigue 
svmptom  it  points  to  nervous  exhaustion  and  not  to  any  other  neuro- 
sis.    It  differentiates  this  disease. 

In  all  neurasthenics  certain  symptoms  appear  with  a  remarkable 
degree  of  persistency  when  one  remembers  the  generalized  and  ex- 
tensive character  of  the  trouble.  Among  these  may  be  mentioned  a 
peculiar  type  of  headache,  and  backache,  vertigo,  insomnia,  melan- 
cholia, depression  of  spirits,  bad  dreams,  cardiac  palpitation,  nervous 
dyspepsia  with  constipation  and  general  restlessness  and  fear  of  im- 
pending ruin.  I  will  now  discuss  these  and  some  other  indications  more 
in  detail. 

The  patient's  mental  sphere  is  always  invaded  by  the  disease  and 
hence  we  find  that  all  of  his  psychic  occurrences  are  depressed.  His 
memory  is  poor,  especially  for  names  and  the  more  recent  events.  His 
power  of  attention  and  concentration  are  annoyingly  diminished.  When 
reading  his  mind  wanders  off  upon  other  subjects  though  his  eyes 
may  go  on  taking  in  the  printed  words.  He  cannot  sustain,  as  he 
used  to  do,  a  continuous  line  of  argument.  His  thoughts  at  times  seem 
to  vanish  and  thus  for  a  moment  cause  him  to  lose  the  thread  of  his 
discourse.  His  wall  power  has  lost  its  old  vigor;  he  plans  this  and 
that  but  he  finds  it  hard  to  muster  the  energy  to  start  his  plans.  His 
imagination  is  irritable  and  active  in  depicting  disagreeable  and  hor- 
rible scenes.  His  dreams  are  all  of  an  unpleasant  and  depressing  char- 
acter. This  vicious  activity  of  his  imagination  is  often  the  cause  of 
the  partial  aboulia. 

The  patient  imagines  all  sorts  of  disasters  and  unfavorable  condi- 
tions that  may  arise  and  so  dreads  to  begin  any  undertaking.  His 
judgments  are  all  tinctured  with  this  gloomy,  negative  view  of  life. 
He  sees  everything,  as  it  were,  through  blue  glasses  and  therefore  all 
his  acts  and  thoughts  and  conversations  are  suggestive  of  gloom,  pes- 
simism and  depression.  His  whole  mind  is  in  a  state  of  psychic  pain, 
mild  psychalgia.  Often  the  melancholia  is  so  severe  that  insanity  is 
thought  of  by  the  patient,  his  family  and  family  physician.  Occasion- 
ally it  leads  to  suicide. 

These  cases  must  be  carefully  separated  from  dementia  precox, 
attacks  of  melancholia  or  manic  depressive  insanity,  and  such  phrenas- 
thenic  conditions  as  dipsomania,  hysteria,  obsessions  and  the  exhaustion 
psychoses. 


THE    NEURONIC    DISEASES  163 

Strange  to  say,  neurasthenics  with  all  their  melancholy  and  de- 
pression are  not  hopeless  of  getting  well  as  the  hypochondriacs  are.  I 
make  it  a  rule  to  question  all  of  them,  and  gloomy  as  they  may  say 
they  feel  at  times,  they  almost  invariably  declare  they  believe  they  will 
get  well  if  the  proper  line  of  treatm-ent  can  but  be  hit  upon.  I  almost 
regard  this  in  itself  as  a  valuable  sign  of  true  neurasthenia. 

The  feeling  of  dread  which  these  patients  have  is  usually  indefinite 
and  unaccountable.  Often,  however,  it  assumes  the  definite  form  of 
a  mild  phobia. 

The  phobias  of  neurasthenia  are  innumerable  so  that  only  a  few 
of  them  need  be  named  by  way  of  illustration.  Agoraphobia  (fear  of 
crossing  a  large  open  square),  potamophobia  (fear  of  crossing  a  run- 
ning stream),  claustrophobia  (fear  of  being  alone  in  a  narrow  place), 
astrophobia  (fear  of  storms),  pantophobia  (fear  of  everything)  are  a 
few  of  the  special  varieties.  It  is  unnecessary  to  dignify  these  phobias 
as  special  "fear  neuroses,"  as  Hecker,  Freud  and  some  others  have 
done,  for  they  do  not  occur  alone  or  without  some  other  neurasthenic 
symptom  being  present.  They  are  of  the  nature  of  an  obsession  or 
fixed  idea  which  is  not  an  uncommon  symptom  of  neurasthenia. 

I  had  a  neurasthenic  lad  under  my  care  who  saw  the  body  of  his 
drowned  brother  shortly  after  it  was  taken  out  of  the  water.  He  was 
so  much  the  victim  of  potamophobia  and  fear  that  he  would  himself 
drown  some  day  that  he  never  could  be  induced  to  cross  over  water. 
When  inveigled  into  approaching  a  bridge  he  would  suddenly  turn  and 
run  to  his  room,  lock  himself  in  and  suffer  from  severe  trembling  and 
fright.  He  recovered  in  about  a  year,  the  phobia  and  obsession  dying 
out  as  his  other  neurasthenic  symptoms  disappeared. 

A  young  clerg3'man  under  my  care  was  harassed  with  the  fixed 
notion  that  he  w_as  offensive  and  ridiculous  in  the  eyes  of  every  human 
being  he  met,  though  as  a  matter  of  fact  he  was  most  agreeable  and 
much  sought  after. 

These  patients  are  all  mentally  irritable.  They  are  oversensitive 
and  easily  offended ;  hence  they  appear  egotistical  at  times  and  lead 
a  more  or  less  solitary  life.  Their  lack  of  sustaining  power  makes 
them  often  appear  changeable,  frivolous,  weak  and  inconsistent. 

Nearly  every  neurasthenic  complains  sometime  of  vertigo.  This 
is  not  a  continuous  symptom,  nor  is  it  very  severe.  It  is  usually  of 
the  objective  type.  The  patient  feels  as  if  he  were  stationary,  while 
objects  are  whirling  about  him.  Occasionally  in  severe  cases  it  is  sub- 
jective, the  patient  feeling  as  if  he  himself  were  the  spinnmg  object.  It 
is  provoked  generally  by  sudden  and  unexpected  movements.  Often 
the  floor  seems  as  if  it  were  rising  up.  It  is  not  accompanied  by  vomit- 
ing often,  though  it  is  associated  not  infrequently  with  a  feeling  of 
nausea.  It  never  occurs  at  night  nor  when  the  patient  is  lying  down. 
It  is  experienced  in  the  morning  soon  after  rising.  It  is  felt  when 
the  patient  ascends  high  places,  stands  upon  the  edge  of  a  precipice  or 
looks  at  rapidly  moving  objects,  such  as  a  passing  train.  Under  these 
conditions  it  sometimes  takes  the  form  of  an  impulsive  desire  tO'  jump 
from  a  high  place,  to  rush  in  front  of  the  train  or  attempt  a  sort  of 
bird-like  flisrht. 


164  THE    NEURONIC    DISEASES 

These  vertiginous  impulses  are  occasionally  very  distressing  and  T 
have  known  people  to  be  in  constant  dread  from  them  of  committing 
suicide.  It  is  not  at  all  improbable  that  some  cases  of  unexplainable 
self-destruction  by  leaping  from  high  places  and  plunging  into  deep 
cataracts  may  have  been  vertiginous  attacks  of  this  sort. 

Insomnia  is  a  remarkably  constant  symptom  of  neurasthenia.  The 
patient  undoubtedly  loses  a  great  deal  of  sleep,  but  not  as  a  rule  so 
much  as  he  imagines  he  loses.  Tlie  sleep,  such  as  it  is,  is  broken  and 
fitful  and  more  or  less  disturbed  with  troubled  dreams.  Sleep  during 
the  day  is  almost  impossible,,  even  when  the  conditions  are  made  par- 
ticularly inviting.  The  early  part  of  the  night  may  be  occupied  with 
sleep,  but  about  two  or  three  o'clock  in  the  morning  the  patient  awakens 
and  thereafter  remains  awake  until  the  next  night.  More  rarely  the 
patient  passes  the  night  in  short,  cat-like  naps.  Such  sleep  does  not 
bring  refreshment  and  as  a  consequence  neurasthenics  always  feel 
tired  and  reluctant  to  get  up  when  morning  arrives. 

Among  the  subjective  symptoms  the  sensory  phenomena,  both 
general  and  special,  hold  an  important  place.  As  aids  to  neurological 
diagnosis  all  subjective  symptoms,  and  especially  the  sensations,  must 
be  studied  with  great  care.  The  value  of  the  patient's  statements  in 
regard  to  himself  must  be  weighed  with  caution.  Xevertheless,  so 
constant  and  so  uniformly  similar  are  some  of  these  symptoms  that  we 
cannot  but  help  accepting  them  as  distinct  a,nd  valuable  signs  of  the 
disease. 

The  sensations  of  neurasthenia  are  generally  of  the  nature  of 
pafsesthesia,  very  rarely  hypersesthesia  or  hyperalgesia,  and  most  rarely 
anaesthesia  or  analgesia. 

Nearly  every  neurasthenic  complains  of  some  form  of  pain. 
Headache  is  the  most  frequent.  Even  the  headache  is  not  a  well-defined 
pain,  but  rather  a  form  of  cephalic  pargssthesia.  The  patient  complains 
of  the  head  feeling  loaded  and  full ;  or  it  is  compressed  as  in  a  vise ; 
or  it  seems  as  if  it  were  covered  w"ith  a  heavy,  leaden,  tight-fitting  skull- 
cap. One  patient  described  it  as  though  there  were  a  thousand  strings 
attached  to  her  brain  and  some  one  were  steadily  pulling  upon  them  all 
at  the  same  time.  Another  corrected  me  every  time  I  used  the  word 
headache,  for  she  wanted  me  to  distinctly  understand  that  this  distress 
was  nothing  at  all  like  the  distmct  and  painful  headaches  which  she 
frequently  suffered  from. 

These  neurasthenic  headaches  vary  in  severity,  though  they  are 
always  more  or  less  present.  A  close  observation  of  them  reveals  the 
fact  that  they  exacerbate  almost  always  after  some  unusual  or  pro- 
longed exertion.  Therefore  they  usually  appear  shortly  after  the  pa- 
tient rises  in  the  morning.  As  the  stimulation  and  distraction  of  the 
dav's  duties  proceed  they  seem  to  partly  die  out,  or  at  least  are  not  so 
noticeable.  But  in  the  latter  part  of  the  afternoon,  when  more  or  less 
phvsical  and  mental  exhaustion  begins  to  come  on  the  headache  re- 
turns with  greater  intensity  even  than  it  had  in  the  early  forenoon. 

No  other  form  of  organic  or  non-organic  cephalalgia  occurs  in  ex- 
actly this  way  or  possesses  exactly  these  characteristics ;  hence  the 
headache  of  neurasthenia  is  a  valuable  s3"mptomx  of  the  disease. 


THE    NEURONIC    DISEASES  165 

Backache  is  another  very  constant  sensory  symptom.  It  also  is 
fairly  characteristic,  at  least  enough  so  to  aid  materially  in  making  a 
differential  diagnosis  from  other  affections  in  which  dorsal  pains  are 
present.  The  entire  spine  of  the  neurasthenic  feels  sore  and  tender, 
not  more  so  in  one  part  than  in  another.  Pressure  and  percussion  do 
not  specially  provoke  tender  spots  nor  does  the  passage  along-  the  spine 
of  a  hot  sponge  or  a  piece  of  ice.  The  pain  seems  to  be  eminently 
subjective,  being  more  like  a  feeling  of  heaviness,  burning,  chilliness 
or  aching ;  it  is  of  the  nature  of  paresthesia  rather  than  a  hyperalgesia. 

Some  patients  complain  of  a  numbness  or  stiff  feeling  in  the  spine 
and  its  related  muscles.  They  attribute  this  feeling  often  to  cold, 
rheumatism,  or  lumbago.  It  is  usually  relieved  by  the  recumbent 
posture. 

The  nerves  of  common  sensation  are  implicated  in  nervous  ex- 
haustion. The  patient  complains  of  ill-defined  feelings  of  distress  all 
over  the  body  and  in  the  viscera;  of  pressure,  of  flashes  of  cold  and 
heat;  of  ill-defined,  fugitive  pains  here  and  there.  The  very  indefi- 
niteness  and  indescribable  character  of  these  sensations,  their  varia- 
bility in  intensity  and  their  dependence  upon  the  patient's  feelings  and 
his  condition  of  weariness  are  their  characteristic  attributes. 

There  are  such  pains  about  the  heart,  leading  to  a  fear  of  organic 
heart  disease.  This  fear,  with  the  neurasthenic  trait  of  introspection, 
superinduces  palpitation. 

Pains  in  and  about  the  stomach  are  frequently  referred  to.  As 
they  are  not  influenced  especially  by  the  ingestion  of  food  or  associated 
with  nausea  and  vomiting  and  other  signs  of  organic  gastric  trouble, 
but  are  accompanied  by  nervous  dyspepsia  and  troublesome  eructations 
and  feelings  of  distension,  their  nature  is  easily  determined. 

The  cutaneous  as  well  as  the  visceral  paresthesia:  are  sometimes 
very  curious.  Formication  is  common.  It  seems  as  if  ants  or  worms 
were  crawling  under  the  skin.  Pinchings  here  and  there  and  flea-bites 
are  imagined  and  give  much  annoyance.  More  frequently  there  is  a 
feeling  of  coldness  in  the  hands  and  feet,  which  the  patient  invariably 
attributes  to  poor  circulation.  Sometimes  this  peripheral  coldness  sud- 
denly alternates  with  a  sense  of  heat  as  if  hot  irons  were  touching  the 
skin. 

Among  the  visceral  parassthesise  are  such  feelings  as  rectal  con- 
striction and  paralysis.  I  have  seen  some  ludicrous  cases  of  this. 
Pruritus  ani  is  in  most  cases  a  cutaneous  parajsthesia  of  neurasthenic 
origin. 

*  The  bladder  may  seem  to  be  overdistended,  obliging  the  patient  to 
get  up  unnecessarily  often  to  empty  it  at  night. 

These  visceral  parsesthesise,  when  associated  with  morbid  fear, 
sometimes  give  rise  to  most  amusing  situations  and  lead  the  neuras- 
thenic in  his  ignorance  to  suggest  very  humorous  anatomical  and 
physiological  explanations. 

One  told  me  once  she  knew  she  was  losing  her  mind  because  she 
could  actually  feel  her  brain  slowly  but  steadily  softening. 

Patients  have  insisted  that  they  had  a  tape-worm,  that  their  lungs 


l66  THE    NEURONIC    DISEASES 

were  entirely  rotted  away,  that  their  wombs  were  misplaced  or  their 
testicles  were  shrunken. 

Such  patients  go  the  rounds  of  the  physicians'  offices  and  too  often, 
alas !  find  men  who  treat  them  for  this  or  that  local  ailment  so  long 
as  their  money  holds  out. 

Cutaneous  and  visceral  hypercesthesia  is  not  infrequently  met  with. 
Simple  increase  of  sensitiveness,  without  special  perversion,  may  be 
neurasthenic  in  origin;  it  is  frequently,  however,  a  sign  of  organic 
disease.  Care  must  be  exercised  when  making  a  differential  diagnosis 
in  the  study  of  sensations  that  show  a  simple  increase. 

In  neurasthenia  hyperaisthesia  is  revealed  by  the  patient's  abnormal 
sensitiveness  to  cold  and  heat,  the  distress  caused  by  the  pressure  of  his 
clothing.  The  ill-defined  internal  sensations  associated  with  the  viscera 
are*undoubtedly  due  sometimes  to  hypergesthesia. 

It  is  a  very  rare  thing  for  the  victims  of  true  neurasthenia  to  com- 
plain of  hypercEsthesia  or  ancesthesia;  such  sensory  feelings  belong 
more  to  hvsteria  and  organic  diseases.  As  hysteria  and  neurasthenia 
are  so  often  combined  in  the  same  individual,  the  anaesthesia  is  more 
apt  to  be  a  symptom  of  the  former.  Nevertheless  I  have  seen  cases  of 
pure  neurasthenia  of  a  profound  type  in  which  objective  signs  of  a 
localized  hypaesthesia  (never  anaesthesia)  were  complained  oi.  In 
these  cases  examination  with  the  faradic  brush  seemed  to  show  that 
there  was  not  a  real  loss  of  sense,  at  least  to  any  marked  degree. 

The  symptoms  dependent  upon  involvement  of  the  special  senses 
are  among  the  most  important  in  neurasthenia  because  they  are  so 
uniformly  present.  Tinnitus  auriuni,  ringing,  bussing,  whistling 
sounds  in  one  or  both  ears  are  very  common.  Frequently  the  left  ear 
is  the  seat  of  the  trouble  and  at  times  it  is  so  annoying  that  the  patient 
declares  it  will  set  her  crazy.  In  spite  of  removal  of  cerumen  and  local 
treatment  for  chronic  otitis,  which  these  patients  so  often  insist  upon, 
the  annoyance  continues.  Aural  hypersensitiveness,  on  account  of 
which  the  patient  starts  at  every  little  noise,  is  rather  a  psychic  trouble 
than  an  auditory  nerve  weakness. 

Visual  disturbances  are  represented  by  spots  flying  before  the 
eyes,  so-called  musccB  volitantes,  by  szvimming  and  vibrating  and  bhcr- 
ring  of  the  printed  page  during  reading.  The  eyes  tire  easily  and 
water  freely.  Before  a  glare  of  bright  light  they  may  even  pain  sharp- 
ly. Vision  itself  may  remain  normal ;  in  fact,  it  may  even  be  ex- 
ceptionally keen. 

Taste  and  smell  are  rarely  if  ever  affected.  I  have  seen  a  hyper- 
sensitiveness of  these  senses  which  was  probably  a  mental  or  ps3^hic 
symptom. 

The  motor  symptoms  of  neurasthenia  are  of  minor  importance  as 
compared  with  the  mental  and  sensory  symptoms,  but  they  are  of 
value  on  account  of  their  objective  character.  They  include  chiefly 
weakness,  tremor,  rapid  exhaustion  and  fatigue.  The  patient  never 
puts  forth  his  entire  strength  when  he  attempts  to  perform  a  muscular 
movement.  He  shows  a  marked  disinclination  and  thus  in  part  reveals 
the  psychic  nature  of  his  trouble.  Sometimes,  on  the  other  hand,  he 
exerts  considerable  force,  but  it  soon  relaxes. 


THE    NEURONIC    DISEASES  167 

This  weakness  of  muscular  action  in  neurasthenia  never  advances 
to  the  point  of  actual  paralysis.  In  fact,  it  bears  no  similarity  to  or- 
ganic paresis.  It  is  generalized  throughout  the  entire  muscular  ap- 
paratus and  is  unaccompanied  by  atrophy  or  electrical  reactions. 

Muscular  overaction  or  true  spasm  never  occurs  in  neurasthenia 
in  the  common  acceptation  of  the  term.  The  tremors  and  tvvitchings 
are  not  so  much  of  the  nature  of  spasms  as  they  are  of  perversion  and 
irritability  of  normal  muscular  contraction.  Blepharospasm,  or  twitch- 
ing in  the  outer  corners  of  the  eyelids,  is  common.  It  is  in  part  a 
sensory  disturbance  and  m  part  a  fine  iibrillary  tremor,  myokymia. 

Tremor  is  a  frequent  symptom  and  usually  consists  of  rapid  vibra- 
tory movements  of  narrow  excursion.  Mental  excitement  and  active 
movements  in  general  are  accompanied  by  this  tremor.  The  patient 
says  his  hands  shake  when  he  writes,  his  head  trembles,  or  his  lips 
or  his  knees,  when  he  becomes  unusually  excited.  Fibrillary  tremor 
in  the  muscles  of  the  leg  is  often  a  most  distressing  symptom.  It  may 
attack  any  of  the  muscles  of  the  body.  Many  people  have  cramps  in 
the  calves  of  their  legs,  especially  when  they  are  suffering  from  night- 
mare, but  such  cramps  are  not  specially  indicative  of  neurasthenia. 

Closely  related  to  the  sensory  and  motor  symptoms  is  the  state  of 
the  reflexes.  As  a  rule  the  deep  reflexes  are  exaggerated,  both  those 
of  the  leg  and  those  of  the  arm.  A  foot  clonus  is  sometimes  elicited. 
Oppenheim  declares  that  all  other  signs  of  muscular  rigidity  are  absent, 
notwithstanding  the  statements  of  Binswanger  and  others.  The 
myotatic  irritability  as  well  as  the  nerve  excitability  are  both  increased. 
In  the  severest  forms  of  emaciation  the  knee-jerks  may  be  diminished. 
Though  largely  true,  it  is  not  absolutely  so,  as  Oppenheim  asserts  that 
the  absence  of  the  knee-jerks  means  always  and  only  a  symptom  of 
organic  disease.  I  know  a  woman,  perfectly  healthy  in  every  respect 
except  for  a  slight  nervous  dyspepsia,  in  whom  the  patella  tendon  re- 
flexes are  completely  absent. 

The  pupillary  reflexes  are  somewhat  exaggerated,  though  the  con- 
dition of  the  pupils  is  generally  normal. 

The  irritable  weakness  of  neurasthenia  is  revealed  symptomatically 
in  the  vasomotor,  secretory  and  trophic  mechanisms,  also.  Flushing 
and  a  rush  of  blood  to  the  head  are  spoken  of  by  nearly  all  patients. 
This  is  often  associated  with  the  vertiginous  feeling  of  faintness  and 
cardiac  palpitation.  The  condition  is  observable  objectively,  for  the 
skin  is  suffused  with  a  general  redness  and  its  temperature  is  slightly 
elevated. 

Under  the  name  of  erythrophobia  has  been  described  a  most  stub- 
born and  troublesome  form  of  morbid  fear  of  blushing. 

As  Hartenberg  has  pointed  out,  the  blushing  disease,  erythropathy, 
should  be  distinguished  from  the  vicious  neurotic  circle  set  up  by  the 
fear  of  blushing,  or  erythrophobia.  Shyness  or  shame,  not  related  to 
fear,  causes  the  flushing.  This  is  a  well-defined  and  frequent  phenome- 
non. When  fear  is  added  to  it,  the  two  emotions  influence  and  react 
upon  each  other.  Blushing  creates  the  fear  of  blushing  and  the  fear 
creates  the  blushing.    The  latter  becomes  a  veritable  obsession. 

The   vasomotor  disturbance  mav   even   be   so   great  as   to   cause 


l68  THE    NEURONIC    DISEASES 

wheals,  as  in  urticaria  factitia.  I  had  a  highly  emotional  young  man,  a 
professional  musician  with  a  high  order  of  poetic  temperament,  once 
under  my  care,  who  almost  nightly,  as  soon  as  the  irritation  and  warmth 
of  the  bedclothes  encompassed  him,  suffered  from  a  form  of  neuras- 
thenic hives.  Redness,  local  oedema  and  itching  were  marked.  /\t  first 
I  thought  it  was  a  case  of  angioneurotic  oedema.  He  fully  recovered 
under  the  treatment  for  neurasthenia  after  a  number  of  months. 

Certain  special  functions  are  so  frequently  affected  in  neurasthenia 
that  they  have  come  to  occupy  a  place  of  considerable  prominence  in 
its  symptomatology.  I  refer  especially  to  the  alimentary,  circulatory 
and  sexual  functions.  These  troubles  are  largely  subjective  in  char- 
acter and  yet  are  not  without  certain  objective  features. 

Nervous  dyspepsia  in  the  broad  sense  of  the  term  is  practically 
always  present.  The  patient  complains  of  not  being  able  to  digest  his 
food.  It  often  seems  to  lie  in  his  stomach  like  a  heavy  weight.  His 
appetite  is  capricious;  usually  it  borders  well  upon  anorexia  or  the 
entire  want  of  appetite.  The  taste  for  certain  articles  of  food  may  be 
changed.  There  is  a  craving  for  stimulants,  like  tea,  coft'ee  and  alcohol. 
Shortly  after  taking  the  food  there  is  a  feeling  of  distension  and  fre- 
quently an  annoying  eructation  of  gas.  Pyrosis  or  heartburn  with  water 
brash  then  follows.  Finally  this  passes  into  a  feeling  of  rawness  and 
irritation  in  the  stomach,  with  which  is  associated  the  old  gnawing, 
empty  feeling  so  unlike  normal  hunger.  Nausea  is  not  common  and 
vomiting  still  less  so.  Persistent  thirst  and  dryness  of  the  mouth  are 
common,  especially  at  times  of  special  nervous  excitement.  It  is 
strange  that  there  is  not  more  deterioration  of  the  physical  health  with 
all  these  gastric  troubles !  To  be  sure,  the  patients  do  lose  flesh  from 
a  failure  to  eat,  but  the  anorexia  is  the  result  of  the  dread  of  these 
vague  sensations  of  gastric  distress  coming  on,  and  even  in  the  severest 
cases,  wherein  there  may  be  vomiting,  suffocation,  cardiac  palpitation 
and  meteorism,  it  is  out  of  all  proportion  to  the  actual  loss  in  the 
physical  condition.  The  shgbtly  coated  tongue,  the  eructations  and  the 
frequent  hyperacidity  add  objective  confirmation  to  the  patient's  un- 
doubted distress. 

Constipation  is  almost  universal,  depending  upon  peristaltic  torpor 
and  muscular  atony. 

Borbarygmi  and  rumbling  in  the  bowels  are  frequent. 

Occasionally  there  may  be  attacks  of  temporary  diarrhoea  and  in 
some  cases  there  is  a  constant  tendency  to  diarrhoea,  which  must  be 
guarded  against  by  the  avoidance  of  every  sort  of  emotional  excite- 
ment.    Scybalous  fecal  and  mucous  masses  appear  in  the  stools. 

In  very  rare  cases  these  symptoms  lead  to  a  high  degree  of  ema- 
ciation. This  emaciation  with  pallor  and  loss  of  strength  can  be  initiat- 
ed by  the  nervous  dyspepsia  and  continued  insomnia.  Nevertheless  it 
is  a  fact  that  a  large  number  of  neurasthenics  do  not  suffer  from  bad 
general  nutrition.  Some  of  the  greatest  sufferers  I  have  seen  have 
been  people  who  were  outwardly  the  very  picture  of  health. 

Palpitation  of  the  heart  is  a  symptom  very  commonly  complained 
of.  To  a  certain  extent  it  is  subjective  in  character  and  is  associated 
with  feelings  of  suffocation  and  precordial  pain  which  may  shoot  down 


THE    NEURONIC    DISEASES  169 

the  arm.  I  have  noticed  that  a  fear  of  organic  heart  disease  has  often 
been  the  only  thing  that  sent  these  patients  forth  for  medical  advice. 
The  so-called  "tobacco  heart"'  is  a  good  example  of  a  neurasthenic  heart 
It  is  subject  to  tachycardia,  every  wave  of  psychic  activity  causing  it  to 
vary  in  its  rhythm,  Intennittency  of  the  beat  is  not  uncommon. 
Allorhythmia  and  arrhythmia  and  even  bradycardia  have  all  been  at- 
tributed to  neurasthenia.  Anaemic  and  systolic  murmurs  may  be  heard, 
but  they  are  not  sufficiently  common  to  make  them  very  valuable  as 
signs.  Vascular  murmurs  are  spoken  of.  It  is  claimed  by  Gerhardt 
that  more  than  one-half  of  those  who  had  consulted  him  for  palpitation 
of  the  heart  had  some  functional  disorder  of  this  organ  and  not  valvular 
disease. 

As  a  result  of  all  these  cardiac  manifestations  a  special  form  of 
neurasthenia---neurasthenia  cordis — has  been,  somewhat  arbitrarily, 
established. 

Attempts  have  been  made  to  locate  the  trouble  in  the  sympathetic 
nerve  or  in  the  vagus,  but  without  any  very  satisfactory  results.  For 
the  present  the  irritable  and  weakened  ner\^ous  apparatus  is  enough 
to  account  for  the  irregularity  of  action  in  an  organ  so  directly  under 
the  influence  of  the  nervous  apparatus  as  the  heart  is. 

In  the  sexual  sphere  neurasthenia  reveals  itself  in  various  ways. 
In  regard  to  some  of  these  manifestations  it  is  a  difficult  matter  to 
determine  always  the  proper  relationship  as  to  cause  and  effect.  There 
is  no  good  reason  for  segregating  the  sexual  symptoms  into  a  special 
form  of  disease  and  calling  it  sexual  neurasthenia.  The  other  mani- 
festations of  the  defective  nervous  system  may  be  less  noticeable  on  ac- 
count of  the  prominence  of  the  sexual  aberrations,  but  they  will  always 
be  found  if  carefully  sought  for.  In  congenital  neurasthenia  there  are 
weaknesses  and  perversions  in  the  sexual  sphere  that. show  themselves 
early  and  are  difficult  to  overcome.  Masturbation  is  sometimes  an  early 
evidence  of  the  nervous  instability  and  irritability  in  both  the  mental 
and  physical  constitution  of  the  congenital  neurasthenic.  Indeed  Op- 
penheim  makes  the  assertion,  and  I  am  inclined  to  agree  with  him, 
that  the  tendency  to  masturbate  can  be  inherited.  The  habit  once 
established,  and  ever  increased  as  it  always  is,  puts  a  strain  upon  the 
nervous  mechanism  and  reacts  upon  the  patient's  mind  through  fear, 
shame  and  other  depressing  mental  processes  in  such  a  way  that  the 
neurasthenia  out  of  which  the  habit  originally  grew  is  all  the  more 
developed.  Thus  the  vicious  circle  is  agam  established,  just  as  it  is 
in  the  gastric  and  other  special  troubles. 

Sometimies  these  congenital  neurasthenics,  whether  addicted  to 
the  habit  of  masturbation  or  not,  are  chagrined  to  find  themselves  im- 
potent. Usually  this  is  psychic  in  origin  and  is  due  to  local  irritability. 
Such  individuals  find  that  they  have  their  erections,  emissions,  nocturnal 
pollutions  and  even  the  orgasm,  all  more  or  less  associated  with  what 
seems  to  be  a  normal  sexual  desire,  but  under  peculiar  and  abnormal 
conditions,  such  as  when  out  in  society  or  under  the  strain  of  prolonged 
work,  or  of  intense  emotion.  When  they  attempt  to  cohabit  normally 
the  erection  fails  to  take  place,  or  it  is  too  brief,  or  ejaculation  with 
relaxation    occurs   before   penetration.      If   the   intercourse   is    accom- 


I70  THE    NEURONIC    DISEASES 

plished  there  is  such  a  sudden  and  complete  reversal  of  the  feelings 
from  pleasure  to  disgust  that  the  act  becomes  one  to  be  avoided  rather 
than  indulged  in.  All  of  this  still  more  depresses  the  patient  and  in- 
creases his  nervous  weakness  and  irritability. 

Many  of  the  cases  of  sexual  perversion  are  probably  congenital 
neurasthenics.-  Sadism,  Masochism,  fetichism,  pederasty  and  all 
forms  of  abnormal  modes  of  cohabitation  may  in  some  instances  be  due 
to  the  neurasthenic  congenital  twist  of  the  mind ;  in  other  words,  the 
result  of  a  distinct  psychosis :  or  they  may  be  due  to  the  efiforts  of  a 
congenital  neurasthenic  to  gratify  his  passion  in  some  way,  since  he 
is  deprived,  by  reason  of  his  abnormal  irritability,  of  gratifying  it  in 
the  normal  way.  These  abnormal  excitations  all  increase  the  original 
trouble  and  the  patient  becomes  still  more  neurasthenic. 

Spermatorrhoea,  prostatorrhoea  and  all  forms  of  seminal  emission 
may  be  the  result  of  a  congenital  or  acquired  neurasthenic  weakness. 
Many  patients  have  such  discharges  every  time  they  defecate.  Often 
the  urine  contains  some  spermatozoids.  All  of  this  worries  and  cha- 
grins and  acts  as  the  real  depressing  agent  and  causes  the  nervous  ex- 
haustion more  than  does  the  physical  effect  of  the  seminal  loss.  Fiir- 
bringer  speaks  of  an  onanistic  neurosis  and  Kraift-Ebing  makes  the 
attempt  of  dividing  sexual  neurasthenia  into  the  three  stages,  a  genital 
local  neurosis,  a  lumbar  or  spinal  neurosis  and  a  general  cerebro- 
spinal neurasthenia.  This,  it  seems  to  me,  is  an  unwarranted  and  con- 
fusing refinement  of  classification.  The  sexual  phenomena  are  but 
one  phase  of  a  general  cerebrospinal  neurasthenia.  The  prominence  of 
the  sexual  manifestations  is  due  to  many  factors,  such  as  the  con- 
genital or  acquired  nature  of  the  neurasthenia,  the  mental  characteris- 
tics of  the  patient,  the  particular  conditions  and  environment  in  which 
he  lives.  The  sexual  symptoms  are  distinctly  psychoneurotic  in  origin 
and  are  dependent  upon  both  general  and  local  influences.  They  are 
always  in  part  both  symptomatic  and.  causative  of  neurasthenia  and 
therefore  enter  into  the  constitution  of  a  vicious  circle.  The  recogni- 
tion of  this  fact  has  an  important  bearing  upon  the  treatment  of  the 
cases  in  which  the  sexual  features  seem  to  be  so  prominent. 

The  condition  of  the  urine  in  neurasthenia  is  not  pathog-nomonic. 
As  a  rule  it  is  more  or  less  condensed  and  reveals  variable  evidences  of 
a  defective  metabolism.  The  daily  amount,  as  well  as  the  specific 
gravity,  is  apt  to  be  somewhat  below  normal.  An  excess  of  phosphoric 
and  oxalic  acid  is  frequent,  but  not  characteristic,  as  is  too  often  as- 
sumed. Indican  in  pathological  quantity  occasionally  occurs  and  the 
relation  of  uric  acid  to  the  urea  varies  from  i  to  40,  or  i  to  30,  instead 
of  from  I  to  45,  or  I  to  60,  as  in  normal  urine.  A  transitory  glycosuria 
is  occasionally  met  with.  Less  frequently  a  temporary  albuminuria 
without  casts  or  other  signs  of  renal  disease  is  seen. 

There  is  no  alteration  of  temperature  in  neurasthenia,  though  of 
course  vasomotor  disturbances  may  modify  the  local  heat. 

Hyperidrosis  is  common  enough  to  make  it  a  valuable  symptom 
when  taken  in  conjunction  with  others.  Sometimes,  however,  the  skin 
is  dry. 

Alopecia  and,  according  to  Beard,  a  tendency  to  an  early  decay 


THE    NEURONIC    DISEASES  171 

of  the  teeth  are  to  be  noted  among  the  trophic  general  disturbances. 
I  have  seen  oedema  as  a  hystero-neurasthenic  symptom 

In  spite  of  the  frequent  anzemia  and  loss  of  weight  in  many  neuras- 
thenics, their  blood  is  not  found  to  be  markedly  abnormal.  The  cor- 
puscular richness  may  be  up  to  the  normal  and,  according  to  Hosslin, 
ihere  is  a  healthy  amount  of  hjemoglobin. 

A  thoughtful  consideration  of  the  entire  symptomatology  of  neu- 
rasthenia, I  think,  will  convince  any  one  that  it  is  a  disease  of  the  whole 
nervous  apparatus.  Confusion  in  the  mind  of  the  practitioner  may 
result  from  the  fact  that  all  of  the  symptoms  do  not  stand  out  with 
«qual  prominence  in  every  case.  In  fact,  each  neurasthenic  is  a  law 
unto  himself  in  regard  to  the  outward  expression  of  his  nervous  ex- 
haustion. If  his  inclinations  and  previous  mode  of  life  have  been 
intellectual  his  psychic  symptoms  will  be  the  more  obtrusive ;  if  he  has 
l>een  a  mere  physical  laborer  his  symptoms  of  physical  weakness  will 
he  the  more  prominent :  if  his  environment  and  education  have  been 
immoral  his  sexual  and  other  moral  delinquencies  will  give  the  prevail- 
ing tone  to  the  picture.  In  all  of  the  cases,  however,  other  manifesta- 
tions will  be  discovered  upon  careful  examination  and  thus  show  that 
the  predominant  symptoms  are  but  a  part  of  a  general  symptom-group. 

It  is  this  symptom.-group  that  we  must  always  search  for,  because 
it  possesses  certain  more  or  less  uniform  and  persistent  characteristics 
that  justify  the  establishment  of  neurasthenia  as  a  specific  entity.  The 
subjective  characteristics  of  this  symptom-group  are  the  more  con- 
stant and  regular  ones  and  include  the  insomnia,  bad  dreams,  melan- 
■cholia,  vertigo,  headache  and  other  pains,  pargesthesise,  gastric,  cardiac 
and  sexual  symptoms,  general  weakness  and  irritability. 

The  objective  traits  of  the  group  are  second  only  to  the  subjective 
in  prominence  and  constancy.  They  are  sometimes  coequal  to  them 
in  value  as  additional  signs  whereon  to  base  a  diagnosis.  They  include 
increase  of  tendon  reflexes,  cardiac,  vasomotor  and  secretory  disturb- 
ances, tremor,  increase  of  muscle  and  nerve  excitability  and  the  general 
history  of  mental  and  physical  irritability. 

Diagnosis. — The  diagnosis  of  neurasthenia  is  usually  easy;  at 
times  it  is  extremely  difficult.  It  is  the  safest  plan  to  always  diagnose 
it  by  exclusion,  because  it  so  often  simulates  other  affections  and  not 
infrequently  is  a  part  of  the  clinical  manifestation  of  distinct  organic 
-disease.  For  example,  the  cardiac  symptoms  at  times  resemble  those 
of  various  heart  diseases ;  and  again  in  the  earliest  appearances  of  syph- 
ilis of  the  central  nervous  system  the  clinical  picture  is  very  frequently 
that  of  simple  neurasthenia. 

Much  assistance  is  afforded  the  diagnostician  when  endeavoring  to 
■determine  whether  a  symptom  is  neurasthenic  or  not  by  remembering 
that  a  neurasthenic  symptom  is  always  the  expression  of  an  irritable 
weakness ;  is  one  of  a  number  of  similar  symptoms ;  is  variable  and 
changeable  both  as  to  location  and  time  of  appearance;  and  is  a  per- 
■version  of  the  normal  function  rather  than  a  mere  increase  or  diminu- 
tion of  it.  For  example,  in  neurasthenia  the  sensory  phenomena  run 
more  to  bizarre  and  variable  parsesthesise  rather  than  to  actual  anaesthe- 
sia or  hypersesthesia;    psychic   and  cerebral  disturbances   assume  the 


172  THE    NEURONIC    DISEASES 

character  of  melancholy  rather  than  true  melancholia,  of  vertigo  of 
psychic  origin  rather  than  true  organic  cerebellar  vertigo  or  ataxia; 
the  motor  weaknesses  are  the  result  of  volitional  inertia  or  absence 
of  psychic  initiative  rather  than  the  expression  of  a  true  neuromuscular 
paralysis,  paresis  or  spasm. 

Neurasthenia  should  never  be  diagnosed  upon  too  small  a  number 
of  symptoms  or  upon  a  set  of  symptoms  lunited  to  one  sphere  of 
physiological  activit}-.  It  may  be  convenient  at  times  to  speak  of  gas- 
tric, sexual,  cerebral,  spinal  and  other  forms  of  neurasthenia  in  which 
certain  symptoms  stand  forth  with  special  prominence,  but  it  is  highly 
injudicious  and  unsafe  to  diagnose  neurasthenia  from  such  prominent 
symptoms  alone. 

The  disease  is  one  of  the  entire  nervous  apparatus  and  the  tont- 
enseinblc  of  its  symptomatology  must  be  more  or  less  discovered  before 
a  clear  and  decisive  opinion  can  be  formed.  The  same  may  be  said  of 
the  diagnosis  of  those  arbitrarily  classified  forms  of  neurasthenia  some- 
times spoken  of  as  primary  neurasthenia,  hystero-neurasthenia,  cli- 
macteric neurasthenia,  traumatic  neurasthenia,  anxiety  neurosis,  an- 
giopathic  neurasthenia,  neurasthenia  gravis. 

Some  further  points  in  regard  to  the  diagnosis  of  neurasthenia, 
itself  will  be  brought  out  in  the  discussion  of  its  differential  diagnosis- 

The  disease  with  which  nervous  exhaustion  is  perhaps  most  fre- 
quently confounded,  because  some  of  the  symptoms  appear  so  nearly^ 
alike  in  both,  and  because  they  both  frequently  exist  in  the  same  patient 
at  the  same  time,  is  hysteria.  Neurasthenics  sometimes  develop  hys- 
teria, and  hysterics  are  nearly  always  more  or  less  neurasthenic.  Never- 
theless, when  both  aft'ections  are  present  at  the  same  time  it  is  possible 
often  to  clearly  determine  which  of  the  symptoms  are  due  to  the  neu- 
rasthenia and  which  to  the  hysteria. 

The  etiology  of  the  two  diseases  has  so  much  in  common,  as  for 
example  heredity,  environment  and  education,  it  is  not  to  be  wondered 
at  that  a  certain  resenlblance  should  obtain  betw^een  the  two  sets  of 
symptoms.  On  the  other  hand,  the  differences  between  their  patho- 
genetic bases — namely,  the  purely  psychic  nature  of  true  hysteria  and 
the  purely  physiological  and  histological  nature  of  neurastfien:a — ex- 
plain and  emphasi/.e  most  clearly  the  differences  in  the  symptoms — 
even  the  same  symptoms — of  the  two  diseases. 

As  Wundt,  the  great  exponent  of  modern  physiological  psychol- 
ogy, has  shown,  m_ental  phenomena  are  compounds  representing  inter- 
connections between  certain  elementary  sensations  and  feelings.  Con- 
cepts, judgments,  memory,  imagination  and  volition  are  not  actual 
entities  with  a  local  habitat  in  the  brain ;  they  are  mere  processes,, 
occurrences  resulting  from  the  interplay  of  the  psychic  elements,  sen- 
sations and  feelings.  The  latter  are  the  only  psychic  phenomena  known 
to  have  a  distinct,  local,  anatomico-physiological  basis.  This  being  so,, 
it  is  obvious  how  the  symptoms  of  a  pure  psychosis,  as,  for  instance, 
hysteria,  should  be  so  changeable,  variable  and  abrupt,  and  should 
represent  more  or  less  faithfully  normal  physiological  activities,  but  iri 
an  exaggerated  or  diminished  form  rather  than  in  an  actual  perversion^ 
In  hysteria,  therefore,  we  observe  an  irritability  with  a  heightened  sug- 


THE    NEURONIC    DISEASES  I73 

^estibility  and  the  individual  symptoms  assume  the  character  of  a 
psychoneural  anaesthesia  or  hypersesthesia,  paralysis  or  spasm,  exalted 
imagination  or  absent  volition.  The  striking  peculiarity  of  these  symp- 
toms is  their  psychoneural  distribution,  and  above  all  their  incom- 
parable changeableness  and  sudden  variability.  They  are  utterlv  de- 
void of  anything  like  stability  and  permanency  ;  they  are  mere  increases 
or  diminutions  along  normal  lines ;  they  are  the  results  of  an  unin- 
lierited  or  overinherited  clash  of  two  or  more  psychic  forces  represented 
in  the  elementary  psychic  sensations  and  feelings.  They  are  the  ex- 
pression of  a  true  psychosis  and  can  only  be  effectively  reached  and 
managed  through  psychic  means. 

Neurasthenia,  on  the  other  hand,  while  necessarily  revealing  itself 
in  part  through  the  psychic  sphere,  is  not  a  true  psychosis.  It  is  an 
organic  disease,  using  the  term  organic  in  the  sense  that  disturbance  of 
function  necessarily  presupposes  disturbances  of  the  nervous  elements. 

It  does  not  matter  whether  our  present  means  of  investigation  fail 
to  reveal  to  us  the  nature  of  the  molecular,  chemical  or  other  dis- 
turbance, whatever  it  may  be,  in  the  neuroses  or  not.  The  fact  remains 
that  they  are  altered,  else  they  would  have  functionated  normally. 

The  outward  expression  of  this  alteration  of  the  elements  in  the 
neurasthenic  state  is  that  of  an  irritability  with  inability  for  sustained 
activity;    in  other  words,  an  irritable  weakness. 

lliis  organic  basis  of  neurasthenia,  about  which  we  know  so  little 
positivel}'  as  yet,  lends  a  certain  degree  of  permanency  and  persistency 
to  the  symptoms,  a  more  or  less  definite  anatomico-physiological  dis- 
tribution to  them,  and  a  tendency  towards  positive  aberrations  and 
perversions  in  them,  rather  tlian  mere  exaltations  and  diminutions  of 
normal  psychic  and  sensory-motor  activities.  One  or  two  brief  illus- 
trations will  make  this  clear.  Headache  is  a  symptom  of  both  hysteria 
and  neurasthenia.  In  h}steria  it  is  a  distmct  pain,  often  in  the  vertex, 
when  it  is  known  as  clavus.  The  pain  sense  is  one  of  the  normal 
psychic  elementary  senses.  In  hysteria  this  normal  elementar}-  sense 
is  psychically  exaggerated.  In  nerirasthenia  the  headache  assumes 
more  of  the  character  of  a  pargesthesia.  It  is  described  as  a  pressure,  a 
constriction,  a  pulling,  a  vise-like  cap,  but  never  as  a  distinct  pain. 
Many  times  I  have  had  neurasthenics  stop  me  when  I  have  used  the 
word  headache,  in  referring  to  their  head  trouble,  saying  that  they  had 
had  headaches,  but  felt  sure  that  this  feeling  was  not  like  their  distinct 
attacks  of  headache.  Again,  anaesthesia  of  psychic  origin  is  peihaps 
the  typical  symptom  of  hysteria ;  no  such  anaesthesia  ever  occurs  in 
even  the  most  profound  state  of  nervous  exhaustion.  The  rare  form 
of  numbness  sometimes  complained  of  by  neurasthenics,  if  examined 
objectively,  is  seen  to  be  not  an  anaesthesia  at  all,  but  rather  a  subjective 
form  of  parassthesia. 

And  so  on  through  the  whole  list  of  symptoms  common  to  both 
■diseases.  A  careful  consideration  of  them  from  the  two  standpoints 
just  described  will  enable  one  to  determine  whether  they  are  hysterical 
or  neurasthenic  in  origin,  even  when  they  appear  in  a  patient  afflicted 
with  both  diseases  at  the  same  tim^e. 

Hypochondriasis,  a  mental  malady  in  which  the  notion  of  disease 


1/4  THE    NEUROiSilC    DISEASES 

is  persistently  and  definitely  localized  b}'  the  patient,  often  resembles 
neurasthenia  with  anxiety  and  fixed  ideas.  The  hypochondriac  insists 
that  he  is  never  going  to  recover,  but,  on  the  other  hand,  is  steadily 
growing  worse,  while  objectively  he  is  seen  to  be  steadily  improving. 
The  neurasthenic,  when  asked,  always  feels  that  he  is  going  to  get 
well  if  he  is  only  fortunate  enough  to  get  the  right  treatment. 

Hypochondriacs  brood  over  their  supposed  trouble,  but  they  are 
not  wearily  depressed  or  typically  melancholic  as  neurasthenics  are. 
Moreover,  they  do  not  reveal  the  weakness,  the  bodily  emaciation,  the 
inability  to  take  prolonged  exercise  and  the  other  sensory,  motor  and 
vasomotor  symptoms  of  the  latter.  In  a  word,  hypochondriasis  is  a 
pure  psychosis  of  a  restricted  sort ;  the  somatic  and  anatomico-physio- 
logical  functions  are  but  little  disturbed. 

The  form  of  insanity  commonly  known  as  melancholia  is  some- 
times hard  to  differentiate  from  the  melancholy  of  neurasthenia.  In 
the  former  there  is  a  strikingly  persistent  insomnia,  a  severe  bodily 
emaciation,  great  restlessness,  a  high  degree  of  causeless  emotionalism, 
hallucinations  and  delusions,  and  a  tendency  toward  suicide. 

Melancholia  is  a  pure  psychosis  with  secondary  physical  mani- 
festations ;  it  is  subject  to  abrupt  changes  in  its  symptomatology,  es- 
pecially outbursts  of  mania.  The  face  often  shows  an  insane  expres- 
sion and  the  acts  of  the  pa.tient,  if  closely  watched,  reveal  a  mental 
derangement. 

In  melancholia  the  psychic  predommance  of  the  clinical  picture  is 
emphasized ;  in  neurasthenia  the  psychic  depression  is  merely  a  part 
of  a  symptomatology  that  includes  an  irritability  and  weakness  of  the 
entire  nervous  apparatus,  motor,  sensory,  vasomotor  and  sympathetic. 
And  yet  it  must  iDe  frankly  admitted  that  there  are  cases  of  melancholia 
and  neurasthenia  that  lie  on  the  borderland  between  the  two  diseases 
and  in  part  actually  overlap.  These  are  the  cases  that  give  the  real 
trouble  in  diagnosis. 

It  should  not  be  forgotten  that  a  melancholia  patient  may  at  the 
same  time  be  the  victim  of  a  neurasthenia  and  vice  I'crsa.  Time  and 
close  observation  alone  can  solve  the  true  nature  of  some  of  these 
cases. 

Many  gross  organic  dis'^ases  depress  the  patient  mto  a  state  of 
neurasthenia,  especially  in  their  incipient  stages.  Among  such  diseases 
may  be  mentioned  syphilis  of  the  central  nervous  system,  multiple 
cerebrospinal  sclerosis,  the  parasyphilitic  diseases,  locomotor  ataxia 
and  dementia  paralytica,  cerebral  tumor  or  abscess,  and  certain  forms 
of  toxaemia  involving  the  nervous  apparatus  and  resulting  in  gross 
lesions  later  on.  The  differential  diagnosis  of  these  will  be  discussed 
under  the  head  of  the  respective  diseases. 

Myasthenia  gravis  occasionally  suggests  neurasthenia.  The  weak- 
ness is  here,  however,  more  decidedly  neural.  It  verges  more  upon  a 
distinct  paralysis.  The  bulbar  prominence  of  the  manifestations,  their 
remarkable  remissions,  and  the  absence  of  sensory  and  psychic  mani- 
festations are  to  be  noted. 

Neurasthenic  symptoms  may  be  provoked  in  a  reflex  way  by 
gross  lesions  and  disease  outside  of  the  nervous  system.     The  constant 


THE    NEURONIC    DISEASES  1/5 

and  severe  pain  of  cancer,  for  instance ;  the  ceaseless  distress  caused  by 
an  inflamed  uterus  or  bladder ;  the  anxiety  and  worry  incident  to  a 
knowledge  of  organic  heart  disease  may  so  strain  the  patient's  nervous 
inhibition  and  self-control  as  to  wear  it  out  functionally  and  thus  set 
up  a  condition  of  neurasthenia. 

The  value  of  this  observation  lies  in  the  direction  of  urging  the 
examiner  to  spare  no  pains  in  searching  for  all  such  possible  extraneural 
sources  of  the  neurosis.  The  mere  removal  of  this  extraneural  trouble 
may  not  cause  the  neurasthenia  to  immediately  vanish,  for  the  latter 
has  grown  into  a  distinct  entity  and  needs  attention  solely  on  its  own 
account. 

Neurasthenia  is  a  slow  on-coming  disease.  Even  those  cases  which 
seem  to  develop  suddenly  or  rapidly  after  some  violent  mental  shock 
or  physical  traumatism  do  not  at  first  exhibit  the  typical  neurasthenia 
that  they  do  later  on. 

Sometimes  the  disease  steadily  progresses  for  a  number  of  months 
or  years  and  after  reaching  a  degree  of  moderate  severity  remains  sta- 
tionary. In  all  this  long  period  there  may  be  remissions  and  exacerba- 
tions of  the  trouble,  due  to  various  influences  acting  upon  the  patient, 
but  there  is  scarcely  ever  any  absolute  return  to  health  unless  there  is 
a  more  or  less  complete  change  of  habits  and  environment. 

Exceptionally  there  are  instances  of  neurasthenia  gravis  which  run 
a  very  rapid  course,  and  in  spite  of  everything  sooner  or  later  die  of 
inanition  and  complete  exhaustion. 

Prognosis. — The  prognosis  of  neurasthenia  is  generally  favorable. 
It  is  never  a  fatal  disease  per  se,  though,  as  Oppenheim,  Tlioma,  Regis, 
Frsenkel  and  others  point  out,  it  may  through  continual  fear  and  emo- 
tion set  up  incessant  acceleration  of  the  heart's  action  until  an  organic 
disorder  may  result  or  favor  the  early  development  of  atheroma  of  the 
heart  and  blood  vessels,  which  ultimately  may  be  the  cause  of  death. 
When  a  neurasthenic  worries  himself  into  committing  suicide  the 
mental  condition  is  probably  the  expression  of  a  pure  psychosis. 

Every  case  of  uncomplicated  neurasthenia  is  amenable  to  treat- 
ment, and  under  proper  conditions  most  cases  get  well.  This  is  par- 
ticularly true  of  the  acute  acquired  cases.  It  is  even  true  of  the  chronic 
cases.  The  congenital  cases,  of  course,  are  only  partially  amenable 
to  treatment.  Medicine  cannot  recreate  an  inherited  neuropathic  con- 
stitution, but  it  can  do  a  great  deal  in  preventing  and  overcoming  the 
acute  outbreak  of  the  disease  in  such  constitutions. 

The  character  of  the  heredity,  the  patient's  station  in  life  and 
means  for  accepting  what  may  prove  to  be  an  expensive  method  of 
cure,  and  the  absence  of  all  signs  of  other  mental  and  physical  disease 
obviously  determine  the  prognosis.  Given  certain  conditions,  some  of 
the  most  brilliant  results  in  neurology  are  obtained  in  the  cure  of  neu- 
rasthenia. Complete  recovery  from  the  most  distressing  conditions  is 
often  obtained  and  gratefully  appreciated.  This  is  shown  by  the  fact 
that  such  patients,  knowing  their  neuropathic  tendency,  guard  them- 
selves, when  once  they  have  recovered,  and  often  live  to  a  long  and 
happy  old  age. 


1/6  THE    XEUROXIC    DISEASES 

Treatment.  The  successful  treatment  of  neurasthenia  depends 
upon  several  conditions. 

In  the  hrst  place  there  must  be  a  clear  comprehension  of  the  na- 
ture of  the  disease  and  of  its  underlying  physical  basis.  In  other  words 
a  clear  diagnosis  must  be  made,  not  merely  of  the  patient's  condition  in 
general,  but  of  the  individual  symptoms  as  well.  For  example  a 
psychic  symptom  may  be  due  to  nerve-cell  malnutrition  (neurasthenic) 
or  to  disturbed  psychic  processes  (hysteric).  To  attempt  to  combat 
it  always  in  the  same  way  will  undoubtedly  lead  to  frequent  failure. 
The  paraesthesise  of  neurasthenia  whether  cerebral  or  neural  in  origin 
are  quite  different  from  the  psychic  anaesthesias  and  hypenesthesias  of 
hysteria. 

In  neurasthenia  there  is  an  anatomico-physiological  derangenient 
either  within  or  without  the  nervous  system  dependent  upon  malnu- 
trition, toxaemia,  exhaustion  or  reflex  irritation.  In  the  treatment  of 
neurasthenia,  therefore,  the  center  of  attack  must  be  made  against  one 
or  more  of  these  factors.  Psychic  treatment  is  of  no  avail  except  in 
those  cases  in  which  there  are  hysterical  tendencies. 

In  the  second  place,  the  successful  management  of  neurasthenia 
demands  the  absolute  confidence  and  ready  acquiescence  of  the  patient, 
on  the  one  hand,  and  the  highest  degree  of  tactfulness,  authority  and 
wisdom  of  the  physician  upon  the  other.  Failure  to  obtain  a  cure  not 
infrequently  results  from  the  non-fulfillment  of  one  or  both  of  these 
conditions.  From  a  want  of  confidence  and  obstinacy  the  patient  fol- 
lows directions  in  a  half-hearted  manner,  or  delights  in  combating 
everything  that  is  done  or  suggested,  or  listens  too  readily  to  all  sorts 
of  counsel  from  neighbors  and  friends  and  religious  cranks.  The  result 
is  obvious. 

The  physician  sometimes  offends  from  want  of  tact,  or  he  attributes 
to  hysteria,  a  pure  psychosis,  symptoms  that  are  neurasthenic  and 
anatomico-pathological  in  origin  and  adopts  a  manner  and  mode  of 
treatment  that  quite  insults  the  patient,  such  as  questioning  the  veracity 
of  her  statements :  or  he  is  less  intellectual,  less  well  informed  and 
less  cultured  than  his  patient.  All  of  which  foretells  the  inevitable 
result. 

The  third  and  too  often  the  most  difficult  condition  to  secure  for 
the  successful  treatment  of  neurasthenia  is  one  that  involves  the  ques- 
tion of  the  patient's  finances,  time  and  general  ability  to  carry  out  air 
expensive  and  prolonged  course  of  treatment.  If  the  same  unlimited 
freedom  were  given  the  physician  treating  a  case  of  severe  neurasthenia 
that  is  necessarily  given  to  one  who  is  managing  a  case  of  typhoid  fever 
or  pneumonia,  the  results  would  not  only  be  better  for  neurasthenics, 
but  the  art  and  science  of  medicine  would  shine  more  brilliantly  in  the 
management  and  cure  of  the  neurosis  than  it  now  does  in  the  manage- 
ment and  cure  of  the  infection. 

The  latter  diseases  are  not  cured  by  medicine,  but  inevitably  run 
their  course.  The  physician  merely  guards  them  from  certain  possible 
complicating  conditions. 

In  neurasthenia  the  disease  in  toto  is  made  to  right-about  face  and 


THE    NEURONIC    DISEASES  I// 

Start  upon  an  upward  grade  the  moment  the  requisite  environment  and 
regimen  are  obtained. 

The  failure  of  medicine  to  make  a  better  showing  in  the  treatment 
of  neurasthenia  is  largely  due  to  the  fact  that  the  patient's  financial 
condition,  or  his  inability  to  leave  his  business,  obliges  us  to  temporize 
and  substitute  therapeutic  measures  that  are  not  absolutely  the  best. 
In  all  candor  and  as  a  matter  of  personal  comfort  and  professional  repu- 
tation, when  the  charge  of  such  a  case  is  undertaken,  the  practitioner 
had  better  tell  the  truth  about  the  temporizing  character  of  the  treat- 
ment. 

There  is  no  routine  treatment  with  established  formulae  for  neu- 
rasthenia. Each  case  must  be  managed  in  accordance  with  its  own 
individual  peculiarities. 

Rest  and  nutrition,  both  terms  being  used  in  the  broadest  sense, 
are  the  two  words  that  cover  the  whole  line  of  treatment  for  pure 
neurasthenia.  Every  amusement  and  exercise,  every  prescription,  must 
be  suggested  with  only  those  two  ideas  in  view  if  the  case  is  one  of 
pure  exhaustion. 

Not  many  cases  are  purely  neurasthenic.  Certain  hysterical  mani- 
festations of  a  mild  character  usually  develop  along  with  the  neuras- 
thenic. Therefore  many  of  the  therapeutic  measures  adopted  for  the 
purpose  of  procuring  more  rest  and  better  nutrition  of  the  nervous 
elements  may  in  part  be  made  to  subserve  the  purpose  of  combating  the 
psychic  or  hysteroid  manifestations.  In  this  way  we  sometimes  hit 
two  birds  with  one  stone  by  changing  the  pa,tient's  environment,  by  pre- 
scribing particular  forms  of  electricity,  baths,  gymnastics,  outdoor 
games,  travel,  reading  and  other  occupations.  Even  the  medicines  and 
dietary  ordered  may  be  made  to  apply  to  all  three  demands,  rest,  nutri- 
tion and  psvchic  change,  when  all  three  are  combined  in  the  same 
patient. 

The  mode  and  means  of  combating  the  third  demand  will  be  found 
discussed  under  the  head  of  hysteria.  Here  the  discussion  will  be 
limited  to  the  treatment  of  pure  neurasthenia. 

A  little  ingenuity  will  enable  the  practitioner  to  combine,  when 
necessary,  the  two  lines  of  treatment. 

The  first  great  requisite  is  rest.  Now  rest  is  a  broad  term  and  is 
not  synonymous  with  idleness.  Ofttimes  rest  means  change  of  occupa- 
tion, and  occasionally  a  change  that  may  involve  greater  occupa- 
tion. ,  The  rest  must  be  mental  and  physical.  It  is  rest  for  a  man  en- 
grossed in  the  cares  and  worries  of  a  great  financial  undertaking  to 
arrange  his  affairs  temporarily  so  that  he  can  go  out  into  the  woods 
and  exercise  his  mind  and  body  close  to  the  heart  of  nature.  It  is  rest 
for  a  woman  worn  out  with  the  physical  exertion  of  caring  for  a  large 
household  of  children  to  lie  for  a  time  idle  on  a  bed  and  have  her  un- 
used faculties  exercised  with  a  bit  of  literature,  art  or  music.  It  is  rest 
for  one  who  has  ahvays  lived  upon  lower  mental  and  physical  levels  to 
climb  up  the  heights  of  mental  and  physical  mountains  where  the 
horizon  is  larger,  the  skies  more  expansive  and  the  play  of  color  greater. 

A  small  back  room  in  a  private  hospital  with  a  congenial  nurse 
and  a  small  but  well-selected  librarv  will,  with  other  accessories,  afford 


178  THE    NEURONIC    DISEASES 

the  hig'hest  type  of  rest  to  one.  To  another  a  trip  up  the  Nile,  a  jaunt 
through  Europe,  a  cHmb  up  the  peaks  of  Colorado,  a  hunting  expedi- 
tion through  [Montana,  canoeing  in  Canada,  farming  in  Illinois  or  even 
golf,  tennis  and  ball  in  the  park  may  be  genuine  rest. 

By  not  carefully  considering  the  patient's  previous  mode  of  life,  his 
temperament,  his  mental  and  physical  demands,  mistakes  have  often 
been  made  when  change  of  environment  has  been  recommended.  A 
European  trip  has  only  aggravated  some  cases  of  neurasthenia ;  the 
so-called  secluded  "rest-cure"  in  a  hospital  has  brought  still  more 
misery  upon  others. 

Rest  in  the  broad  sense  of  change,  mental  and  physical  rest,  is  the 
sine  qua  non  for  beginning  the  treatment  of  this  disease. 

When  all  things  are  taken  into  consideration,  perhaps  the  largest 
number  of  neurasthenics  can  obtain  the  required  rest  in  a  private  hos- 
pital or  home.  In  this  way  the  expense  of  travel,  the  distant  separa- 
tion from  family  and  medical  adviser,  and  all  the  annoyances  of  de- 
parture and  return  are  obviated.  A  change  of  the  mental  and  physical 
atmosphere  is  thus  secured  with  the  least  amount  of  discomfort.  There- 
fore most  cases  of  neurasthenia  are  benefited  by  a  preliminary  sojourn 
away  from  their  usual  environment  in  a  rest  cure  sanitarium,  home  or 
suburban  hospital. 

It  is  assumed,  of  course,  that  the  management,  location  and  fitting 
of  these  places  are  all  that  they  should  be,  otherwise  they  are  to  be 
shunned  absolutely. 

To  Weir  Mitchell  a  debt  of  gratitude  is  owing  for  the  thorough 
manner  in  which  he  has  studied  and  outlined  the  rest  cure.  Its  main 
features  consist  of  more  or  less  seclusion,  physical  and  mental  rest  and 
forced  nutrition.  Only  a  small  percentage  of  cases  of  neurasthenia,  and 
those  the  more  severe  ones,  need  the  absolute  rest  cure  carried  out  in 
all  of  its  details.  The  general  purpose  and  principles  of  the  treatment 
being  kept  well  in  mind,  it  may  be  varied  by  the  attendant  so  as  to  be 
adapted  to  the  particular  needs  of  the  case  in  hand.  The  details  of 
the  treatment  may  be  briefly  discussed  under  the  heads  of  hydrotherapy, 
massage,  electricity,  diet  and  medicines. 

In  a  general  way  my  own  method  of  procedure  with  a  moderately 
severe  case  of  genuine  neurasthenia  is  about  as  follows :  After  get- 
ting the  patient  away  from  her  usual  environment  into  a  private  hos- 
pital or  home,  or,  if  circumstances  will  not  permit  otherwise,  into  the 
home  of  some  friend  of  the  patient,  where  there  is  a  sunny,  well- 
ventilated  room  fitted  up  with  furniture,  pictures,  books,  flowers,  etc., 
that  suggest  quiet  and  cheerfulness,  I  limit,  sometimes  prohibit,  the 
visitation  of  friends  and  relatives. 

A  willing  and  refined  nurse  is  selected  and  requested  to  continue  in 
constant  attendance  so  long  as  she  proves  congenial  to  the  patient. 

A  few  simple  gam^es  and  a  list  of  a  dozen  or  more  books  selected 
from  the  essayists,  historians,  travelers,  poets,  philosophers,  novelists 
and  humorists  to  meet  the  patient's  particular  mental  requirements  are 
recommended. 

For  the  first  week  or  so  very  little  is  done  in  the  way  of  active 
treatment.     The  patient  is  requested  to  remain  on  the  bed  or  couch 


THE    NEURONIC    DISEASES  I79 

most  of  the  time,  to  receive  a  few  friends  only,  to  pass  the  time  chat- 
ting and  getting  acquainted  with  the  nurse  and  otherwise  becoming 
famihar  with  the  new  surroundings.  During  this  first  week  the  bowels 
are  freely  moved  daily  with  calomel  or  enemata ;  the  kidneys  are 
slightly  stimulated  with  diuretin ;  and  the  diet  is  quite  closely  limited 
to  milk  and  broths  given  in  small  quantity  every  hour  or  two.  Sleep  is 
enforced  by  nightly  doses  of  trional  or  sulphonal.  A  certain  amount  of 
psychic  suggestion  is  made  upon  each  visit  to  the  patient,  which  visits 
are  daily  or  every  other  day  at  first.  This  is  to  inspire  confidence,  to 
increase  the  docility  and  hopefulness. 

At  the  end  of  the  first  week  or  ten  days  of  this  preliminary  treat- 
ment the  patient  usually  recognizes  that  her  physician  can  dominate 
the  disease,  for  she  finds  she  has  slept  and  that  though  she  is  apparently 
more  collapsed  and  ready  to  take  to  her  bed,  she  is  slightly  less  irritable 
and  melancholy. 

Now  the  patient  is  ordered  to  keep  her  bed  constantly.  The  calo- 
mel and  diuretin  are  stopped  and  only  the  morning  enemata  continued ; 
the  trional  and  sulphonal  are  gradually  diminished  each  night ;  and 
a  slightly  more  generous  dietary  is  allowed.  By  this  time  the  particu- 
lar requirements  of  the  case  are  so  well  revealed  that  a  daily  program 
is  carefully  written  out  and  left  with  the  nurse  to  execute.  The  follow- 
ing program  suggested  by  Dr.  John  K.  Mitchell  may  be  taken  as  an 
illustration : 

7  a.  m.     Cocoa. 

Cool  sponge  bath  with  rough  rub  and  toilet  for  the  day. 

8  a.  m.     Milk.     Breakfast. 

Rest  an  hour  after. 

10  a.  m.     8  oz.  peptonized  milk. 

11  a.  m.     Massage. 

12  m.     Milk  or  soup. 

Reading  aloud  by  the  nurse. 
I  :30  p.  m.     Dinner. 
Rest  an  hour. 

3  '30  P-  ^-     8  02-  peptonized  milk. 

4  p.  m.     Electricity. 

6  p.  m.     Supper  with  milk. 

8  p.  m.     Reading  aloud  by  nurse  one-half  hour. 

9  p.  m.     Light  rubbing  by  nurse  with  drip  sheet. 

8  oz.  malt  extract  with  meals,  tonic  after  meals. 
8.0Z.  peptonized  milk  with  biscuit  at  bedtime  and  a  glass  of 
milk  during  the  night  if  desired. 

Such  a  program  as  the  above  should  never  be  adopted  as  a  routine 
for  all  cases.  Its  chief  value  is  in  giving  the  approximate  time  for  each 
of  the  manoeuvres  and  in  forming  a  skeleton  ground  plan  whereon 
special  indications  may  be  made  to  meet  special  requirements.  Not  the 
least  advantage  in  the  use  of  such  a  program  is  the  regularity  and 
system  which  it  establishes. 

In  regard  to  the  dietary  suggestions  for  such  a  program,  it  should 
be  well  understood  that  a  forced  nutrition  is  the  desideratum  and  that 


l8o  THE    NEURONIC    DISEASES 

therefore  the  only  Hmitations  surrounding  it  are  the  digestibility  and 
nutritious  character  of  the  food  and  the  digestive  powers  of  the  patient. 
Sometimes  I  find  it  necessary  to  study  closely  the  patient's  idiosyncrasies 
in  regard  to  food ;  at  other  times  I  urge  the  use  of  all  kinds  of  food,  in- 
discriminately, that  the  patient  will  enjoy  most,  assisting  its  digestion, 
when  necessary,  with  the  artificial  digestants.  I  get  the  food  into  the 
patient,  sometimes  with  the  regular  meals,  sometimes  with  small,  fre- 
quently repeated  meals,  knowing  that  in  spite  of  some  temporary  dis- 
tress, with  digestants  some  assimilation  of  it  will  be  accomplished.  In 
the  early  dietary  milk  plays  almost  the  entire  role.  Even  throughout 
the  whole  six  weeks'  or  two  months'  course  of  treatment  milk  is  made 
a  staple  article.  The  quantity  (two  to  four  quarts  a  day),  mode  of 
preparation,  frequency  of  administration  and  method  of  rendering  it 
continuously  palatable  are  subject  to  variation. 

The  nitrogenous  foods  are  usually  considered  the  best  for  neuras- 
thenics. Meats,  fish,  eggs,  green  vegetables,  fruits,  with  occasionally 
a  little  tea  and  cofifee,  and  at  all  times  abtmdance  of  water,  may  be 
taken. 

It  is  well  for  this  class  of  patients  to  avoid  such  viands  as  pork, 
stews,  hashes,  veal  and  salt  meats  in  general,  thin  soups,  cooked  oysters 
and  clams,  turkey,  thick  gravies,  pickles,  pies,  pastry  and  preserves 
and  all  made  dishes.  Howbeit  as  nervous  starvation  is  so  largely  at  the 
base  of  nervous  exhaustion,  I  would  in  some  cases  even  allow  some  of 
these  undesirable  articles  of  food  if  the  patient's  idiosyncrasy  called 
for  them  to  the  exclusion  of  the  more  digestible  ones.  The  need  of 
nutrition  is  so  great  that  for  the  time  being  a  certain  amount  of  gastric 
distress  may  be  risked  if  thereb}  more  food  stuff  is  accepted  by  the 
patient. 

Stomachic  tonics,  acids  and  digestants  can  do  much  towards  aiding 
the  stomach  under  these  circumstances. 

Hydrotherapy  is  a  most  valuable  factor  in  the  treatment  of  neu- 
rasthenia. It  should  be  employed  for  its  tonic  rather  than  its  stimulat- 
ing or  its  psychic  effect.  Therefore  I  prefer  warm  or  tepid  baths  daily, 
either  upon  rising  in  the  morning  or  just  before  the  massage  in  the 
forenoon.  The  tepid  sponge  bath  in  bed  every  morning,  or  the  drip  in 
the  evening,  may  be  employed  in  the  early  period  of  the  treatment.  In 
exceptional  cases  and  sometimes  late  in  the  treatment  when  stimulation 
is  indicated  I  use  the  cold  bath  or  the  cold  wet  pack.  I  am  convinced, 
however,  that  the  vast  majority  of  the  cases  of  neurasthenia  are  better 
off  without  such  vigorous  stimulation,  at  least  until  they  are  well  along 
in  convalescence. 

Whether  the  water-  is  applied  cold  or  hot,,  in  sprays,  douches  or. 
packs,  in  full  baths,  half  baths  or  sitz  baths,  for  a  long  or  short  time, 
are  details  that  must  be  decided  by  the  physician  in  individual  cases. 

Massage,  especially  for  women,  is  a  most  grateful  form  of  passive 
exercise.  It  should  not  be  too  vigorous  at  first,  though  it  may  be 
administered  daily.  Gentle  rubbing  of  the  entire  body  towards  the 
heart,  sometimes  with  the  use  of  olive  or  cocoanut  oil,  is  usually  all 
that  is  necessary.  Occasionally  pinching,  stroking  and  slapping  are 
beneficial.    Later  on  active  and  passive  gymnastics.  Swedish  movements 


THE    NEURONIC    DISEASES  l8l 

and  other  forms  of  medico-mechanical  treatment  should  be  systemati- 
cally employed.  About  this  time  short  walks  with  the  nurse,  or  rides 
in  the  open  air,  may  be  indulged  in,  always  under  the  physician's  in- 
structions, however. 

Electrotherapy  is  sometimes  abused  in  the  treatment  of  neuras- 
thenia. It  should  never  be  begun  too  early,  say  before  the  second  or 
third  week  in  the  hospital.  It  should  be  used  at  first  rather  tentatively, 
and  had  better  be  dispensed  with  entirely  if  it  tires  or  irritates.  Above 
all  it  should  never  be  used  in  pure  neurasthenia  under  the  notion  that 
its  good  effects  are  psychic  upon  the  patient.  Central  galvanization  of 
the  spine  with  general  faradization  of  the  whole  body,  the  former  for 
five  minutes  and  the  latter  for  three-quarters  of  an  hour,  in  some  cases 
produces  a  marvelously  restful  feeling  and  provokes  the  fine,  fibrillary 
contraction  of  the  muscles.  I  never  saw  any  benefit  from  the  use  of 
static  electricity  in  pure  neurasthenia.  High  frequency  currents,  it  is 
said,  are  being  used  vvith  a  certain  degree  of  success.  The  same  is 
claimed  for  the  light-cure. 

Psychotherapy  from  the  very  nature  of  things  has  some  influence 
in  the  management  of  neurasthenia,  though  that  influence  is  infinitely 
less  than  it  is  in  hysteria.  It  consists  chiefly  in  the  confident  and  assur- 
ing manner  of  those  who  are  m  attendance  upon  the  patient. 

]\Iedicine3  are  valuable  only  as  adjuvants  to  the  other  lines  of  treat- 
ment. They  are  chiefly  tonics,  stomachics,  chalybeates,  carthartics  and 
hypnotics. 

Before  speaking  of  them  more  in  detail  I  want  to  protest  against 
the  too  frequent  use  of  stimulants,  such  as  strychnia,  alcohol,  etc.,  in 
the  early  treatment  of  this  disease.  To  whip  up  an  exhausted  and  badly 
nourished  nervous  system  is  not  only  illogical,  but  positively  harmful. 
Not  only  in  patented  nervines,  but,  alas !  too  often  in  the  prescriptions 
of  intelligent  physicians  do  we  find  these  stimulants  when  neurasthenia 
is  the  disease  in  hand. 

Among  the  tonics  available  are  small  doses  of  nux  vomica,  the 
mineral  acids,  quinine,  arsenic,  phosphorus  and  iron.  Any  preparation 
of  these  may  be  employed  that  is  most  easily  assimilable  and  that  upon 
trial  seems  to  fit  the  case  best.  Among  the  cathartics  the  salines  and 
cascara  are  the  best  for  continuous  use.  I  always  gradually  reduce  the 
laxatives  and  depend  for  a  while  longer  on  gradually  diminished  ene- 
mata.  The  bromides,  sulphonal  and  trional  are  the  hypnotics  of  choice, 
though  these  should  only  be  used  early  in  the  treatment  and  should  soon 
be  replaced  by  other  means  of  inviting  sleep. 

I  deem  it  unwise  to  make  specific  suggestions  for  the  treatment 
of  individual  symptoms.  Besides  emphasizing  the  one-sided  conception 
of  his  trouble  already  held  by  the  patient,  it  is  apt  to  cause  the  attend- 
ants to  lose  sight  of  the  fact  that  neurasthenia  is  a  disease  of  the  entire 
nervous  apparatus  and  therefore  always  needs  treatment  along  general 
lines.  This  statement  applies  especially  to  the  treatment  of  the  special 
organs  at  fault  in  what  is  called  sexual  neurasthenia. 

After  the  patient  leaves  the  hospital  or  home  it  is  well  for  him  to 
still  keep  under  the  observation  of  his  physician  for  several  weeks 
longer,  and  above  all  to  avoid  returning  into  the  same  environment  from 


i82  ri[i:  xiiUROA'ic  diseases 

which  he  emerged  at  the  beginning  of  the  treatment.  His  exercise,  diet 
and  tonics  still  need  some  oversight.  ^loreover  the  medical  adviser 
can  even  at  this  period,  when  the  patient  is  starting  a  new  sort  of  a  life, 
as  it  were,  offer  suggestions,  propose  restraints  and  lend  encourage- 
ment that  may  prevent  a  much-dreaded  relapse.  During  the  long  course 
of  hospital  treatment  a  bond  of  friendship,  closer  than  a  mere  profes- 
sional association,  has  not  infrequently  sprung  up  that  reveals  itself 
when  the  patient  has  returned  to  his  normal  course  of  life  in  a  mutual 
confidence  which,  if  properly  exercised,  will  keep  the  patient  from 
ever  falling  into  his  old  state  of  distressing  invalidism. 

THE  TRAUMATIC  NEUROSES. 

A  few  years  back  the  discussion  about  these  troubles  was  loud 
and  heated.  To-day  it  has  retired  almost  wholly  into  the  courtroom 
where  it  is  unfortunately  mixed  up  with  damage  suits.  From  the  very 
nature  of  the  case  it  will  probably  continue  to  be  heard  there. 

By  a  traumatic  neurosis  is  meant  the  more  or  less  sudden  appear- 
ance of  abnormal  manifestations  or  symptoms  of  disease  in  one  who  has 
recently  passed  through  a  severe  accident,  railway  or  other  sort,  and 
W'ho  shows  nowhere  upon  his  person  any  outward  sign  of  physical 
injury. 

It  is  evident  that  a  condition  such  as  this  definition  would  cover 
opens  the  way  for  simulation,  fraud  and  malingering.  The  heat  of  the 
debate  in  the  past  was  undoubtedly  fanned  to  an  exalted  degree  by  the 
dift'erences  of  opinion  as  to  whether  all  such  conditions  outlined  in  the 
definition  were  not  simulations. 

In  most  damage  suits  it  is  obviously  the  interest  of  the  plaintiff' 
to  establish  beyond  question  the  actual  reality  of  his  trouble ;  whereas 
it  is  the  interest  of  the  defendant  to  belittle,  to  prove  the  unreality  of, 
the  disease,  and  even  to  establish  the  simulation  of  it.  The  first  ques- 
tion that  always  presents  itself  in  regard  to  these  manifestations,  there- 
fore, is  whether  there  is  any  abnormality  present  or  whether  the  com- 
plainant is  not  a  malingerer.  This,  of  course,  involves  detective  work 
of  all  sorts,  medical  as  well  as  lay. 

As  cases  of  trouble  following  accidents  of  all  kinds  continued  to 
appear,  some  in  search  of  damages  and  some  not,  it  became  evident 
that  there  was  actual  disease  of  some  sort  in  them  and  that  the  ques- 
tion of  malingering  should  be  set  aside  as  an  entirely  distinct  and 
separate  one.  Can  there  be  a  disease  from  shock  or  other  accident  to 
the  nervous  system  and  yet  no  change  be  found  in  the  tissues  of  the 
body? 

At  last  the  question  was  narrowed  down  to  something  that  scien- 
tifically was  worth  while  answering.  It  was  a  question,  however,  in 
which  it  seemed  there  could  be  honest  differences  of  opinion  between 
equally  learned  and  scientific  investigators.  In  other  words,  it  was  the 
old,  old  problem  looming  up  again,  but  under  another  guise,  as  to 
whether  disturbance  of  function  can  occur  without  change  of  structure. 
There  were  those  who  answered  "No"  to  this,  but  there  were  also  those 
who  answered  "Yes."    The  reality  of  the  symptoms  was  granted. 


THE    NEURONIC    DISEASES  183 

Those  who  held  that  disease  always  meant  some  discoverable 
change  in  the  tissues  at  once  started  to  search  for  such  changes  in  these 
accident  cases.  In  some  of  them  were  found  effusions,  small  hem- 
orrhagic foci,  minute  degenerative  areas,  meningeal  alterations,  vascu- 
lar obstructions,  etc.  On  the  strength  of  these  few  findings  and  upon 
the  character  of  some  of  the  symptoms,  a  pathology  was  erected. 

The  influence  of  the  distinguished  surgeon,  Erichsen,  was  so  great 
that  he  led  the  medical  world  into  adopting  the  view  that  the  trouble 
was  a  spinal  concussion  with  early  molecular  changes  and  secondary 
inflammatory  retrogressive  processes  in  the  cord.  He,  Riegler  and 
others  regarded  the  condition  as  essentially  organic,  as  a  chronic 
meningom.yelitis.  Page  then  took  up  the  subject  and  in  a  volume 
argued  against  Erichsen  that  no  such  damage  to  the  cord  could  possi- 
bly be  produced  by  railway  accidents. 

Thus  the  ball  was  set  a-rolling  again  and  as  investigators  lined  up 
on  one  side  or  the  other  we  were  edified  wdth  a  vigorous  scientific  de- 
bate on  the  question  of  the  causation  of  organic  and  non-organic  dis- 
eases. 

But  still  the  cases  appeared  in  which  the  symptoiiis  were  unde- 
niable, but  in  which  the  usual  signs  of  organic  disease  of  the  cord  were 
wanting  or  were  woefully  confused. 

The  pros  and  cons  having  all  now  been  heard,  it  is  to-day  prac- 
tically conceded  by  the  authorities  of  most  reliability  that  the  acci- 
dents which  are  supposed  to  cause  these  diseases  can  and  do  cause 
them,  but  that  they  are  not  by  any  means  new  diseases.  The  troubles 
which  we  observe  after  a  severe  shock,  physical  and  mental,  are  of  the 
nature  of  psychoneuroses,  though  they  may  have,  in  the  beginning  or 
later  on,  associated  with  them  vascular,  meningeal,  inflammatory, 
sclerotic  and  other  changes  of  the  brain,  spinal  cord,  nerves  and  sym- 
pathetic system. 

It  is  at  last  recognized  that  the  traumatic  nervous  troubles  are 
of  many  types.  There  are,  first,  the  gross  surgical  cases  with  their 
fractures,  luxations,  hemorrhages  and  compressions  of  the  spinal  cord. 

Then  there  are  the  true  neuroses  or  psychoneuroses.  These  are 
classified  in  modern  neurology  as  neurasthenic,  hysterical  and  hypo- 
chondriacal cases.  Associated  with  and  sometimes  following  later  on 
these  neurotic  and  psychoneurotic  states,  there  are  the  hemorrhagic, 
inflammatory  and  degenerative  troubles,  or  their  combinations,  in  the 
nervous  centers. 

The  symptomatology  of  all  these  is  well  known,  and  as  I  have 
described  them  in  detail  elsewhere  they  will  not  be  repeated  here.  A 
traumatic  hysteria  is  the  same  as  any  hysteria.  A  traumatic  com- 
pression of  the  cord  needs  no  further  description  than  what  has  been 
given  it  under  the  head  of  spinal  diseases.  Were  these  traumatic  cases 
never  to  enter  court  or  be  mixed  up  with  damage  suits,  their  discus- 
sion as  a  separate  and  peculiar  set  of  troubles  would  disappear  from  the 
text-books. 

In  court,  however,  there  is  still  much  debate  as  to  what  is  meant 
by  a  neurosis  or  a  psychoneurosis.  Why?  Because  the  law  as  it  is 
framed  does  not  concern  itself  with  hypotheses,  however  they  may  seem 


184  THE    NEURONIC    DISEASES 

to  be  well  founded ;  and  those  who  administer  the  law  are  not  wdlling- 
or  well  enough  informed  in  medicine  to  fully  comprehend  what  is  meant 
by  a  functional  disease.  The  law  and  the  lawyer  demand  what  are 
commonly  called  physical  proofs,  evidences  that  can  be  actually  per- 
ceived by  our  senses  in  some  way.  They  do  not  care,  when  in  court 
at  least,  if  they  are  told  that  a  large  amount  of  scientific  knowledge, 
even  the  ultimate  foundation  of  all  human  knowledge,  consists  of 
inference  drawn  by  a  logical  deduction  from  given  data.  How  often 
the  witness  in  a  criminal  trial  is  reminded  to  tell  only  what  he  actually 
saw,  or  what  he  can  swear  that  he  perceived  in  some  way  through  his 
five  senses !  The  court  does  not  want  to  know  what  he  thinks  or 
infers.  It  cares  nothing  for  his  forms  of  reasoning  or  the  logic  of  his 
argument.  It  wants  from  him  merely  cold,  bare  facts  which  it  can 
itself  behold  or  could  have  perceived  under  the  same  circumstances. 

This,  of  course,  is  the  only  stand  to  adopt  in  legal  matters  where 
the  conflicts  of  human  judgment  are  brought  to  a  maximum,  but  it  is 
an  absurd  one  to  adopt  as  the  ground  for  the  determination  of  knowl- 
edge. Upon  such  a  basis  we  could  not  swear  that  we  knew  an}i;hing 
positively.  Distant  planets  would  have  to  be  brought  into  court,  atoms 
and  molecules  would  have  to  be  magically  enlarged,  gravitation  would 
have  to  be  materialized  and  weighed,  and  the  vibrations  of  sound  would 
have  to  be  caught  and  held  up  for  the  jury's  personal  inspection. 

Facts  as  the  law  defines  them  are  not  the  same  as  facts  constantly 
recognized  in  the  scientific  world. 

Among  these  facts  which  science  accepts  but  the  law  does  not  is 
the  one  that  we  can  have  a  functional  disturbance  in  a  nervous  cell 
and  yet  not  be  able  to  discern  it  directly  by  means  of  any  of  our  five 
senses.  Logic  can  penetrate  where  the  latter  fail.  It  is  just  as  legiti- 
mate to  reason  from  effect  back  to  cause  in  medicine  as  it  is  in  astron- 
omv  or  biology.  It  is  just  as  legitimate  to  accept  the  existence  of 
inherent  changes  in  cellular  structures  of  the  nervous  apparatus  when 
the  manifestations  are  constant  and  uniform,  as  it  is  to  infer  the  ex- 
istence of  an  unseen  world  when  certain  constant  and  uniform  perturba- 
tions are  observed  in  the  heavens. 

In  medicine  we  have  long  since  advanced  to  the  point  where  we 
recognize  a  neurosis  or  psychoneurosis  as  an  entity,  a  disease,  an  abnor- 
mality,  due  infereiitially  but  logically,  to  some  molecular,  chemical  or 
nutritional  change  in  the  minute  nervous  elements. 

At  the  present  day  it  is  not  incumbent  upon  the  victim  of  the 
disease  to  defend  that  proposition.  If  the  lawyer  of  the  defendant 
wishes  to  deny  it,  he  has  the  whole  scientific  world  of  medicine  and  of 
logic  to  combat,  and  to  permit  him  to  waste  the  time  of  the  court  in 
such  a  stupendous  task  is  sheer  folly. 

At  the  present  day  to  discuss  and  deny  the  reality  of  the  neuroses 
because  forsooth  we  can't  minutely  define  their  pathological  basis  Is 
as  ludicrous  as  it  would  be  to  discuss  and  deny  some  forms  of  insanity 
in  \vhich  no  known  pathological  changes  have  yet  been  observed. 

In  a  word,  then,  these  court  trials  should,  if  properly  conducted, 
narrow  themselves  down  to  the  question  of  the  existence  of  or  simula- 
tion of  the  neurosis ;    and  in  the  event  that  the  former  is  proved  to  be 


THE    XEUROXIC    DISEASES  l8^ 

the  case,  they  should  have  regard  to  the  relation  of  the  disease  to  the 
accident  as  one  of  cause  and  effect,  and  they  should  determine  the 
severity  of  it  as  regulating  the  amount  of  damages  to  be  awarded. 

In  fine.  th€  medico-legal  consideration  of  the  traumatic  neuroses 
relates  at  the  present  day  only  to  the  establishment  of  their  presence, 
their  etiology  and  their  prognosis. 

Etiology. — One  of  the  questions  always  brought  up  in  court,  in 
fact  the  question  upon  which  the  awarding  of  damages  actually  de- 
pends, concerns  the  general  and  the  particular  causes  of  the  neurosis. 

Can  a  neurosis  be  produced  b}-  shock  in  an  individual  previously 
well  in  every  respect,  or  has  the  plaintiff's  condition  been  caused  solely 
by  the  admitted  accident  ? 

Another  question  that  also  arises  is,  after  granting  that  the  acci- 
dent has  sensed  merely  to  awaken  a  latent  diseased  state  in  the 
plaintiff,  how  much  damages  should  be  awarded  for  a  disease  simply 
aroused  into  activity,  in  comparison  with  one  actually  originated  ? 

It  is  admitted  by  all  neurologists  at  the  present  day  that  shock, 
both  physical  and  psychic,  can  set  up  an  abnormal  state  in  an  individual 
sufficient  to  be  termed  disease.  Lightning  strokes,  railway  collisions, 
concussions  can  and  do  produce  symptoms  which  som.etimes  betray  an 
actual  physical  basis  and  sometimes  do  not.  In  the  latter  case  they 
constitute  almost  universally  the  clinical  pictures  of  hysteria  and 
hystero-neurasthenia  of  variable  degree. 

We  call  these  diseases  or  symptom-complexes  functional  for  want 
of  a  better  term,  but  we  assume  that  they  are  dependent  upon  molecu- 
lar alterations,  involving  change  of  metabolism. 

Severe  fright  and  excitement,  mental  and  physical  shocks  of  all 
kinds  have  been  followed  by  these  troubles  when  there  could  have 
been  no  possible  thought  of  damages.  It  is  perfectly  reasonable,  there- 
fore, that  they  might  occur  when  a  damage  suit  is  possible,  whether  it 
be  probable  or  not. 

It  can  no  longer  be  doubted  that  a  profound  psychoneurosis,  hys- 
terical or  neurasthenic,  with  all  that  we  include  in  those  disease  states, 
may  be  caused  de  novo  by  a  severe  accident  in  which  there  has  been 
a  severe  mental  and  physical  shock. 

Nevertheless  it  is  true  that  in  the  majority  of  cases  there  has  not 
been  a  state  of  ideal  health  before  the  accident.  A  shock  that  would 
produce  a  pronounced  psychoneurosis  in  a  previously  healthy  indi- 
vidual would  be  not  unlikely  to  produce  a  severe  physical  lesion  of  some 
sort.  Not  infrequently  such  is  the  case,  though  it  is  not  often  recog- 
nized until  some  weeks  after  the  accident.  Embolic  and  hemorrhagic, 
inflammatory  and  sclerotic  conditions  of  insidious  character  are  thus 
often  initiated  and  bring  in  their  train  a  long  series  of  grave  mani- 
festations. 

These  are  the  organic  cases,  and  as  a  rule  are  the  type  that  occur 
in  patients  who  are  caught  by  the  accident  when  they  are  in  perfect 
physical  and  mental  vigor. 

A'erv  often,  however,  the  victim  of  the  shock  has  been  the  pos- 
sessor of  a  highly  neuropathic  constitution.  He  may  even  have  been 
all  his  life,  or  recentlv,  a  hvsteric  or  neurasthenic.     His  nervous  ap- 


l86  THE    NEURONIC    DISEASES 

paratus  may  have  been  already  on  the  verge  of  collapse  with  alcoholic 
or  nicotine  poisoning.  ]\Ieeting  with  an  accident  under  such  circum- 
stances, an  unusual  psychoneurotic  state  is  suddenly  evolved  in  him 
and  he  is  profoundly  prostrated,  violently  hysterical  or  pitifully  hypo- 
chondriacal, though  he  may  show  no  physical  sign  of  injury  and  may 
even  not  have  been  as  badly  shaken  up  as  some  others  in  the  accident. 

The  latter  is,  therefore,  a  definite  exciting  cause  of  his  trouble, 
though  not  the  primary  originator  of  it.  The  results  may  be  lasting 
and  later  on  even  evidences  of  physical  degenerative  conditions  may 
make  their  appearance. 

The  relative  amount  of  damages  for  an  accident  that  originates 
and  for  one  that  merely  awakens  a  latent  disease  state  must  be  decided 
by  the  legal  authorities. 

Symptoms. — There  is  nothing  to  be  said  of  the  symptoms  of  these 
neuroses  more  than  what  has  already  been  said  under  the  heads  of 
hysteria  and  neurasthenia. 

The  detection  of  malingering  depends  almost  wholly  upon  symp- 
tomatology. Familiarity  with  the  diseases  that  are  simulated  and  nat- 
ural shrewdness  alone  will  enable  the  examiner  to  detect  a  fraud.  To 
lay  down  rules  of  procedure  would  be  absurd.  Each  case  must  be 
studied  by  itself.  The  whole  clinical  picture  must  be  taken  into  view  as 
well  as  the  various  manifestations  in  detail. 

Most  simulators  are  dishonest  and  fraudulent.  A  hysteric  may 
be  an  incorrigible  simulator  and  yet  not  be  dishonest  or  fraudulent. 
The  examiner  must  be  careful  to  difterentiate  the  two.  One  of  his 
most  difficult  tasks,  if  the  case  goes  into  court,  will  be  to  convince  the 
jury  that  there  is  a  difference  between  the  hysterical  and  the  fraudulent 
simulator.  It  is  a  fact  that  the  laity  still  loOk  upon  hysteria,  with  its 
high  degree  of  susceptibility  to  suggestion,  as  a  sort  of  a  make-believe 
on  the  part  of  the  patient,  that  gives  strength  to  the  defendant's  side 
in  the  courtroom.  If  a  case  is  hysterical  I  urge  against  all  litigation. 
A  prompt  settlement,  though  small,  will  be  better  than  to  run  the 
risk  of  trying  to  explain,  in  the  presence  of  an  opposing  lawyer,  to 
the  average  panel  of  layman,  what  is  meant  by  hysteria  and  to  prove  to 
them  that  it  is  an  actual  disease  as  much  as  typhoid  fever  or  pneu- 
monia. The  task  is  herculean  and  even  though  heavy  damages  be 
reallv  deserved,  the  chances  are  strong  that  the  verdict  will  be  against 
the  plaintiff. 

A  very  good  principle  to  remember  in  detecting  malingering  is 
that  it  is  safer  for  the  malingerer  to  imitate  an  organic  disease  than  to 
imitate  a  neurosis,  but  that  it  is  easier  to  diagnose  a  simulated  neurosis 
than  to  diagnose  a  simulated  organic  trouble.  The  reason  of  this  is 
obvious.  The  neuroses  are  so  much  more  changeable  in  their  symp- 
toms and  have  so  many  more  of  them  than  the  organic  diseases,  that 
the  chances  of  inattention  on  the  part  of  the  malingerer  are  better  in 
the  former  than  in  the  latter.  A  local  paralysis  or  anaesthesia  such  as 
we  observe  in  an  organic  disease  can  be  imitated  by  a  shrewd  criminal. 
His  attention  being  confined  to  so  limited  a  phenomenon,  he  cannot  be 
thrown  off  his  guard  by  the  tests  of  the  examiner.  On  the  other  hand, 
scarcely  a  simulator  is -so  well  posted  on  disease  as  to  be  able  to  present 


THE    NEURONIC    DISEASES  IS/ 

a  complete  and  typical  picture  of  a  neurosis.  He  either  overacts  or 
underacts  his  part. 

One  of  the  shrewdest  simulations  that  I  was  ever  asked  to  unmask 
was  that  of  a  woman  who  for  years  had  been  representing  herself  as 
an  epileptic.  She  had  clearly  studied  the  disease  well  from  the  books. 
Several  physicians  who  had  seen  her  in  her  fits  had  pronounced  her 
epileptic.  The  family  history  was  neuropathic  and  there  had  been  a 
trauma.  In  all  details  she  acted  her  part  to  perfection.  When,  how- 
•ever,  the  entire  history  and  total  picture  of  the  case  were  brought  into 
the  light  of  scrutiny  it  w^as  obvious  enough  that  the  case  was  not  one  of 
typical  epilepsy.  It  was  not  hysterical,  nor  was  it  organic.  I  pro- 
nounced it  one  of  simulation  and  the  later  results  proved  the  correct- 
ness of  my  suspicion. 

Another  case  that  I  saw  was  one  of  genuine  hysteria  in  which 
imitation  had  played  such  a  strong  role  that  in  the  absence  of  certain 
stigmata  of  hysteria  some  of  my  colleagues  thought  it  was  one  of  pure 
simulation.  The  total  picture  of  the  case  formed  the  basis  of  my 
opinion. 

I  recently  saw  in  consultation  a  traum.atic  hysteria  in  a  man  who 
could  not  move  his  left  arm,  could  not  hear  with  his  left  ear  and  was 
afflicted  with  complete  aphonia.  .  A  stroke  of  lightning  had  hurled  him 
across  the  room  and  he  was  examined  about  a  week  later.  No  organic 
lesion  would  have  given  the  peculiar  complexus  of  symptoms  that  he 
presented.  Simulation  was  excluded  by  the  rapid  action  of  the  pupils 
to  light,  with  sluggish  action  to  accommodation,  and  by  the  entire 
early  and  late  history  of  the  case. 

Simulators  who  attempt  to  nnitate  the  neuroses  do  not  render  the 
picture  changeable  enough.  They  adopt  a  type  of  the  disease  and 
then  give  its  manifestations  such  a  permanency  and  a  uniformity  as 
belongs  only  to  organic  disease. 

Of  course,  electricity,  a  psychic  shock,  etherization  and  the  state 
•of  the  pupils  will  serve  when  in  doubt  as  invaluable  aids  in  differen- 
tiating organic  from  functional  disease  and  distinguishing  either  from 
pure  malingering. 

Prognosis. — ^the  prognosis  of  the  traumatic  neuroses  is  always  an 
important  question  in  court.  Much  is  said  on  the  side  of  the. defense 
about  the  rapid  recoveries  that  occur  after  the  payment  of  the  damages. 
The  insinuation,  of  course,  is  that  deception  has  been  practiced.  That 
is  undoubtedly  the  case  sometimes.  However,  there  is  something  to  be 
-said  in  favor  even  of  those  who  thus  recover  after  damages  and  yet  are 
not  simulators.  It  is  a  fact  that  the  recovering  of  a  large  award  and 
the  satisfaction  of  having  won  one's  case  is  a  powerful  stimulant.  A 
neurosis  is  a  functional  depression,  a  continuous  autosuggestion  in  some 
cases.  Let  such  a  case  be  given  an  experience  that  would  make  almost 
any  human  being  glad,  honestly  glad,  and  it  is  not  surprising  that 
-sometimes  it  takes  a  turn  and  recovers.  Psychotherapy  is  a  potent 
agent  when  administered  by  a  court  as  much  as  wdien  administered  by 
a  physician  in  the  hospital. 

As  a  matter  of  fact,  however,  there  are  numerous  cases  of  trau- 
matic neurosis  that  do  not  recover  immediately  or  at  any  time  after 


l88  THE    NEURONIC    DISEASES 

the  awarding-  of  suitable  damages.  Indeed,  some  of  them  even  get 
worse  and  not  a  few  develop  in  the  course  of  a  year  or  so  distinct  indi- 
cations of  serious  organic  trouble.  If  the  outlook  of  every  case  could 
be  foretold,  the  amount  of  damages  to  be  awarded^ could  be  nicely 
adjusted.    Unfortunately  there  are  no  safe  guides  in  this  respect. 

The  traumatic  neuroses  have  a  prognosis  that  is  a  little  worse 
than  otiier  forms  of  neuroses.  If  there  has  been  a  latent  neuropathic 
state  prior  to  the  accident,  the  prognosis  is  rendered  very  grave.  It  is 
to  be  remembered  that  tabes,  dementia  paralytica,  disseminated  sclerosis, 
or  spastic  paraplegia  may  have  been  latent  or  just  beginning  to  show 
themselves  with  mild  neurasthenic  symptoms  about  the  time  of  the 
accident  and  that  they  may  be  suddenly  started  into  a  full  and  rapid 
progress  by  the  nervous  shock  of  the  accident. 

"Aside  from   such  facts  as  these  the  prognosis  of  th^  traumatic 
trouble  follows  that  of  the  disease,  however  it  may  have  originated. 

Treatment. — For  treatment,  see  the  sections  on  hysteria  and  neu- 
rasthenia. 

EPILEPSY. 

There  are  some  twenty  or  more  synonyms  for  this  disease,  so  long 
has  it  been  known  and  so  varied  have  been  the  explanations  of  it.  Its- 
protean  manifestations  have  caused  students,  from  ancient  times  down 
to  the  present,  to  regard  it  all  the  way  from  a  divine  possession  to  a 
mere  gross  anatomical  defect.  The  numerous  names  of  the  disease- 
in  a  general  way  either  describe  some  particular  feature  in  its  symp- 
tomatology or  suggest  an  imaginary  pathology  for  it.  Falling  sickness,, 
fits,  apoplexia  parva  and  morbus  sacer  are  among  the  more  striking^ 
synonyms.  Epilepsy,  from  a  Greek  root  meaning  to  seize  upon,  is  now 
the  recognized  title  of  the  disease  everywhere. 

It  is  easy  to  say  that  epilepsy  is  a  condition  in  which  loss  of  con- 
sciousness with  convulsive  movements  constitutes  the  principal  phe- 
nomenon. Such  a  definition,  however,  is  inadequate  to  cover  all  of  the 
various  types,  many  of  the  aberrant  forms  and  the  general  mental 
state,  while  it  gives  no  clue  whatever  to  the  underlying  pathological 
anatomy.  In  fact,  it  is  not  probable  that  any  short  definition  of  so  pro- 
found and  varied  a  malady  will  ever  prove  entirely  satisfactory.  This- 
is  especially  important  to  remember  when  the  physician  is  placed  upoit 
the  witness  stand  in  court  and  pressed  to  give  in  a  few  words  a  ae- 
scription  of  the  disease.  Preceding  his  testimony  with  this  explanation, 
he  may,  upon  the  urgent  request  of  the  court,  attempt  a  definition, 
somewhat  in  this  wise,  remembering  all  the  while  that  the  two  cardinal 
features  of  the  clinical  ensemble  are  the  sudden  loss  of  consciousness, 
and  the  impairment  or  loss  of  motor  coodination  :  Epilepsy  is  a  dis- 
ease of  the  brain  in  which  paroxysmally  and  somewhat  periodically, 
abruptly  and  for  a  brief  period  of  time,  the  consciousness  is  wholly  or 
partially  lost  and  the  muscles  are  or  are  not  thrown  into  a  condition  of 
incoordination  with  the  tonic  and  clonic  convulsive  movements. 

There  are  four  well-recognized  types  of  the  disease  based  largely 
upon  their  symptomatic  differences.  They  are  the  grand  mal,  the  petit 
mal,  the  partial  (Jacksonian)  type  and  the  psychic  type. 


THE    XEUROXIC    DISEASES  189 

There  are  certain  neuroses  that  are  beheved  by  many  to  be  minor 
manifestations  or  types  of  epileptic  seizure,  such  as  migraine,  certain 
iorms  of  angina  pectoris,  asthma,  nocturnal  pollution,  gastralgia, 
enteralgia,  etc.  These  will  be  again  referred  to  under  the  head  of 
■epileptic  equivalents. 

Status  epilepticus  is  a  culmination  of  the  disease,  but  hardly  a 
-special  type. 

The  old  division  into  primar}'  or  idiopathic  and  secondary,  organic 
or  symptomatic  epilepsy  is  rapidly  being  obliterated.  As  our  knowl- 
edge increases  we  are  realizing  more  and  more  that  an  organic  change 
of  some  sort  in  the  cortical  structures  underlies  the  whole  trouble.  The 
reason  for  and  the  exact  nature  of  this  change  are  the  problems  still 
awaiting  solution. 

Etiology. — The  one  great  truth  that  stands  out  beyond  all  others 
in  regard  to  the  causation  of  epilepsy  is  that  a  hereditary  taint,  more  or 
less  pronounced,  lies  behind  it.  By  this  I  do  not  mean  to  say  that 
it  is  a  hereditary  disease  directly,  though  it  is  often  observed  itself  in 
the  progenitors.  \'arious  influences  of  a  neuropathic  sort,  such  as  hys- 
teria, migraine,  gout,  insanity,  alcoholism,  nervous  strain  and  dissipa- 
tion, syphilis,  etc.,  in  the  ancestors  often  reveal  themselves  in  the  off- 
spring in  the  production  of  epilepsy.  In  this  broad  sense,  therefore, 
genuine  epilepsy  is  an  inherited  disease.  The  predisposing  factor  in 
its  etiology  is  an  inherited,  developmental  defect  in  the  nervous  system 
whereby  certain  exciting  prenatal,  natal  and  postnatal  accidents  and 
influences  cause  the  cortical  neurones  to  functionate  in  this  abnormal 
manner.  A  clear  heredity  can  be  traced  in  about  one-third  of  all 
cases.  In  two-thirds  of  these  the  inheritance  is  direct  and  of  like  sort. 
In  the  remaining  cases  an  indirect  heredity  is  so  constantly,  though 
ofttimes  remotely,  discovered  that  one  is  almost  justified  in  saying  that 
the  so-called  exciting  causes  of  the  disease  depend  for  their  potency 
upon  the  existence  of  this  predisposing  element. 

Sometimes  where  the  heredity  cannot  be  elicited  clearly  from  the 
ancestral  history,  collateral  defects  and  stigmata  of  degeneracy  in  other 
children  will  point  it  out.  A  woman  whom  I  saw  recently  had  never 
had  any  trouble  until  she  was  forty-seven  years  of  age.  The  family 
history,  so  far  as  it  was  confessed  to  me,  was  entirely  negative.  A  sis- 
ter of  the  patient,  however,  had  cleft  palate.  Another  patient  claiming  to 
come  of  a  strong  and  sturdy  German  stock  had  had  migraine  of  a  most 
severe  type  until  her  first  fit,  and  volunteered  the  information  that  her 
sister,  as  well  as  herself,  were  the  victims  of  paroxysmal  asthmatic 
attacks. 

Injuries,  depressing  irdlnenc.es  and  other  factors  that  may  affect 
the  growing  brain  in  its  early  years  ^^'ill  cause  congenital  defects  that 
may  express  themselves  in  epileptic  seizures.  Freud  goes  so  far  as 
to  say  that  all  epilepsy  is  due  to  the  developmental  defect  left  in  the 
train  by  the  ordinary  lesions  of  the  cerebral  palsies  of  childhood.  In 
these  cases,  of  course,  what  hereditary  influence  there  is  must  be  of  an 
indirect  sort  and  probably  vascular  in  character.  The  traumatic  cerebral 
palsies  which  provoke  brain  atrophy,  sclerosis  and  other  defects  out  of 
which  epilepsy  is  evolved  cannot  be  spoken  of  as  hereditary. 


190  THE    XEUROXIC    DISEASES 

The  disease  may  declare  itself  at  any  age.  Partly  on  account  of 
the  hereditary  and  congenital  nature  of  it,  three-fourths  of  the  cases 
begin  to  show  symptoms  under  twenty  years  of  age.  I  have  often 
noticed  that  an  epileptic  equivalent,  such  as  migraine,  asthma  or  neu- 
ralgia, will  suddenly  cease  and  epileptic  seizures  take  its  place  at  about 
the  age  of  physiological  stress,  as  puberty  and  the  climacteric.  It  is 
said  that  nearly  fifty  per  cent  of  the  cases  occur  in  the  second  decade  of 
life,  when  the  awakennig  of  the  sexual  function  and  the  consequent 
emotional  strain  are  overwhelmingly  dominant. 

Partly  as  predisposing  and  partly  as  exciting  causes  infections  and 
toxcEmias  are  particularly  significant.  The  acute  infectious  fevers  of 
childhood,  and  above  all  scarlet  fever,  are  responsible  for  the  disease. 
As  the  cerebral  palsies  of  childhood,  from  which  so  many  cases  of 
epilepsy  are  to  be  dated,  are  also  largely  due  to  the  acute  infectious 
diseases,  it  is  difficult  to  say  whether  the  epilepsy  is  the  direct  result  of 
the  infection  or  the  secondary  result  of  the  brain  defect.  Pertussis, 
thermic  fever,  malaria,  pneumonia,  influenza,  diphtheria,  measles,, 
typhus,  typhoid  and  yellow  fever  and  meningitis  have  all  been  credited 
with  the  disease.  Gastro-intestinal  disorders  with  auto-intoxication 
may  well  be  the  cause  of  epilepsy,  in  view  of  our  modern  nutritive 
conception  of  its  pathogenesis.  Toxsemia  from  lead  poisoning,  exces- 
sive use  of  tobacco,  renal  diseases,  alcohol  and  such  poisons  as  cocaine,, 
antipyrin,  arsenic,  ph}'30stigmin,  chloroform,  etc.,  are  to  be  remembered 
as  possible  instigators  of  epileptiform  and  probably  epileptic  fits. 

Acquired  syphilis  may  cause  epilepsy,  though  as  a  rule  the  seizures 
are  indicative  of  gross  lesions  of  a  vascular  nature  so  familiar  in 
cerebral  lues.  Inherited  syphilis  is  undoubtedly  responsible  for  some 
cases. 

Other  chronic  infectious  states  that,  like  syphilis,  predispose  to  the 
disease  are  rheumatism,  scrofula,  rickets,  gout,  severe  anaemia,  cancer,, 
drunkenness  of  parents  at  the  time  of  conception,  diabetes  and  possibly 
chorea. 

Dentition  in  a  predisposed  child  may  provoke  the  disease.  In- 
fantile eclampsia  may  be  the  beginning  of  it,  a  fact  which  should  warn 
us  not  to  make  light  of  infantile  convulsions  about  the  period  of  teeth- 
ing, as  is  so  often  done. 

Traumatic  epilepsy  is  usually  focal,  partial  and  Jacksonian  in  type. 
Nevertheless  injuries  to  the  head  may  provoke  general  epilepsy  in 
various  ways.  Depressed  bone,  fracture  of  the  inner  table,  hemorrhage, 
embolic  obstruction,  degenerative  focal  encephalitis  or  meningo-en- 
ceplmlitis  may  be  the  immediate  cause  of  the  trouble. 

Mental  shock  is  another  factor  and  has  often  been  the  starting 
point  of  the  severest  types  of  the  disease.  Mental  strain,  such  as  pro- 
longed anxiety,  Avorry,  grief  and  exertion  in  those  whose  heredity  is 
unfavorable,  are  of  the  nature  of  mental  traumatic  causes.  I  place  here 
the  influence  of  masturbation.  Usually  this  is  an  evidence,  in-'early 
cases  at  least,  of  a  neuropathic  condition,  rather  than  the  cause  of  it. 
And  yet  it  is  clear  that  the  shame,  the  fear  of  detection,  the  periodica} 
excitement  and  the  popular  notion  that  the  practice  invariably  leads 
to  insanity,  is  of  the  nature  of  a  mental  rather  than  a  physical  cause. 


THE    NEURONIC    DISEASES 


191 


The  mental  poAver  of  the  old  Roman  eunuchs  shows  that  the  loss  of 
the  vita  sexiialis  alone  is  not  the  cause  of  mental  deterioration,  whereas 
the  worry  and  continued  distress  that  such  a  condition  may  provoke 
may  be.  The  horrible  results  liable  to  follow  masturbation  may  be 
depicted  to  a  susceptible  lad  in  order  to  frighten  him  out  of  the  dis- 
gusting practice,  but  they  ought  not  to  be  set  dow^n  in  a  scientific  work 
to  that  which  is  not  the  real  cause  of  them.  Indeed  it  is  questionable, 
in  my  opinion,  whether  we  do  well  to  play  upon  the  mind  of  the  patient 
in  order  to  coerce  him  into  a  better  state  of  morality.  The  remedy 
may  be  worse  than  the  disease  and  by  reason  of  the  fright  and  dread  set 
up,  a  serious  mental  shock,  with  all  its  evil  consequences,  may  be  put 
in  place  of  a  mere  filthy  habit.  Masturbation,  I  can  well  understand, 
may  as  a  secret  and  vicious  practice  well  provoke  in  a  neuropath 
epileptic  seizures.  It  should  be  discouraged,  therefore,  as  strenuously 
as  possible,  without,  however,  resorting  to  measures  that  still  more  tend 
to  disturb  and  depress  the  mind. 

Psychic  outbursts,  ungovernable  passion,  intense  anger  and  electric 
shocks  have  formed  the  starting  point  of  the  disease. 

Heart  disease  is  so  often  found  in  company  with  epilepsy  that  a 
causal  relationship  is  more  than  a  suspicion.  Mitral  regurgitation  was 
the  chief  cardiac  symptom  in  the  1,070  cases  examined  by  Spratling. 
Some  form  of  heart  trouble  occurred  in  238  of  them. 

ReUcx  epilepsy  is  still  a  battle  ground  of  argument  and 
opinion.  Xo  one  believes  in  the  sole  causation  of  the  disease 
by  peripheral  irritation.  There  must  be  already  present  a  strong 
predisposition.  The  unstable  equilibrium  of  the  nervous  elements  must 
be  already  in  existence.  That  being  so,  it  is  both  conceivable  and  dem- 
onstrable that  irritating  diseases  of  the  internal  organs,  intestinal  para- 
sites, elongated  prepuce,  laryngeal  polyps,  carious  teeth,  eye  strain  and 
foreign  bodies  in  the  ear  may  provoke  the  seizures.  That  is  very  differ- 
ent, however,  from  the  statement  that  reflex  irritations  are  the  cause 
of  epilepsy.  Putting  a  stop  to  the  fits  is  not  always  curing  the  epilepsy. 
The  removal  of  these  various  sources  of  reflex  irritation  usually  puts 
a  stop  merely  for  a  time  to  the  seizures.  Too  often  the  patient's  early 
delight  and  belief  in  the  cure  are  transformed  into  bitter  disappoint- 
ment and  hopeless  indifference  at  finding  that  the  fits  are  beginning  to 
return  again.  These  may  be  due  to  some  new  source  of  peripheral 
irritation,  and  had  the  exact  value  of  these  causes  in  the  production 
of  the  disease  been  honestly  presented  to  him,  he  would  be  willing  to 
continue  further  treatment  instead  of  basing  his  resisting  obstinacy 
against  all  further  attempts  at  relief  upon  the  false  hopes  that  were 
raised  by  the  earlier  treatment. 

Senile  epilepsy  has  been  attributed  to  an  atheromatous  condition 
of  the  blood  vessels.  It  is  just  as  liable  to  be  due  to  the  general  senile 
decay  and  toxaemia  from  functional  insufficiency  of  the  various  organs 
as  from  anything  else. 

It  is  obvious  that  predisposing  causes  play  the  initial  role  in  the 
etiology  of  epilepsy  and  that  innumerable  exciting  causes  may  provoke 
the  former  into  an  outward  expression. 

The  great  predisposing  causes  are  heredity,  infection  and  physical 


192  THE    NEURONIC   DISEASES 

defects  in  the  brain  of  a  congenital  or  acquired  nature.  Cerebral  in- 
stability is  thus  established  and  constitutes  the  essential  disease.  Its 
presence  may  be  discovered  and  typical  epileptic  seizures  may  be  pre- 
cipitated, however,  only  when  one  or  more  of  a  long  list  of  possible 
exciting-  agents  begin  to  bear  upon  it. 

Pathology  and  Pathogenesis. — It  would  be  interesting  but  un- 
profitable to  rehearse  all  the  explanations  that  have  been  vouchsafed  in 
the  past  in  regard  to  the  pathogenesis  of  epilepsy.  Some  of  the  scien- 
tific accounts  of  it  were  no  less  fanciful  and  no  more  founded  upon 
actual  pathological  findings  than  were  the  superstitious  and  religious 
belief  that  it  was  due  to  some  divine  or  devilish  form  of  possession. 
As  in  all  the  great  neuroses  the  number  and  variety  of  hypotheses  have 
been  in  inverse  proportion  to  the  number  and  constancy  of  the  post 
mortem  findings.  It  is  only  withm  the  last  few  years  that  we  have 
approached  anything  like  a  scientific  and  well-founded  explanation  of 
the  disease.  Much  still  remains  to  be  discovered,  but  what  we  already 
know  indicates  in  the  clearest  manner  along  what  lines  future  investi- 
gations should  proceed. 

It  would  be  well  in  discussing  the  modern  explanation  of  epilepsy 
to  always  keep  a  sharp  line  of  demarkation  between  the  actual  patho- 
logical findings  and  the  mere  surmises  and  logical  deductions  that  are 
based  upon  those  findings.  The  former  may  always  be  referred  to 
with  a  certain  degree  of  positiveness ;  the  latter  must  always  be  looked 
upon  with  a  certain  amount  of  reserve. 

After  noting  briefly  the  actual  macroscopical  and  microscopical 
changes  commonly  found  in  epileptics  who  have  died,  as  well  as  some 
functional  abnormalities  frequently  observed  during-  life,  I  will  follow 
the  recent  excellent  work  of  Prout  and  Clark  and  indicate  the  prob- 
able relationship  of  these  various  pathological  conditions  to  the  cardinal 
symptoms  and  the  disease  itself. 

In  the  gross  pathology  of  the  disease  we  find  various  more  or  less 
constant  changes  in  and  about  the  head  and  the  brain.  Some  of  these 
are  of  the  nature  of  stigmata  of  degeneracy,  some  are  the  residua  of  old 
diseased  conditions,  others  are  the  results  of  arrested  development, 
and  still  others  are  the  direct  products^  of  the  epileptic  seizures.  In 
all  of  this  the  one  fact  that  stands  out  with  embarrassing  prominence 
is  that  these  changes,  whether  macroscopic  or  microscopic,  cannot 
always  be  determined  as  the  cause  or  the  result  of  the  disease. 

Almost  every  sort  of  lesion  of  the  cerebrospinal  axis,  its  mem- 
branes and  their  bony  envelope,  has  been  seen  in  epileptics.  Deformi- 
ties of  the  skull,  thickenings  of  the  bones,  anatomical  changes  in  its 
minute  structure  are  almost  constantly  observed.  They  may  have 
something  to  do  with  the  production  of  the  disease,  but  it  is  more 
likely  that  they  are  the  expression  of  a  physical  degeneracy  of  which 
the  epilepsy  is  in  part  also  an  expression.  The  membranes  are  opaque, 
adherent,  thickened  m  many  cases,  showing  signs  of  an  old  inflamma- 
tion, hemorrhage  and  other  vascular  troubles.  The  brain  itself  not 
infrequently  shows  a  partial  or  general  atrophic  change  with  alterations 
in  its  contour  and  convolutions.  Like  the  skull,  it  is  often  undersized 
and  deformed.     On  the  other  hand,  it  may  appear  perfectly  normal. 


irf- 


THE    NEURONIC    DISEASES  I93 

The  most  frequent  findings  in  it  are  the  remains  of  the  old  lesions  of  an 
infantile  cerebral  hemiplegia.  Spots  of  softening,  old  hemorrhagic 
scars,  cysts,  depressions,  porencephalic  deficiencies  and  atrophy  may 
be  discovered.  These  are  the  remains  of  pre  and-  postnatal  cerebral 
hemorrhages,  embolism,  thrombosis  and  meningo-encephalitis.  Freud, 
as  before  mentioned,  believes  that  all  epileptics  owe  their  disease  to  the 
lesions  that  cause  the  cerebral  palsies  of  childhood,  so  frequently  are 
they  found  in  the  post  mortem  examinations.  With  or  without  atrophy, 
the  brain  is  sometimes  hardened  by  an  over-production  of  neurogliar 
tissue,  a  general  gliosis.  This  is  thought  by  many  to-  be  a  result  and 
not  a  cause  of  the  fits. 

**  A  sclerosis  of  the  cornu  ammonis  was  at  one  time  dignified  by 
Meynert  and  others  as  the  pathogenetic  factor  in  the  disease.  It  cer- 
tainly occurs  frequently,  but  is  only  a  part  of  the  general  cortical 
sclerosis  or  neurogliosis. 

Cerebral  tumors  are  not  commonly  the  cause  of  epileptic  seizures, 
but  that  they  may  be  influential  in  the  production  of  the  disease  must 
not  be  lost  sight  of.  They  provoke  epileptiform  rather  than  epileptic 
seizures. 

So  varied,  irregular  and  disconnected  are  all  these  gross  conditions 
that  one  can  only  mention  their  existence  in,  without  being  able  to 
■postulate  definitely  their  relationship  to,  the  disease  proper.  They 
may  be  the  outgrowth  of  the  same  etiological  influences  that  establish 
the  epilepsy,  while,  on  the  other  hand,  they  may  by  pressure  and  other- 
wise so  disturb  the  circulation  and  nutrition  in  the  brain  as  to  set  up 
the  epileptic  state  and  habit  in  the  cortical  cells. 

There  is  no  question  at  the  present  day  but  that  epilepsy  is  a  dis- 
ease of  the  brain  cortex.  For  this  reason  I  pass  by  the  older  theories, 
such  as  that  of  Kussmaul  and  Nothnagel,  which  places  the  primary 
trouble  in  the  medulla  and  pons,  where  the  vasomotor  centers  are 
located,  that  send  out  impulses  which  cause  spasm  of  the  cerebral 
vessels  and  cortical  anaemia.  Through  its  S3'mptomatology  and  by 
means  of  experimentation  it  is  settled  that  the  source  of  the  manifesta- 
tions of  epilepsy  resides  in  the  cortical  cell-bodies.  Attempts  have 
been  made  to  determine  the  immediate  cause  and  character  of  these 
cell  changes.  Here  again  theory  has  been  rife,  while  the  demonstrable 
proofs  have  been  wanting. 

Among  the  more  notable  theories  that  have  been  propounded  upon 
the  slight  histological  basis  of  the  cortical  findings  may  be  noted  the 
cerebral  gliosis  irritative  explanation  of  Fere,  Chaslin  and  Sommer ; 
the  undemonstrable  fiiie  molecular  changes  in  the  cells  assumed  by 
Binswanger,  Gowers,  Jackson ;  the  autointoxication  view  and  all  its 
minute  possibilities  upheld  by  Voisin,  Agostini,  Coloban,  Krainsky ; 
and  the  views  of  those  like  Prus,  Hering,  Redlich,  Bischoff,  Rothman 
and  Von  Bechterew,  who  have  attempted  to  localize  the  origin  and 
-extension  of  the  fits. 

By  the  work  of  all  these  investigators  many  isolated  and  sug- 
gestive facts  have  been  brought  to  light,  in  uniting  and  comparing 
of  which  certain  broad  deductions  may  be  made  which  will  lead  us  to  a 
fairly  definite  conception  of  the  modern  pathogenesis  of  the  disease. 


194  THE    NEURONIC    DISEASES 

The  examination  of  the  cortex  of  twenty  epileptics  who  ched  at 
the  Craig  Colony  in  Xew  York  warranted  Prout  and  Clark  to  assert 
that  the  most  striking  changes  were  found  in  the  cells  of  the  second 
cortical  layer,  cells  distinctly  sensory  in  type.  This,  as  well  as  the 
general  symptomatology,  favors  the  view  that  epilepsy  is  primarily  a 
sensory  disease  with  certain  secondary  motor  disorders.  In  these  cells 
the  nucleus  was  most  affected.  It  was  granular,  swollen  and  poorly 
outlined.  The  nucleolus  was  often  absent,  many  hundred  times  more 
so  in  sections  from  status  epilepticus  cases  than  in  sections  from  normal 
brains.  The  nucleus  being  damaged,  the  cell  nutrition  is  injured,  and 
as  a  result  chromatolysis.  often  spoken  of  b}'  other  investigators  as  well, 
occurs.  The  cortex  is  invaded  with  leucocytes,  especially  after  status 
and  serial  fits,  which  assume  the  phagocytic  property  of  removing  the 
products  of  the  tissue  metamorphosis.  A  neurogliosis  accompanies  the 
process,  filling  up  the  spaces  vacated  by  the  wasting  cells. 

Upon  these  histological  findings  and  the  chemical  changes  and 
alteration  of  secretions  noted  but  not  positively  established  by  others 
in  the  bodies  of  epileptics,  Prout  and  Clark  deduce  that  epilepsy  is  a 
cerebral  disease  attended  and  followed  by  profound  and  dift'use  cortical 
degeneration  ;  that  the  morbid  changes  concern  chiefly  the  destruction 
of  the  nuclei  of  the  cells  of  the  sensory  type  from  v/hich  the  primary 
departure  of  the  disease  originates  and  often  and  in  the  course  of 
which  a  progressive  and  more  or  less  marked  and  diffuse  gliosis  oc- 
curs ;  that  it  is  as  a  disease  essentially  a  sensory  phenomenon  with  a 
secondary  motor  manifestation ;  that  its  etio-pathology  rests  with  a  ■ 
variety  of  toxic  or  autotoxic  agents  not  as  yet  definitely  isolated  or 
determined ;  arid  finally  that  it  is  engrafted  upon  a  cortical  organic 
cellular  anomaly  which  is  induced  largely  by  a  faulty  heredity,  the  exact 
anatomic  nature  of  which  is  not  known. 

The  two  chasms  still  to  be  bridged  before  the  circle  of  our  knowl- 
edge of  the  pathogenesis  of  epilepsy  can  be  said  to  be  complete  are  the 
nature  of  the  heredity  and  the  change  it  produces  in  the  cortical  cells 
whereby  they  become  epileptogenous,  and  the  nature  and  source  of  the 
toxic  agent  that  provokes  these  predisposed  cells  into  the  actual  state 
of  disease. 

In  regard  to  the  former  we  know  absolutely  nothing  except  what 
is  hidden  beneath  the  phrase  developmental  inadequacy.  In  regard  to 
the  latter  the  work  of  many  investigations  upon  the  blood,  the  urine, 
the  sweat  and  the  secretions  of  the  ductless  glands  is  suggestive  and 
worthy  of  more  than  a  passing  notice.  There  is  a  hypotoxic  state  of 
these  various  fluids  of  the  body  in  the  interpasoxysmal  periods  of  the 
disease,  a  hypertoxic  state  just  before,  during  and  after  the  fit.  Krain- 
sky  and  Weber  attribute  the  toxicity  to  carbonate  of  ammonium, 
Donath  to  cholin  and  neurin,  Haig  to  uric  acid. 

In  this  connection  it  is  worthy  of  note  that  the  disease  has  been 
attributed  to  acetone,  to  leucomaine  poisoning  and  to  a  diminished  alka- 
linity of  the  blood. 

There  is  no  conclusiveness  or  uniformity  about  the  autointoxication 
basis  of  the  disease  as  yet  to  warrant  more  than  a  passing  brief  mention. 

Symptoms. — The  symptomatology  of  epilepsy  may  be  studied  in 


THE    NEURONIC    DISEASES  I95 

an  orderly  manner  from  several  different  standpoints.  Types  of  the 
disease  have  been  constructed  out  of  the  predominance  of  certain  symp- 
toms so  that  there  is  a  marked  difference  between  the  clinical  accounts 
of  grand  mal,  petit  mal,  status  epilepticus,  partial  or  Jacksonian  epilepsy, 
psychic  epilepsy  and  the  so-called  epileptic  equivalents. 

A  disconnected  account  of  the  seizures  may  be  given  as  though 
they  alone  constituted  the  disease,  and  the  patient's  condition  between 
the  attacks  be  assumed  as  one  of  health. 

Emphasis  may  be  laid  upon  the  slim  data  which  we  possess  in 
regard  to  the  exact  etiology  and  pathology  of  the  disease  and  the 
clinical  description  be  varied  so  as  to  suit  the  so-called  idiopathic  or 
primary  and  secondary  or  symptomatic  cases. 

In  my  own  opinion  the  best  plan  upon  which  to.  study  the  outward 
manifestations  of  epilepsy  is  to  regard  all  cases  as  practically  the  same, 
with  the  same  general  etiology,  the  same  pathological  basis  and  the 
same  general  clinical  exhibition.  I  will  regard  the  disease,  when  once 
established,  as  a  continuous  and  more  or  less  persistent  one  with  mere 
exacerbations,  as  it  were,  in  the  seizures.  In  other  words,  an  epileptic 
is  such  not  because  of  his  fits  merely,  but  because  he  has  a  cerebral 
lesion  or  disorder  which  reveals  itself  occasionally  by  certain  violent 
outbursts.  The  patient  is  as  much  of  a  victim  of  disease  between 
attacks  or  fits  as  during  themi.  He  is  in  no  sense  in  perfect  health 
until  all  evidence  or  possible  evidence  of  the  disease  is  removed  per- 
manently and  completely. 

I  will  make  no  distinction  between  idiopathic  and  symptomatic 
epilepsy,  for  in  their  essential  pathogenesis  they  are  the  same ;  nor 
between  the  general  and  localized  forms,  for  they  toO'  are  practically 
the  same,  except  for  extent  of  symptomatic  distribution.  In  other 
words,  in  the  following  description  I  will  assume  that  epilepsy  is  a 
disease,  one  and  uniform,  characterized  by  a  more  or  less  orderly  series 
of  events  in  all  cases  and  with  only  some  slight  variations  in  its  clinical 
presentation  as  the  result  of  some  unimportant  variations  in  the  extent, 
origin  and  location  of  the  lesion.  I  will  note  these  variations,  but 
I  will  not  emphasize  them  as  special  forms,  separate  types  or  distinct 
diseases.  Syphilitic  meningitis  that  focalizes  itself  in  the  cervical  part 
of  the  cordis  not  spoken  of  as  a  different  disease  from  syphilitic  menin- 
gitis that  focalizes  itself  chiefly  in  the  lumbar  part  of  the  cord,  and  yet 
the  symptoms  of  the  one  are  radically  more  unlike  those  of  the  other 
than  are  the  symptoms  of  the  various  so-called  types  of  epilepsy  fromi 
one  another. 

The  essential  characteristics  of  epilepsy  are  certain  premonitory 
warnings,  a  fit  or  sudden  exacerbation  with  peculiar  mental  and  motor 
phenomena,  a  group  of  seciuelse  and  a  quiescent  interval  until  the  next 
exacerbation.  This  is  the  uniform  series  of  events  that  makes  up  the 
clinical  picture.  There  may  be  and  usually  are  many  variations  in  the 
details  of  this  picture. 

The  premonitory  symptoms,  for  instance,  may  be  of  every  sort  in 
which  involvement  of  the  cerebral  functions  are  implicated.  They  may 
be  so  slight  as  to  be  practically  nil. 

The  mental   disturbance  may  be  profound  and   accompanied  by 


196  THE    NEURONIC    DISEASES 

Other  most  violent  and  appalling  demonstrations,  while,  on  the  other 
hand,  it  may  be  so  slight  that  it  alone  seems  to  constitute  the  entire 
disease. 

The  sequelae  may  be  so  pronounced  that  they  seem  quite  like  essen- 
tial traits  of  the  disease ;  but,  on  the  other  hand,  they  may  be  entirely 
wanting.     Sometimes  they  assume  the  role  of  the  so-called  equivalents. 

Finally  the  quiescent  interval  may  resemble  perfect  health  or  con- 
stitute a  mild  degree  of  general  physical  and  mental  invalidism  or  even 
be  occupied  by  an  extension  of  the  exacerbation  into  the  serious  con- 
dition of  status  epilepticus. 

So-called  symptomatic  epilepsy  has  nO'  place  in  this  description, 
unless  it  sets  up  and  is  accompanied  by  the  form  of  the  disease  novv^ 
under  consideration.  Symptomatic  epilepsy  due  to  gross  irritative 
lesions  is  nothing  but  an  epileptiform  symptom  of  the  particular  disease 
in  which  it  occurs,  and  should  so  be  referred  to  under  the  symptomatol- 
ogy of  that  disease. 

The  first  evidence  of  the  disease  is  always  a  Ut.  A  person  may 
have  been  born  of  epileptic  parentage  with  all  the  predisposing  heritage 
of  the  disease,  nay,  more,  he  may  actually  be  the  victim  of  the  disease, 
but  no  decisive  evidence  of  it  occur  for  years  or  until  he  is  well  along 
in  middle  life.  If  the  fits  should  be  mild  and  nocturnal,  not  even  his 
family  may  know  of  his  trouble.  Whether  they  occur  during  the  day 
or  night,  it  sometimes  happens  that  the  patient  has  no  very  distinct 
knowledge  of  them,  particularly  when  they  begin  or  are  first  discovered 
by  the  friends.  In  some  forms  of  the  disease  in  which  the  psychosis 
is  the  predominant  element,  the  patient's  own  diary  written  by  him 
while  in  the  epileptoid  state  is  a  surprise  to  him.  In  petit  mal  he  is 
usually  unaware  of  his  attack  and  when  it  is  over  goes  on  about  his 
business  as  though  nothing  whatever  had  taken  place.  Very  often 
early  in  the  onset  of  even  the  seizure  types  of  the  disease  the  patient 
has  only  a  vague  sort  of  idea  that  something  has  happened.  I  have 
actually  been  asked  thus  by  epileptics,  especially  those  who  have  had 
their  attacks  at  night,  what  could  have  happened  to  have  caused  their 
tongue  to  be  so  sore  and  jagged.  It  is  almost  pathetic  at  times  to 
observe,  especially  in  the  young,  this  wonder,  mystery  and  confusion, 
nay,  even  total  ignorance  and  indifference  sometimes,  displayed  by 
those  who  are  apparently  unaware  of  the  nature  of  their  trouble.  In 
such  cases  the  testimony  of  friends  and  witnesses  of  the  attacks  alone 
has  to  be  depended  upon  for  an  account  of  the  disease.  The  signs  are 
all  objective,  the  subjective  being  so  slight  or  swallowed  up  in  the 
period  of  overwhelming  unconsciousness  that  the  patient  himself  can 
give  no  intelligent  account  of  himself.  If  the  attack  is  thus  capable 
of  being  verified  and  is  typical,  epilepsy  can  be  positively  diagnosed. 
That  does  not  mean,  however,  that  the  attacks  alone  constitute  the 
disease  and  the  patient  may  not  be  the  victim  of  it  without  the  actual 
occurrence  of  the  typical  fits. 

There  are  cases  that  are  undoubtedly  epileptic,  as  are  shown  by 
the  later  appearance  of  the  typical  fits  which  in  the  meantime  have 
gone  on  exhibiting  for  years  periodical  attacks  of  severe  headache, 
asthma,  cardiac  disturbances,  local  and  visceral  neuralgia,  unaccounta- 


THE    NEURONIC   DISEASES  I97 

ble  moods  and  spells  of  eccentricity,  vomiting,  nocturnal  pollution, 
nightmare  and  other  so-called  epileptic  equivalents.  In  such  cases 
these  manifestations  may  awaken  the  suspicions  of  the  medical  at- 
tendant, but  cannot  in  any  way  constitute  the  basis  for  a  diagnosis  of 
the  disease.    Only  the  typical  fit  can- afford  such  a  basis. 

How  often  have  we  all  sought  in  vain  for  an  earlier  evidence  of 
the  disease  in  which  the  first  typical  outbreak  occurred  well  along  in 
adult  life,  knowing  all  the  time  that  it  was  a  hereditary  trouble  and 
should  have  given  some  warnings  in  the  earlier  years  of  the  patient's 
life !  And  how  often  have  we  been  almost  inclined  to  doubt  the  pos- 
sibility of  finding  any  pronounced  underlying  neuropathic  premonition 
in  the  history  of  the  patient's  life  until  we  were  volunteered  the  state- 
ment that  an  abnormal  periodical  hunger  and  freakishness  of  appetite, 
a  dysmenorrhcea  without  any  apparent  organic  cause  for  it,  an  oc- 
casional insane  outburst  of  ungovernable  temper,  or  a  peculiar,  irresisti- 
ble impulse  to  do  and  say  certain  things,  have  been  noted ! 

Epilepsy  is  a  much-abused  term  and  many  and  varied  are  the 
phenomena  that  have  been  recorded  under  it.  Many  diagnosticians 
have  come  to  deny  the  wisdom  even  of  ever  declaring  the  presence  of 
the  disease  until  more  than  one  fit  has  actually  been  observed  by  him 
who  is  called  upon  to  make  the  diagnosis.  This  seems  to  be  rather  a 
tightly  drawn  position  to  take,  and  yet  it  was  inevitable  almost  from 
the  loose  manner  in  which  every  form  of  convulsion  and  mental  oblit- 
eration was  looked  upon  as  epileptic.  My  own  position  is  that  epilepsy 
is  present  in  the  patient  as  a  distinct,  positive  disease  even  when  there 
are  no  fits  as  yet  in  evidence ;  that  in  such  cases  the  equivalents  of 
the  disease  may  awaken  suspicion  and  put  the  physician  on  his  guard ; 
but  that  only  upon  the  occurrence,  all  other  things  being  considered, 
of  the  actual  typical  attack,  varied  even  as  this  may  be,  should  a  posi- 
tive diagnosis  ever  be  founded.  If  possible  the  physician  himself 
should  see  the  attack,  and  better  still,  more  than  one :  nevertheless  if 
those  describing  it  to  him  are  honest,  observant  and  intelligent  indi- 
viduals, he  may  base  a  positive  diagnosis  of  the  disease  if  their  account 
presents  a  clean-cut,  typical  picture.  Too  much  caution,  however, 
cannot  be  exercised  by  him  in  makmg  his  diagnosis  in  such  a  way, 
for  epilepsy  is  a  disease  often  simulated  by  malingerers  and  so  closely 
resembles  other  diseases,  or  is  so  closely  imitated  by  other  diseases, 
that  even  the  most  intelligent  of  the  laity  will  give  a  description  with 
all  honesty  of  it  such  as  to  mislead  the  medical  man  into  pronouncing  it 
genuine  epilepsy. 

In  nearly  all  cases  there  are  premonitions  of  an  attack.  These 
may  be  very  pronounced  and  exist  for  several  minutes,  hours  or  days. 
On  the  other  hand,  they  may  be  so  slight  and  brief  that  they  are  not 
recognized  by  the  patient  or  spoken  of  until  after  a  most  searching 
inquiry  is  made  by  the  examiner.  In  some  cases  no  premonitory  signs 
can  seem  to  be  discovered,  though  I  have  found  that  these  cases  have 
gradually  diminished  in  number  as  I  have  learned  to  make  my  exam- 
inations more  searching. 

These  forewarnings  may  be  studied  under  the  heads  of  sensory, 
psychic,  motor  and  irregular  aurje. 


198  THE    NEURONIC    DISEASES 

The  term  aura  is  particularly  applicable  to  the  sensory  premoni- 
tion, for  there  is  a  suggestion  of  a  sort  of  ascending  "spirituous  vapor" 
which  Pelops,  the  master  of  Galen  and  first  user  of  the  name,  sup- 
posed passed  up  through  the  extremities  to  the  head  by  way  of  the 
veins.  A  peculiar  sensation  starting  in  the  toes  or  tips  of  the  fingers, 
from  the  stomach  or  region  of  the  heart,  and  rapidly  and  lightly  sweep- 
ing up  towards  the  head,  is  very  often  felt  just  before  the  stroke  of 
unconsciousness  falls.  Tlie  sensation  is  varied  an'd  uncertain.  Many 
patients  declare  it  is  indescribable,  especially  the  very  frequent  gastric 
form  of  it.  It  may  resemble  the  globus  of  hysteria  or  retching.  At 
other  times  it  may  consist  of  actual  pain,  especially  in  the  vicinity 
of  the  heart.  In  the  -limbs  it  consists  of  some  form  of  paraesthesia, 
such  as  tingling,  pins-and-needles  sensation.,  formication  or  numbness. 
There  may  be  slight  dull  headache.  Not  always  does  this  sensation 
ascend  ;  occasionally  it  descends.  It  may  not  appear  at  all  or  in  aborted 
attacks  it  may  die  out  without  the  onset  of  any  other  symptom  what- 
ever. 

When  it  was  thought  at  one  time  that  this  sensory  aura  Vv^as 
somehow  the  direct  cause  of  the  fit,  bands  were  tightly  drawn  around 
the  arm  and  leg  to  check  its  progress.  As  in  a  certain  percentage  of 
cases  this  manoeuvre  was  followed  by  an  aborted  attack,  the  belief 
in  the  causative  influence  of  the  aura  was  strengthened  as  the  result  of 
a  sort  of  post  hoc  propter  hoc  reasoning. 

It  is  usually  stated  that  these  sensory  forerunners  of  the  attack 
occur  in  about  half  of  all  the  cases.  I  am  skeptical  of  all  statistics 
founded  upon  subjective  phenomena,  and  especially  upon  such  varied, 
elusive  and  intensely  personal  phenomena  as  are  the  sensory  aurge  of 
epilepsy.  I  have  a  suspicion  they  are  present  in  more  than  half  the 
cases,  for  I  have  not  infrequently  learned  of  them  in  long-subsec[uent 
visits  upon  the  patient  or  from  the  testimony  of  friends  with  better 
memories,  or  in  other  direct  and  indirect  ways  when  the  closest  ques- 
tioning of  the  patient  himself,  who  may  have  belittled  or  forgotten 
them,  failed  to  elicit  their  existence. 

After  the  general  sensory  aurre  the  most  frequent  and  important 
are  those  of  the  special  senses.  Of  these  vision  furnishes  the  largest 
number.  Flashes  of  light,  fortification  figures,  stars,  lightning-like 
lines,  increase  and  diminution  in  the  size  of  objects,  bright  colors  and 
darkness  are  all  mentioned.  Actual  hallucinations  and  real  pictures, 
curious  illusions,  the  vanishing  and  approaching  of  persons  and  things 
are  epileptic  aurae  that  go  a  long  way  to  explain  some  of  the  wonderful 
assertions  of  mystics,  religious  devotees,  hysterical  recluses  and  other 
superstitious  neuropaths.  Much  fascinating  and  romantic  literature, 
especially  in  the  Middle  Ages,  when  religiosity  was  rampant  and 
ignorance  was  its  handmaid,  has  been  written  on  the  basis  of  these 
visions. 

In  the  sphere  of  smell  and  taste  some  extraordinary  phenomena 
are  sometimes  met  with,  though  usually  the  patients  who  experience 
them  describe  them  as  bitter,  sweet,  pleasant,  disagreeable,  metallic,  etc. 
Numbness  of  the  tongue  and  palate  may  occur.  One  of  Spratling's 
patients  spoke  of  the  aura  as  "a  snuff  of  bad  air." 


THE    XEUROXIC    DISEASES^  I99 

Xext  to  the  visual  the  auditcry  aurae  have  furnished  the  strangest 
and  most  weird  descriptions.  Xot  only  noises,  but  the  ringing  of  bells, 
blowing  of  whistles,  sweet  music,  voices,  human  speech  and  other 
sounds,  both  in  and  out  of  nature,  pleasant  and  terrifying,  are  heard. 
It  is  easy  to  conceive  how  these  may  be  the  basis  of  heavenlv  com- 
mands, spiritualistic  whisperings  and  divine  inspirations.  The  range 
of  the  auditory  aurse  stretches  all  the  way  from  intolerable  roaring  and 
shrieks  to  actual  deafness. 

Were  these  special  sense  aur^e  only  more  frequent  than  they  are, 
and  did  they  occur  relatively  more  often  in  the  grand  mal  type  of  the 
disease,  they  would  probably  be  less  mysterious  and  therefore  less 
misleading  to  the  ignorant  and  superstitious  laity.  The  visual  aurse 
are  twice  as  frequent  as  all  the  other  special  sense  aurse  combined ; 
the  auditory  are  one-quarter  as  frequent  as  the  visual ;  the  olfactorv 
and  gustatory  are  the  least  frequent  of  all.  Usually  only  one  sense  is 
affected:  rarely,  however,  two  or  more  senses  may  exhibit  aurs  simul- 
taneously. 

Still  more  astounding  at  times  than  the  sensory  aur^e,  though 
they  are  less  frequent,  are  the  psychic.  The  mental  processes,  especiallv 
the  imagination  and  intellection,  are  unusually  quickened.  Emotions 
of  a  high  degree,  and  a  rapid  succession  of  ideas,  spring  into  being  and 
continue  until  suddenly  obliterated  by  the  paroxysmal  stroke.  It  is  to 
be  remembered  that  the  sudden,  unaccountable  actions  of  the  patient 
may  be  due  to  the  nature  of  these  exalted  feelings  and  ideas.  Fear  and 
horror  may  cause  him  to  suddenly  run  away  or  strike  at  a  neighbor, 
or  accomplish  his  own  destruction.  It  must  be  undoubtedly  true  some- 
times what  we  are  told  of  the  sudden  illumination  and  inspiration  which 
these  patients  experience  when  they  are  composing,  inventing  or 
attempting  the  solution  of  some  abstruse  problem.  The  fine  frenzy  of 
the  poet  may  sometimes  be  closely  allied  to  a  psychic  aura.  Memory 
m.ay  be  exalted,  so  much  so  that  the  far  past  is  regarded  by  the  patient 
as  being  actually  the  present. 

These  aura  are  at  times  delirious  and  seem  like  a  veritable  pre- 
epileptic insanity.  They  are  mostly  of  the  depressive  and  terrifying 
type,  though  they  may  be  of  the  exalted  and  ecstatic  type  with  rapture, 
joy,  lightness  or  immense  serenity.  Spratling  quotes  from  Dostoieffsky, 
the  Russian  novelist,  who  was  himself  an  epileptic  and  described  his 
own  feelings  in  the  character  he  has  drawn  in  '"Besi".  '"There  are 
moments,  and  it  is  only  a  matter  of  five  or  six  seconds,  when  you  sud- 
denly feel  the  presence  of  eternal  harmony.  This  phenomenon  is  neither 
terrestrial  nor  celestial,  but  is  an  indescribable  something  which  man 
in  his  mortal  body  can  scarcely  endure.  The  terrible  thing  is  the 
frightful  clearness  with  which  it  manifests  itself  and  the  rapture  with 
which  it  fills  you.  During  those  few  seconds  I  live  a  whole  human 
existence."" 

It  is  but  a  step  from  this  to  the  belief  in  and  proclamation  of  one's 
power  of  disembodiment  and  visitation  to  the  supernatural. 

Psychic  aurae,  like  the  sensory,  are  to  be  awarded  the  credit  of 
giving  us  many  strange  beliefs,  surprising  mental  exhibitions  and  what 


2(X)  THE    NEURONIC    DISEASES 

seems    almost   like   omnipotent   clairvoyance.      It   is   just   here   where 
genius  unto  madness  becomes  closely  allied. 

The  motor  aurce  consist  of  jerkings,  local  spasms,  trembling, 
twitching  in  one  or  more  limbs.  They  are  very  brief  as  a  rule  and  are 
more  characteristic  of  partial  or  Jacksonian  epilepsy.  Complicated 
coordinated  movements  of  an  automatic  sort  are  occasionally  observed. 

Procursive  epilepsy  is  that  form  in  which  the  patient  runs  forward 
just  before  the  fit.  Some  epileptics  turn  rapidly  around  and  go  around 
in  a  circle.  Gould  and  Pyle  relate  the  case  of  an  epileptic  workman 
who,  upon  one  occasion,  ran  from  Peterboro  to  Whittlessy.  A  patient 
of  Echeverria's  resorted  quickly  to  violent  exercise  on  a  trapeze  to 
control  the  spasms.  A  patient  of  mine  would  jump  up  and  run  around 
the  dinner  table. 

There  are  many  other  premonitory  signs  of  the  disease  classified 
under  the  head  of  irregular  aiircc.  A  sudden  pallor,  general  erythema 
or  spotted  appearance  of  the  skin  may  represent  a  vasomotor  aura. 
Profuse  perspiration  has  introduced  a  fit.  A  case  reported  by  Moyer 
was  wont  to  have  sudden  attacks  of  uncontrollable  sleepiness.  Tliis 
somnolence  has  been  noticed  in  a  number  of  cases. 

Elevation  of  general  and  local  temperature,  and  sphygmographic 
evidence  of  increased  arterial  tension  have  been  observed  during  an 
aura. 

Immediately  succeeding  the  aura  or,  as  in  some  cases,  without  it,, 
the  patient  abruptly  falls  in  a  state  of  complete  unconsciousness.  He 
may  fall  in  any  direction,  though  usually  it  is  forward.  He  may  strike 
any  near  object,  such  as  a  hot  stove  or  sharp  point  and  thus  acquire  a 
wound  that  may  leave  an  ugly  scar.  A  young  woman  patient  of  mine 
was  found  dead,  having  dropped  while  making  the  bed  in  such  a  way 
that  her  throat  and  chin  became  caught  on  the  sideboard  of  the  bed- 
frame  and  she  was  asphyxiated. 

With  the  fall  and  the  sudden  coma  there  is  a  tonic  spasm  or  sudden 
tetanic  stiffening  of  all  the  muscles  of  the  body.  The  teeth  are 
clenched,  the  arms  are  rigid  and  flexed,  the  thumb  is  pressed  tightly 
down  into  the  palm  of  the  hand  and  the  fingers  firmly  flexed  on  top  of 
it,  the  legs  are  stiff  and  flexed  or  extended.  The  limbs  are  not  all 
contracted  in  the  same  way.  The  patient  appears  therefore  contorted 
and  hideously  deformed.  The  trunk  is  twisted  or  arched.  The  head 
is  turned  to  one  side,  the  facial  muscles  drawn  or  distorted,  the  eyes. 
fixed  with  the  lids  closed  or  open  and  the  pupils  immoble,  or  the  eye- 
balls rolled  up  into  the  head,  the  lips  compressed  and  distended  laterally, 
the  cheeks  bloated  and  disfigured  and  the  color  pale  and  cyanotic. 
Frothy  saliva,  mixed  with  blood  if  the  tongue  happens  to  have  been 
caught  between  the  snapping  teeth,  sometimes  oozes  between  the  par- 
tially opened  lips.  The  muscles  of  the  neck  are  rigid  and  marked  in 
outline.  On  account  of  the  spasm  of  the  laryngeal  and  respiratory 
muscles  a  short,  sharp,  piercing  cry,  or  perhaps  only  a  loud  sigh,  is 
heard.  The  breathing  ceases  or  becomes  a  mere  inspiratory  gurgle. 
The  faeces  and  urine  may  be  involuntarily  extruded. 

After  a  few  seconds  or  fraction  of  a  minute  this  first  or  tonic  stage 
is  followed  by  the  second  or  clonic  period.     The  unconsciousness  con- 


THE    NEURONIC    DISEASES 


201 


tinues  or  may  even  clear  up  a  little,  or  may  have  been  only  partial  from 
the  beginning.  The  face  becomes  flushed.  The  muscles  of  the  entire 
body  twitch  and  jerk  forcibly  and  rapidly  in  a  rhythmical  sort  of  a 
way.  On  account  of  this  the  patient  may  be  thrown  violently  about, 
some  of  his  joints  be  dislocated  or  even  a  bone  be  broken.  These 
movements  are  at  times  very  powerful,  symmetrical  and  regular.  The 
jaw  snaps  and  the  tongue,  being  pushed  forward,  causes  the  teeth  to 
lacerate  its  edges.  The  eyeballs  roll  about.  The  rectum,  bladder  and 
seminal  vesicles   may  all   be  evacuated.     The  respiratory   movements 


FIGURE  38. 


Grand  mal  seizure,   with  partial   retention  of  consciousness.      (.After   Spratling.) 


become  heavy  and  sighing.  A'omiting  and  retching  may  occur.  The 
pulse  increases  in  frequency  along  with  the  respirations.  Perspiration 
breaks  out  over  the  whole  body,  and  the  general  appearance  of  the 
patient  shows  a  beginning  relaxation.  The  vise-like  hold  upon  him  in 
the  tonic  stage  is  clearly  letting  go  during  the  clonic  stage. 

Towards  the  end  of  the  clonic  stage,  which  lasts  from  one  to  five 
minutes,  the  muscular  movements  gradually  quiet  down,  cease  entirely 
in  some  muscles  and  in  all  of  them  later  on,  and  the  patient  lies  limp 
and  exhausted.  Sometimics  he  opens  his  eves,  looks  dazed  and  con- 
fused,, and  then  sinks  into  a  profound  slumber :  at  other  times  he  seems 
to  suddenly  regain  complete  consciousness,  but  is  surprised  and  com- 
plains of  an  intense  headache  and  of  feeling  very  tired  and  sleepy. 

Somnolence  mav  last  several  hours  and  constitutes  what  is  some- 


202 


THE    NEURONIC   DISEASES 


times  called  the  third  stage  cf  the  attack.  The  sleep  is  so  natural  and 
physiological  after  such  a  profound  expenditure  of  nerve  force,  while 
the  rest  of  the  patient's  condition  is  so  little  disturbed,  that  the  pro- 
priety of  calling  this  the  third   stage  of  the   paroxysm   mav   well  be 

FIGURE  39- 


The  order  cf  progression  of  attack  in  a  case  m  which  the  initial  spasm — 519 
times  in  succession  in  forty-nine  hours — was  confined  to  the  first  phalanx  of  the 
right  thumb.     (After  SpratHng.) 

questioned.  From  this  sleep  the  patient  usually  wakes  up  refreshed, 
wdth  his  normal  consciousness  completely  restored  and  only  a  slight, 
decreasing  headache  and  possible  soreness  of  the  tongue  indicating  to 
him  that  something  unusual  has  happened. 


THE    NEURONIC    DISEASES  20^ 

Such  is  the  general  sequence  of  events  in  a  typical  grand  mal 
attack.  There  are  variations  upon  this  clinical  picture  that  must  now 
Tdc  noted. 

In  the  tonic  stage  of  the  fit  the  tetanic  rigidity  of  the  muscles  may 
be  so  powerful,  and  the  cessation  of  the  respiration  so  prolonged,  that 
death  will  occur  under  the  most  extraordinary  circumstances.  A 
woman  once  washing  dishes  at  a  sink  mad%^  a  noise  that  attracted 
attention,  and  w^hen  discovered  a  little  while  after  was  found  dead 
rigidly  standing  in  the  same  position.  Relaxation  occurred  after  thev 
laid  her  on  the  floor. 

Sometimes  in  this  stage  a  fine  series  of  fibrillary  contractions  can 
loe  detected  in  the  muscles.  All  muscles  of  the  body  may  not  be  equally 
stiff  and  in  exceptional  cases  only  those  of  one  side  have  been  involved. 
It  is  not  so  very  uncommon,  even  in  the  so-called  idiopathic  types  of 
the  disease,  for  the  spasm  to  begin  in  one  limb  or  on  one  side  of  the 
l>ody.  This  peculiarity,  with  others,  which  indicates  a  close  resemblance 
"between  idiopathic  and  symptomatic  epilepsy,  gives  ground  for  the 
contention  of  Starr  that  epilepsy  is  an  organic  disease  and  that  there 
is  no  such  distinction  as  the  above  betw^een  types.  The  ciliary  muscles 
of  the  eye  are  also  sometimes  included  in  the  spasm   (Knies). 

When  they  can  be  tested  the  reflexes  are  found  to  be  abolished 
during  the  tonic  stage.  They  have  been  seen  to  be  normal  and  even 
exaggerated  but  in  these  cases  the  unconsciousness  and  general  sup- 
pression may  not  have  been  profound.  The  conjunctiva  is  insensitive 
and  the  pupils  are  dilated  and  irresponsive.  The  fundus  oculi  has  been 
observed  to  be  pale,  then  flushed.  Thomsen  and  Oppenheim  have 
shown  that  not  rarely  concentric  contraction  of  the  visual  field  follow'S 
true  epileptic  attacks.  Transient  paralysis,  aphasia  and  dysarthria  may 
immediately  succeed  a  fit. 

The  skin  and  mucous  membrane  may  be  red  in  spots  and  exhibit 
minute  hemorrhagic  extravasations.  After  the  attack  the  urine  may 
be  discharged  in  excessive  amount,  may  contain  an  mcrease  of  urea 
and  some  albumin.  A  slight  elevation  of  temperature  may  be  noted 
during  the  fit.  High  temperature  belongs  to  the  symptomatology  of 
status  epilepticus.  Cases  in  which  there  are  marked  and  persistent 
post-epileptic  phenomena,  such  as  aphasia,  paralysis,  tremor,  conjugate 
deviation  of  the  eyes,  blindness,  deafness,  diarrhoea  and  vomiting, 
should  always  be  regarded  with  a  high  degree  of  suspicion.  True 
epilepsy  may  not  be  the  cause  of  them  but  rather  some  gross  lesion 
such  as  tumor,  thrombosis  or  hemorrhage. 

After  these  grand  mal  attacks  have  once  started  they  tend  to  re- 
appear periodically,  and  increase  in  number  and  severity.  For  a  time 
they  are  nocturnal,  occurring  mostly  in  the  early  hours  of  the  morning 
w^hile  the  patient  is  sleeping  and  the  physical  forces  are  at  their  lowest 
-ebb.  Sometimes  they  take  place  just  after  retiring  at  night.  As  the 
disease  continues  they  appear  in  the  daytime  and  often  cease  at  night. 
Usually  they  are- single  but  two  or  three  attacks  in  succession  may  oc- 
cur the  same  day  or  on  successive  days.  These  serial  attacks  may  be 
so  numerous,  rapid  and  close  together  that  a  condition  of  status  is 
set  up.     Some  patients  have  grand   mal  attacks  every  few  weeks  or 


204  1HE    XF.UROXIC   DISE-.SES 

months,  with  many  fits  of  the  petit  mal  type  in  the  intervals.     Rarely 
a  patient  may  experience  a  fit  only  once  or  twice  in  a  year  or  two. 

A  most  interesting  and  singular  form  of  epilepsy  is  that  which 
appears  in  the  petit  mal  type.  This  is  characterized  by  frequent,  brief 
disturbances  of  the  consciousness,  entirely  unknown  to  the  patient  and 
without  aurge  and  convulsions.  The  attacks  come  on  without  the 
slightest  warning  and  may  occur  several  times  during  the  day.  The 
patient  suddenly  stops  his  work,  becomes  fixed  and  staring  and  seems 
to  be  in  a  profound  condition  of  mental  abstraction.  This  lasts  but  a 
few  seconds  and  when  it  is  past  the  victim  proceeds  with  his  occupa- 
tion just  as  if  nothing  whatever  had  happened.  Bystanders,  however,, 
can  note  the  fixity  of  the  attitude,  the  partial  or  complete  absence  of  the 
consciousness,  the  momentary  cyanosis,  the  strange  appearance  of  the- 
patient  and  even  the  slight  momentary  spasm.  In  rare  cases  there  may 
be  a  feeble  aura  of  some  sort,  or  the  spasm  may  appear  transiently 
without  loss  of  consciousness.  In  other  cases  the  mind  is  not  so  much- 
absent  as  diverted.  The  patient  responds  but  his  answers  are  irrele- 
vant. He  may  stop  in  the  middle  of  a  sentence  and  mumble  words 
about  something  entirely  difterent,  or  he  may  automatically  get  up 
from  his  desk  and  do  something  else.  If  he  is  directing  envelopes,  for 
instance,  he  may  suddenly  awaken  to  discover  that  he  has  directed  an 
unnecessary  number  all  exactly  alike.  In  such  attacks  there  is  usually- 
partial  amnesia,  the  patient  dimly  remembering  that  he  was  doing- 
something  different,  but  what  or  why  he  cannot  understand.  There  is 
an  automatic,  dream-like  state  under  such  circumstances  in  which  the 
suft'erer  may  do  all  sorts  of  queer  things,  such  as  undressing  himself 
in  public,  striking  those  about  him,  walking  oft  of  dangerous  heights- 
and  writing  long  compositions. 

These  states  may  be  prolonged  for  several  days,  vreeks  or  months^ 
enabling  the  patient  to  travel  long  journeys,  transact  elaborate  busi- 
ness and  do  a  lot  of  strange  things,  of  all  of  w^hich  he  has  only  the 
\'uguest  sort  of  remembrance  when  he  suddenly  comes  to  and  finds  him- 
self in  the  midst  of  strange  surrounding  sand  anomalous  positions.  Tlie 
cases  of  so-called  double  consciousress  such  as  that  of  ]\Iary  Reynolds,, 
reported  by  Weir  ^Mitchell,  and  of  lima  S..  studied  by  Kraftt-Ebing^ 
are  of  this  character. 

The  general  mental  state  of  these  patients,  except  when  they  are 
in  the  fit,  is  not  as  a  rule  much  below  the  normal.  In  fact  the  posses- 
sors of  the  most  brilliant  minds  have  sometimes  been  the  victims  of 
both  grand  mal  and  petit  mal  attacks.  Caesar,  ^Mahomet  and  Napo- 
leon are  the  classical  illustrations.  As  a  rule,  hov\-ever,  there  is  apt  to 
be  more  mental  deterioration  among  the  petit  mal  than  among  the 
grand  mal  epileptics.  In  the  former  there  may  be  terrific  outbursts 
of  passion  and  violence,  with  the  commission  of  great  crimes.  A 
veritable  deliriumi  and  mania  may  even  occur,  or  there  may  be  a  pro- 
found dementia.  Instead  of  violence  a  low  cunning  treachery  may  be 
exercised  in  the  attainment  of  their  strange  purposes. 

There  is  an  obvious  medico-legal  interest  surrounding  these  cases. 
The  degree  of  consciousness  or  its  perversion  should,  of  course,  deter- 
mine such  a  patient's  criminal  responsibility.     This  problem  being  so 


THE    XEURO^■IC    DISEASES  205 

-difficult,  one  need  not  feel  surprise  at  the  unfortunate  wrangles  that 
•sometimes  mar  the  court  proceedings  when  so-called  expert  testimony 
ds  being  taken. 

Some  of  these  attacks  are  less  of  the  type  known  as  petit  mal 
than  they  are  instances  of  what  are  known  as  the  psychic  equivalents 
-of  epilepsy. 

The  whole  question  of  epileptic  equivalents  is  still  under  discus- 
-sion.  By  the  term  is  meant  something  that  is  not  so  much  like  an 
-epileptic  fit  as  that  it  is  a  substitute  for  it,  equivalent  in  value,  force, 
meaning,  compensation,  etc.  J\Iost  writers  recognize  the  existence  of 
'epileptic  equivalents,  though  jMagnan,  Le  Grand  du  Saulle,  Tomlin- 
son  and  others  deny  them.  The  psychic  equivalents  do  certainly  at 
'times  seem  more  like  states  of  insanity,  perhaps  post-epileptic  insan- 
ity. The  propriety  of  characterizing  these  states  as  epileptic  is  doubt- 
ed for  the  reason  that  when  they  are  not  associated  with  typical  fits 
they  are  rarely  if  ever  so  characterized  but  are  then  looked  upon  as 
-distinct  psychoses  or  pure  mental  disorders.  However,  as  epilepsy  is 
in  some  respects  so  largely  a  mental  manifestatioii,  it  is  not  easy  to 
deny  that  a  psychosis  ma}'  be  truly  of  epileptic  origin.  Hence  for  the 
-present,  at  least,  it  will  be  well  to  speak  of  the  epileptic  equivalents, 
-especially  those  in  the  psychic  sphere. 

Spratling  desires  to  keep  a  sharp  distinction  between  true  psychic 
•epilepsy  and  the  psychic  epileptic  equivalents.  The  distinction  rests 
'upon  the  presence  or  absence  of  other  epileptic  signs  such  as  the  motor 
disorders. 

Among  the  equivalents,  the  psychic  always  far  outnumbering  all 
the  others,  may  be  mentioned  the  absences,  the  strange  acts,  the  in- 
decent exposures,  the  mild  manias,  such  as  nymphomania,  klepto- 
Tnania,  etc.,  certain  phobias  and  obsessions  involving  unprovoked  as- 
saults, automatic  laughter,  a  form  of  angina  pectoris,  diaphragmatic 
spasm,  sleep  states,  asthmatic  affections,  spasm  of  the  glottis,  nocturnal 
pollution,  certain  forms  of  pertussis,  neuralgias,  migraines,  the  hunger 
•evil,  sudden  outbreaks  of  perspiration,  verbigeration,  etc. 

There  is  such  a  thing  as  reflex  epilepsy  but  not  in  the  sense  of 
the  old  writers.  A  dormant  epileptic  condition  may  be  aroused  into 
activity  by  various  exciting  peripheral  irritants,  but  a  true  epilepsy 
■can  hardly  be  attributed  to  the  mere  excitation  produced  by  such  peri- 
pheral disturbances.  In  a  person  predisposed  it  is  conceivable  that 
•a  phimosis,  a  cervical  uterine  scar,  a  mass  of  intestinal  parasites,  a 
nasal  polyp,  a  pharyngeal  adenoma,  an  accumulation  of  wax  in  the 
-ear,  and  muscular  anomalies  of  the  eye,  may  be  the  cause  of  initiating 
the  attacks.  To  say  that  such  conditions  can  be  the  cause  of  epilepsy 
in  non-predisposed  individuals  would  have  to  be  followed  by  an  ex- 
planation, before  the  assertion  could  be  accepted,  as  to  why  more  suf- 
ferers from  these  common  conditions  do  not  have  epilepsy,  and  why 
in  those  that  do  have  epilepsy  from  this  condition  there  are  always 
iound  the  great  predisposing  factors  of  heredity,  degeneracy,  intoxi- 
•cation  or  trauma. 

Oppenheim  notes  that  binding  a  limb  on  which  there  is  a  peri- 
pheral cicatrix  will  often  check  an  epileptic  fit.     The  same  thing  will 


206  THE    XEUROXIC   DISEASES 

often  occur,  however,  in  so-called  simple  idiopathic  epilepsy  without 
any  stich  peripheral  irritant.  The  scar  in  such  a  case  may  indeed  be 
a  sort  of  epileptogenous  zone,  but  that  does  not  establish  it  as  the 
sole  or  prime  cause  of  the  disease. 

I  find  there  is  not  a  little  confusion  in  the  minds  of  some  of  the 
profession  between  partial,  or  Jacksoiiian  epilepsy,  and  what  is  called 
symptomatic  epilepsy. 

Every  form  of  local  convulsion  is  not  partial  epilepsy.  It  may  not 
be  epilepsy  at  all  but  merely  epileptiform.  In  a  way  it  may  be  physio- 
logical rather  than  pathological,  for  it  may  represent  the  normal  over- 
action  of  a  vigorous  and  healthy  sensory-motor  apparatus  to  an  ex- 
ternal source  of  constant  irritation.  So-called  symptomatic  epilepsy 
is  therefore  but  a  convulsive  symptom  of  the  disease  of  which  it  is. 
declared  to  be  symptomatic.  A  compressing  lesion  of  the  foot,  say^ 
causing  pains  and  spasms  in  the  area  of  the  nerves  caught  in  the  lesion 
does  not  necessarily  cause  those  pains  and  spasms  to  be  symptoms  of 
a  nervous  disease.  This  is  an  important  distinction  to  bear  in  mind 
when  speaking  of  partial,  or  Jacksonian,  epilepsy.  This,  unlike  mere 
symptomatic  epileptiform  manifestations,  is  a  true  nervous  or  cere- 
bral disease  and  is  epilepsy.  It  may  originate  remotely  from  the  irri- 
tation, disturbed  circulation  or  other  influence  from  an  extra-neural 
growth  or  lesion  of  some  sort.  Gradually,  however,  a  local  change  is 
set  up  by  this  extra-neural  influence  so  that  the  pathological  basis  of 
a  true  epilepsy  is  established.  This  change  may  remain  local,  more 
often  it  spreads  throughout  the  entire  cortex. 

The  great  characteristic  of  Jacksonian  epilepsy,  therefore,  is  its 
local  distribution,  either  during  the  entire  fit  or  at  its  commencement. 
The  sensory'  or  motor  phenomena  begin  in  one  arm  or  leg,  one  fin- 
ger or  side  of  the  face,  then  increase  with  or  without  the  loss  of  con- 
sciousness through  the  entire  epileptic  cycle.  This  is  not  a  mere  aura, 
though  it  may  partake  of  the  nature  of  one  if  the  fit  passes  into  a 
general  one  involving  the  mind  and  body,  as  in  the  ordinary  grand  mal 
type.  It  is,  in  the  purely  local  cases,  the  epilepsy  itself.  Hence  we 
see  the  propriety  of  the  term  partial  epilepsy. 

As  I  have  said  it  may  remain  partial  and  be  free  of  any  asso- 
ciated disturbance  of  the  mind.  In  most  cases,  however,  the  loss  of 
consciousness  comes  on,  somewhat  more  slowly  than  in  the  grand  mal 
seizures  of  the  idiopathic  type,  and  then  the  patient  experiences  the 
typical  generalized  convulsive  seizure.  The  pre-eminent  fact  in  re- 
gard to  it  is  that  the  localization  of  the  phenomenon  never  changes. 

These  cases  are  usually  followed  by  more  or  less  persistent  local 
physical  defects  such  as  paresis,  parassthesise,  aphasia,  etc. 

Their  causes  are  numerous  and  may  be  purely  local  or  general. 
Among  those  that  have  been  enumerated  I  may  instance  injuries  to 
the  skull  involving  the  brain,  cerebral  hemorrhage  with  its  pathological 
sequelae,  thrombus,  embolus,  syphilitic  meningitis,  tumor,  alcoholic  ex- 
cess, old  cicatrices  and  visceral  sources  of  irritation.  This  does  not 
exhaust  the  list  but  indicates  a  few  ways  in  which  the  cortical  cells 
may  be  rendered  epileptogenetic. 

There  has  always  been  a  discussion  among  writers  as  to  whether 


TtlE    NEURONIC    DISEASES  20/ 

simple  tonic  or  clonic  convulsions  alone  can  constitute  epilepsy.  Prich- 
ard  described,  in  1822,  a  violent  and  powerful  form  of  epileptic 
seizure  in  which  a  tetanic  state  of  the  muscles  occurred.  These  cases 
are  rare,  fortunately  so,  for  they  are  very  fatal.  It  seems  to  me  that 
Prichard  described  simply  an  exceptionally  severe  type  of  grand  mal 
in  which  death  occurred  during  the  prolongation  of  the  tonic  stage, 
and  before  the  appearance  of  the  clonic  stage. 

The  myoclonus-cpilepsy,  described  by  Unverricht  in  189 1,  is  an 
association  disease  or  trouble  like  h}stero-epilepsy,  choreic  epilepsy, 
etc.  The  two  diseases  may  run  together  in  the  same  patient,  with 
alternation  or  combination  of  the  symptoms.  The  association,  how- 
ever, does  not  constitute  a  new  disease  or  special  type  of  either.  Occa- 
sionally the  disease  is  really  one  thing  with  a  mere  resemblance  in 
some  of  its  phenomena  to  the  other.  Hystero-epilepsy,  for  instance, 
is  usually  hysteria  whose  outbreaks  resemble  at  times  epileptic  seiz- 
ures. It  serves  no  useful  purpose,  and  is  only  confusing,  to  establish 
new^  diseases  or  even  new  types  of  mere  associated  or  similarly  appear- 
ing affections. 

Much  stronger  is  the  ground,  if  types  are  to  be  noted,  for  sepa- 
rating status  epilepticiis  as  a  special  form  of  the  disease.  Clark  de- 
fines it  as  the  maximum  development  of  epilepsy  in  which  one 
paroxysm  follows  another  so  closely  that  the  coma  and  exhaustion  are 
continuous  between  seizures.  Sooner  or  later  there  is  a  marked  eleva- 
tion of  temperature,  pulse  and  respiratory  movements,  with  profound 
exhaustion  and  death. 

Status  occurs  most  frequently  in  the  grand  mal  type  of  the  disease 
and  partakes  of  all  the  features  of  the  disease  except  in  regard  to  the 
special  points  above  noted. 

To  treat  it  as  a  separate  disease  with  its  own  etiology,  pathology, 
symptoms  and  treatment  is  quite  unnecessar}-.  It  is  a  culmination  of 
epilepsy  and  is  distinguished  by  differences  of  degree  rather  than  kind. 
The  patient  remains  continuously  unconscious.  The  muscles  appear 
to  be  almost  continuously  convulsed.  The  temperature  may  rise  to  109 
degrees  F.  and  even  recovery  occur,  as  in  a  case  reported  by  Spratling 
at  the  Craig  Colony. 

About  half  the  cases  that  attain  the  condition  of  status  die. 

Among  the  sequeke  of  epileptic  convulsions  are  to  be  noted  the 
scars  upon  the  tongue  and  about  the  face  and  body,  extensive  burns, 
fractures,  dislocations,  hemorrhagic  extravasations,  exhaustion,  paraly- 
ses, elevation  of  body  temperature  and  certain  changes  in  the  blood 
and  the  circulation.  Some  of  these,  especially  the  apparent  increase 
of  toxicity  in  the  blood  and  elevation  of  the  blood  pressure,  need  fur- 
ther investigation. 

The  mental  sequelce  of  single  and  multiple  epileptic  seizures  is 
always  a  matter  of  great  anxiety  to  the  patient  and  his  family.  It 
would  not  seem  reasonable  to  expect  so  profound  a  disturbance  of  the 
cerebral  functions  to  continue  long  without  some  deterioration  of  the 
mental  faculties.  Depression,  mistrust,  irritability,  melancholia,  and 
increased  emotionalism  are  usually  noticeable  in  these  patients.  The 
mental  condition  may  get  no  worse  than  this,  and  may  indeed  even 


2o8  THE    MLURONIC  DISEASES 

seem  to  be  not  in  the  least  affected  for  years.  Later  on  the  memory 
grows  weaker,  amnesia  occurs,  the  intelHgence  becomes  blunted,  more 
or  less  stupidity  supervenes  and  ultimately  simple  dementia  appears. 
Hypochondriasis  is  often  -present.  The  mental  deterioration  charac- 
teristic of  the  disease  I  am  convinced  has  been  too  often  charged  to 
the  use  of  bromine. 

When  the  disease  occurs  in  childhood  the  mental  results  are  for 
obvious  reasons  much  more  disastrous.  Imbecility  and  idiocy  are  espe- 
cially liable  to  occur.  All  forms  of  the  disease  without  distinction  are 
responsible  for  the  lowering  of  the  intelligence.  Some  have  thought 
that  there  was  more  danger  in  this  respect  in  the  petit  mal  than  in  the 
grand  mal,  but  it  is  to  be  remembered  that  the  petit  mal  type  of  the 
trouble  is  almost  always  entirely  psychical.  It  represents  as  it  were 
a  considerable  degree  of  mental  degeneracy  in  itself. 

As  bearing  on  the  treatment  it  is  to  be  noted  that  sometimes  epi- 
leptic seizures  are  followed  by  a  disappearance  of  a  certain  amount 
of  stupor  and  mental  indifference.  I  have  long  taught  in  my  lectures 
that  it  is  not  always  wise  or  safe  to  suppress  completely  and  perma- 
nently the  fits  even  when  that  is  possible.  Occasionally  an  epileptic 
who  shows  himself  amenable  and  responsive  to  treatment  is  better  off 
for  a  fit  now  and  then. 

Diagnosis.  Epilepsy  is  usually  easily  diagnosed.  In  doubtful 
cases  it  should  never  be  hastily  decided.  The  longer  a  case  is  ob- 
served the  more  the  diagnosis  becomes  conclusive.  It  is  when  the  dis- 
ease is  first  discovered,  and  when  it  is  wanting  in  some  typical  mani- 
festation, that  the  diagnosis  sometimes  becomes  problematic.  For  this 
reason  and  because  of  the  serious  prognosis  attending  the  disease,  the 
physician  will  do  well  to  rarely  make  a  positive  diagnosis  until  he  has 
been  able  to  watch  the  patient  in  one  of  his  attacks.  The  laity  are  so 
easily  misled,  being  untrained  and  excitable,  that  it  is  never  wise,  ex- 
cept possibly  in  certain  very  obvious  instances,  to  risk  a  diagnosis  upon 
the  description  of  friends  or  relatives.  The  earlier  it  is  in  the  disease 
and  the  more  atypical  the  account  of  it  seems  to  be,  the  more  impera- 
tive is  it  that  the  diagnostician  should  see  the  fits  for  himself,  or 
should  place  the  patient  where  he  can  be  under  the  continual  observa- 
tion for  a  time  of  a  trained  assistant.  Under  such  circumstances  every 
detail,  however  insignificant  it  may  seem  to  be,  should  be  made 
not  e^  of. 

The  presence  and  character  of  the  aurse  should  receive  the  most 
scrutinizing  attention,  for  the  very  nature  of  the  disease  and  its  source 
may  be  indicated  in  the  aura.  Then  the  mode  of  onset  should  be  care- 
fully observed.  Tliis  will  include  the  relative  period  at  which  the 
unconsciousness  took  place,  its  depth  and  duration ;  the  location  of 
the  first  convulsive  manifestation,  its  extension  over  the  rest  of  the 
body,  its  tonic  and  clonic  character,  its  duration  and  its  mode  of  dis- 
appearance ;  the  state  of  the  pupils ;  the  condition  of  the  eyes ;  the 
strength  and  frequency  of  the  respirations  and  pulse  beat ;  the  cyanosis, 
followed  by  flushing  of  the  skin;  the  involuntary  evacuations  of  the 
bowels  and  bladder. 

The  character  of  the  after  effects  will  in  some  cases  help  to  estab- 


THE    NEURONIC    DISEASES  209 

lish  the  diagnosis.  They  are  the  return  to  a  dazed  and  surprised  state 
of  consciousness,  the  headache,  the  profound  exhaustion,  the  transient 
paralyses,  local  muscular  soreness  and  even  slight  mental  aberration. 

In  every  suspected  case  of  epilepsy,  whatever  the  type,  look  for 
some  disturbance  of  the  consciousness.  This  is  undoubtedly  the  car- 
dinal symptom  of  genuine  epilepsy.  It  may  be  the  sole  symptom,  as  in 
some  cases  of  petit  mal,  psychic  epilepsy  and  the  psychic  equivalents 
of  the  disease.  It  is  even  detectable  in  the  cases  of  partial  or  Jackso- 
nian  epilepsy  in  which  the  motor  manifestations  may  be  almost  over- 
whelmingly dominant. 

Note  the  character  of  the  disturbance  in  every  particular  and  the 
order  of  its  progression  for  it  is  pathognom.onic  of  the  disease  and 
is  never  exactly  the  same  as  it  is  in  other  diseases.  If  it  is  accompanied 
by  the  convulsions  and  other  usual  symptoms  of  a  fit,  the  diagnosis 
is  absolutely  easy  and  certain. 

A  good  deal  is  written  about  the  fades  epileptica.  Many  epileptics 
show  in  their  faces  the  indications  of  a  degenerative  heredity,  as  I  have 
often  pointed  out  to  my  classes.  They  also  exhibit  scars  acquired  by 
falls  and  injuries  sustained  in  previous  attacks.  They  may  even  re- 
veal the  facial  acne  from  the  overuse  of  the  bromides.  All  of  this, 
however,  is  of  no  very  great  value  in  the  matter  of  diagnosis  for  with 
such  conditions  present  the  case  is  apt  to  be  a  pronounced  and  ad- 
vanced one,  and  doubtless  already  easily  diagnosed  from  the  other 
symptoms.  As  the  typical  facies  epileptica  is  not  an  early,  sudden 
acquisition,  but  rather  the  result  of  a  slow  development,  it  cannot  as- 
sist us  much  at  that  period  in  the  disease  when  such  assistance  is  most 
needed,  and  when  the  diagnosis  of  the  disease  is  of  the  supremest  im- 
portance. 

There  are  a  number  of  conditions  in  which  mental  and  motor 
disturbances  occur,  with  which  an  epileptic  attack  is  capable  of  being 
confused.  They  are  hysteria,  alcoholism,  drug  intoxication,  syncope, 
urjemic  poisoning,  cerebral  apoplexy,  general  paresis,  vertigo,  tetanus 
and  simulation. 

The  differentiation  between  hysteria  and  epilepsy  is  at  times  a 
matter  of  great  importance  and  difficulty.  There  are  convulsive  seiz- 
ures sometimes  in  hysteria  so  like  those  of  epilepsy  that  for  a  long 
time  they  were  studied  apart  under  the  name  of  hystero-epilepsy.  The 
one  manifestation  that  can  be  absolutely  relied  upon  tO'  establish  the 
distinction  is  the  pupillary  reaction.  In  hysteria  this  is  not  lost  as  it 
invariably  is  in  epilepsy.  Hysteria  being  a  psychosis  primarily  the 
whole  complexion  of  the  case  is  dominated  by  the  mentality  of  the  pa- 
tient ;  in  epilepsy  the  mental  disturbance  is  the  result  of  a  frank  cerebral 
lesion  and  is  therefore  often  accompanied  by  marked  localization  phe- 
nomena. In  other  words  the  mental  side  of  the  picture  and  a  certain 
suggestiveness  of  active  volition  are  more  noticeable  in  hysteria, 
whereas  in  epilepsy  the  convulsions  or  motor  phenomena  and  appear- 
ance of  complete  absence  of  volition  stand  prominently  forth.  The 
suddenness  of  the  attack,  the  initial  cry,  the  involuntary  twitchings, 
the  injury  from  the  fall,  the  involuntary  evacuations,  the  subsequent 
exhaustion,   stupor,   headache   and   somnolence  all   point   to   epilepsy. 


210  THE    NEURONIC   DISEASES 

Hysterics  do  not  injure  themselves  by  falling  unconscious  nor  do  they 
often  bite  their  tongues.  Involuntary  micturition  practically  never  oc- 
curs in  hysteria.  Hysterics  yell  and  cry  and  toss  themselves  about  and 
complain  of  pains  and  develop  their  attacks  at  the  time  of  day,  early 
evening,  when  they  are  likely  to  be  observed.  Their  attacks  are  longer 
in  duration  than  those  of  epileptics  and  are  sometimes  amenable  to 
sharp  suggestion.  Their  symptoms  vary  during  the  attack  and  have 
prominently  among  them  sensory  phenomena. 

The  mental  criteria  are  of  some  value  as  hysterics  are  usually 
keen  and  intelligent,  whereas  epileptics,  especially  of  long  standing, 
are  dull,  somnolent  and  even  demented.  The  facies  epileptica  is  not 
exhibited  by  hysterics  nor  do  they  ever  have  the  post-epileptic  paraly- 
sis, hemorrhagic  extravasations,  wounds,  mental  confusion  and  auto- 
matism that  epileptics  often  show.  They  never  develop  a  temperature 
of  a  degree  or  two,  such  as  occurs  in  the  epileptic.  On  the  other  hand 
they  recover  promptly,  pass  large  quantities  of  urine  after  the  attack 
and  assume  an  entirely  different  manner  when  the  causes  of  the  initia- 
tive emotion  out  of  which  the  attack  grew  are  removed.  A  motive 
lurks  behind  many  outbreaks  of  hysteria,  and  as  the  attack  is  thus 
somewhat  in  the  sphere  of  volition,  painful  pressure  upon  the  ovaries, 
threats  of  discomfort  and  objectionable  manoeuvres  will  often  bring 
a  hysterical  convulsion  to  an  abrupt  termination. 

The  coma  of  acti.te  alcoholism  is  not  so  complete  as  it  is  in  epilepsy 
and  there  are  no  typical  convulsive  movements.  The  odor  of  the 
breath,  the  flushed  face,  the  maudlin  semidelirious  state,  and  the  ab- 
sence of  most  of  the  characteristic  symptoms  of  epilepsy,  such  as  the 
pallor,  the  tu'rned-up  eyes,  the  bloody  frothing  at  the  mouth,  the  rigid 
condition  of  the  muscles,  etc.,  all  distinguish  the  one  disease  easily 
from  the  other. 

Urcemic,  dnig  and  lead  intoxication  are  to  be  distinguished  by 
the  usual  history  of  disease  in  other  organs,  of  drug-taking  and  occu- 
pation in  lead. 

Syncope  occurs  in  feeble  individuals  and  under  special  surround- 
ing conditions  such  as  an  over-heated  room,  shock,  over-exertion. 
Heart  disease  is  often  present.  Syncope  is  wanting  in  the  usual  signs 
of  epilepsy,  such,  as  the  aura,  the  muscular  spasm,  the  initial  moan, 
the  evacuations  and  the  usual  sequelae  of  stupor,  headache  and  somno- 
lence. The  faintings  come  and  go,  several  in  succession,  like  a  soft 
zephyr  without  causing  much  disturbance  in  the  patient's  attitude. 

The  paralytic  symptoms,  the  history  of  the  onset,  the  action  of  the 
pupils,  the  respiration,  the  duration  of  the  coma,  with  the  absence  of 
many  of  the  symptoms  of  epilepsy,  will  help  to  distinguish  the  cerebral 
apoplexia  from  the  latter. 

Aural  vertigo,  or  Meniere's  disease,  is  accompanied  by  aural  symp- 
toms such  as  tinnitus  and  deafness. 

In  the  early  stages  of  dementia  paralytica  the  convulsions  are  apt 
to  be  unilateral,  and  not  accompanied  by  a  loss  of  consciousness.  There 
are  other  well-known  symptoms,  such  as  the  tremor,  the  emotionalism, 
the  eye  symptoms,  that  enable  us  to  recognize  general  paresis. 

However,  it  is  to  be  remembered  that  in  general  paresis,  tumor. 


THE    NEURONIC    DISEASES  211 

cerebral  syphilis,  nephritis  and  arteriosclerosis  the  epileptiform  con- 
vulsions are  more  apoplectic  and  symptomatic  than  are  the  evidences  of 
genuine  epilepsy.  Therefore,  always  search  well  for  the  symptoms  of 
these  diseases  and  regard  the  convulsions  as  wholly  one  of  these  symp- 
toms. In  other  words,  the  examination  is  not  so  much  to  determine  the 
differential  diagnosis  between  an  idiopathic  and  symptomatic  epilepsy, 
so-called,  as  it  is  to  determine  the  diagnosis  of  the  disease  of  which 
the  epileptiform  manifestation  constitutes  one,  and  perhaps  a  minor, 
evidence. 

In  tetanus  there  is  generally  a  history  of  an  injury,  and  the  jaws 
are  characteristically  locked. 

Simulation  sometimes  causes  quite  a  little  trouble.  To  escape 
punishment  for  a  crime,  or  to  win  large  damages  from  a  railroad  or 
other  corporation,  are  two  powerful  motives  to  tempt  cunning  persons 
to  study  and  imitate  epilepsy.  Usually  their  detection  is  easy,  but  I 
have  seen  the  fraud  so  skillfully  practiced  that  the  shrewdest  exam- 
iners were  deceived. 

If  closely  watched  a  simulator  will  omit  or  perform  wrongly  some 
one  manifestation  among  the  many  that  he  has  to  remember.  For 
instance  he  will  not  close  his  thumb  down  and  clench  it  beneath  his 
fingers,  or  he  will  forget  the  cry,  or  fail  to  bite  his  tongue.  His  re- 
flexes will  be  lively,  especially  his  pupillary  reactions.  He  will  ex- 
hibit no  scars,  no  hemorrhagic  extravasations,  no  petechial  spots. 
There  will  be  no  involuntary  evacuations,  nor  will  he  suffer  afterwards 
with  an  exhaustion  paralysis,  a  stupor  and  prolonged  somnolence.  His 
body  temperature  will  not  rise.  He  will  tend  to  overdo  the  part  and 
elaborate  symptoms  that  should  be  kept  in  abeyance,  or  make  little 
of  those  that  should  be  very  prominent.  Without  seeing  the  patient, 
so-called,  I  detected  a  very  cunning  simulator  once  in  a  long  hypothet- 
ical question  constructed  to  correspond  with  the  case,  because  one  part 
of  the  clinical  picture  did  not  harmonize  with  another  part,  whereas  if 
each  had  been  presented  alone  without  the  other  the  deception  would 
have  been  much  harder  to  detect. 

Mairet  emphasizes  the  importance  of  a  urinary  analysis.  The 
toxicity  of  the  urine  is  said  to  be  decreased  after  the  attack,  and  ren- 
dered hypotoxic  in  the  intervals  of  true  epilepsy. 

Spratling  points  out  that  a  simulator  can  reproduce  the  tonic  bet- 
ter than  he  can  the  clonic  contraction. 

Heller  has  suggested  that  the  thigh,  for  instance,  be  firmly  grasp- 
ed, and  in  a  simulator  the  muscles  will  relax  or  be  immediately  con- 
tracted again  if  an  attempt  is  made  to  flex  the  limb. 

Finally  the  simulator  cannot  cause  the  loss  of  the  knee-jerk  and 
ankle  clonus,  which  occurs  after  a  severe  epileptic  attack. 

Prognosis.  There  is  so  much  uncertainty  about  the  course  and 
termination  of  epilepsy  that  it  is  risky  to  assert  an  opinion.  It  may 
contmue  for  years  and  the  patient  die  of  some  other  disease,  such 
as  pulmonary  tuberculosis.  On  the  other  hand  it  may  suddenly  de- 
velop into  the  dangerous  and  fatal  condition  of  status.  Some  patients 
have  attacks  only  once  or  twice  a  year,  others  have     them     several 


212  THE    NEURONIC  DISEASES 

times  a  day.  Often  they  appear  in  a  series  of  several  attacks  during 
several  days  and  then  there  will  be  none  for  a  considerable  time. 

It  is  not  usual  for  the  attacks  to  remain  always  of  the  same  type. 
They  tend  as  a  rule  to  increase  gradually  in  frequency  and  severity. 
In  the  more  common  form  of  the  trouble  the  early  attacks  will  be 
nocturnal  and  for  that  reason  long  unrecognized.  They  will  then  be 
discovered,  by  the  roommate  of  the  patient,  and  if  he  is  not  told  of 
them,  may  continue  as  nocturnal  and  unknown  to  him.  Usually,  how- 
ever, attacks  begin  to  appear  in  the  daytime  along  with,  or  instead  of, 
the  nocturnal  ones.  They  occur  in  the  grand  mal  form  about  every 
two  or  three  months  and  several  times  in  the  interval  in  the  petit  mal 
form.    The  minor  fits  may  occur  many  times  a  day. 

There  is  always  danger  of  accidental  death  in  a  seizure.  Falls 
may  result  in  fracture  of  the  skull,  severe  and  extensive  burns,  chok- 
ing and  asphyxia  by  compression  of  the  throat  from  extraordinary 
position,  drowning  and  in  a  hundred  other  ways. 

Continuously  nocturnal  attacks  are  more  dangerous  than  diurnal 
because  they  occur  more  frequently  in  feeble  persons  and  overtake  the 
individual  when  his  vital  forces  are  at  their  lowest. 

Though  the  immediate  danger  to  life  in  epilepsy  is  not  great,  it  is 
nevertheless  a  serious  disease.  While  not  so  often  killing  the  patient 
directly,  it  greatly  jeopardizes  his  existence  by  the  numerous  fatal  pos- 
sibilities it  surrounds  him  with.  Tuberculosis  of  the  lungs  terminates 
a  considerable  number  of  cases.  Status  epilepticus  comes  next  as  a 
cause  of  the  fatal  issue.    About  half  of  the  cases  of  status  die. 

Sudden  death  in  a  fit  may  be  due  to  rupture  of  the  heart,  passage 
of  food  from  the  stomach  into  the  trachea,  asphyxia  from  position, 
sudden  paralysis  of  the  respiratory  center  and  a  prolonged  tetanic  con- 
vulsion. 

Spratling  furnishes  the  followmg  ratios :  Of  every  one  hundred 
epileptics  who  die,  about  four  do  so  as  the  result  of  a  single  seizure ; 
twenty-four  as  the  result  of  status ;  twenty-four  as  the  result  of  some 
lung  disease,  chiefly  tuberculosis ;  twelve  as  the  result  of  accident  in- 
cluding suffocation  in  bed ;  ten  as  the  result  of  some  organic  heart 
trouble ;  and  about  twenty-six  from  all  other  causes. 

Epilepsy,  apart  from  its  fatalities,  always  tends  to-  shorten  life. 
Early  cases  rarely  pass  beyond  middle  life.  Later  cases  may  continue 
into  old  age.  De^th  is  not  the  worse  thing  to  be  dreaded  by  an  epilep- 
tic. The  terminal  dementia ;  the  occasional  maniacal  attacks ;  the  out- 
bursts of  emotion  and  rage  with  the  commission  of  crime :  are  possi- 
bilities that  death  might  beneficently  forestall.  The  petit  mal  and 
psychic  epilepsies  are  particularly  to  be  regretted  and  guarded  on  this 
account. 

The  question  of  the  cure  of  epilepsy  is  just  now  undergoing  a 
lively  discussion.  A  hundred  years  ago  or  so  the  prognosis  in  this 
respect  was  much  better  than  it  is  to-day.  The  cures  were  rated  then 
even  as  high  as  fifteen  per  cent.  It  is  not  improbable  that  sympto- 
matic and  other  amenable  forms  of  the  disease  entered  into  the  making 
of  these  very  favorable  statistics.     Perhaps  more  attention  of  a  dis- 


THE    XFUROXIC    DISEASES  2I3 

ciplinary  and  hygienic  sort  was  given  to  the  patient  then  than  now, 
as  the  use  of  the  bromides,  undoubtedly  overdone  now,  was  unknown. 

On  the  other  hand  there  are  many  to-day  who  regard  epilepsy  as 
an  absolutely  incurable  disease.  Such  a  pessimistic  view  is  hardlv 
justifiable.  The  term  cure  has  a  varied  significance  and  while  a  res- 
toration back  to  a  condition  of  perfect  normality  would  perhaps  be  a 
Utopian  dream,  a  cessation  of  the  fits  for  years,  and  a  gradual  return 
to  a  better  state  of  mind  is  certainly  to  be  regarded  in  the  light  of  a 
cure. 

If  under  the  enlightened  modern  treatment  of  the  disease  with 
bromides  and  hygienic  measures,  and  especially  with  the  aid  of  the 
colonization  method,  all  epileptics  could  be  rigidly  controlled,  and  if  all 
the  cases  that  improve,  then  wander  away  and  never  seek  for  further 
medical  advice,  could  be  gathered  together,  I  am  sure  a  set  of  tables 
could  be  constructed  showing  statistically  a  much  more  hopeful  out- 
look for  the  cure  of  the  disease.  It  certainly  is  not  an  absolutely  in- 
curable trouble  and  the  percentage  of  restorations,  roughly  and  yet 
conservatively  estimated  under  modern  treatment  as  about  five  per 
cent,  is  enough  to  warrant  the  attempt  in  every  case  that  offers  the 
slightest  degree  of  favorable  indication. 

It  would  be  a  happy  hit  if  we  could  always  determine  just  which 
class  of  cases  are  the  most  amenable  to  treatment.  Turner  and  oth- 
ers declare  that  senile  epilepsy  is  essentially  a  tractable  disease.  The 
least  favorable  cases  are  those  that  begin  under  ten  years  of  age.  If 
arrest  occurs  between  the  fifteenth  and  twentieth  years  the  outlook  is 
particularly  favorable.  The  chances  for  a  cure  then  steadily  decrease 
with  the  advancing  years  but  after  thirty-five  the  intractable  cases 
again  begin  to  diminish. 

Spratling  says  if  there  is  a  difference  in  the  curability  of  the 
two  sexes,  he  is  inclined  to  think  that  it  favors  the  male  side.  Contrary 
to  the  opinion  held  by  some  high  authorities,  the  same  author  finds  that 
the  influence  of  the  catamenia  and  marriage  is  not  good  but  rather 
the  reverse.  The  attacks  have  been  unaltered  in  the  least  in  most  of 
the  cases ;  in  a  few  of  them  they  have  been  increased  in  both  frequency 
and  severity. 

As  is  well  known  the  grand  mal  type  of  the  disease  is  more  sus- 
ceptible of  treatment  than  is  the  petit  mal,  and  the  diurnal  than  the 
nocturnal.  Acquired  and  inherited  mental  weakness  renders  the  out- 
look less  hopeful  in  all  forms  of  the  trouble.  The  previous  duration  of 
the  disease  will  also  determine  the  patient's  future  chances.  The  re- 
moval of  certain  exciting  causes,  such  as  alcohol,  syphilis,  local  mal- 
adies and  reflex  sources  of  irritation  may,  if  done  early,  diminish  or 
even  stop  entirely  the  attacks,  with  all  further  progress  of  the  disease. 

Spontaneous  recoveries  have  been  reported  but  they  are  so  rare 
as  hardly  to  be  taken  into  the  consideration  of  the  prognosis.  The 
strong  tendency  of  the  disease  is  always  to  perpetuate  itself. 

The  probability  of  imbecility  and  idiocy  should  always  be  kept  in 
mind  in  connection  with  infantile  epilepsy. 

Treatment.  Some  one  has  uttered  the  paradox  that  the  way 
to  cure  epilepsy  is  to  stop  the  fits.     This  is  one  of  those  half-truths 


214  THE    XEUROXIC   DISEASES 

which  when  Hved  strictly  up  to  often  do  incalculable  harm.  Were 
the  fits  the  whole  of  epilepsy,  such  an  aphorism  mig'ht  establish  good 
therapeutics.  Unfortunately  we  are  learning  more  and  more  that 
epilepsy  is  a  deep-seated,  continuous,  obstinate  disease  of  the  brain, 
of  which  certain  outbursts  of  a  periodical  sort  constitute  but  one  of 
many  evidences.  To  stop  the  fits  merely  is,  therefore,  not  the  great- 
est good  to  be  obtained  from  treatment.  It  does  not  in  itself  cure  the 
disease.     In  some  cases  it  has  actually  done  harm. 

Ever}-  case  of  epilepsy,  viewed  from  the  therapeutic  standpoint, 
consists  of  two  elemental  factors,  the  disease  proper,  and  its  violent 
exhibition  in  the  fits.  The  latter  are  the  outgrowth  of  the  former  and 
dependent  upon  it.  By  reacting  upon  a  diseased  and  weakened  nervous 
system,  the  frequent  violence  of  the  fits  may  undoubtedly  increase  the 
nervous  weakness  and  underlying  epileptogenous  state. 

All  treatment  of  epilepsy  therefore  must  direct  itself  to  checking 
the  fits  and  to  restoring  the  diseased  nervous  system.  It  must  be  both 
fundamental  and  symptomatic,  general  and  specific,  prophylactic  and 
alterative — in  a  word  it  must  attack  the  trouble  at  its  source  and  it 
must  restrain  it  in  its  violent  outbursts. 

Any  line  of  treatment  that  confines  itself  to  one  or  the  other  of 
these  two  sides  of  the  picture  will  surely  fail  of  attaining  the  best  re- 
sults. The  administration  of  the  bromides  to  svippress  the  convulsions, 
to  the  exclusion  of  all  other  treatment  of  the  patient  as  a  victim  of  a 
profound  general  disease,  is  as  unscientific  and  illogical  as  it  would  be 
to  neglect  the  fits  entirely  and  to  try  and  cure  him  by  attacking  the 
general  underlying  condition. 

The  superior  results  of  institutional  and  colonization  treatment 
over  those  generally  obtained  in  private  practice  are  due  to  the  fact 
that  in  the  latter,  for  obvious  reasons,  medicinal  control  of  the  fits  merely 
takes  precedence  over  the  general  hygienic,  pedagogic,  disciplinary  and 
tonic  measures,  whereas  in  the  former  it  is  just  the  reverse. 

It  is  a  platitude  to  state  that  the  first  step  in  the  treatment  of 
every  case  of  epilepsy  is  to  make  a  thorough  search  for,  and  remove, 
every  possible  source  of  irritation.  This  is  absolutely  necessary  in 
every  case  no  matter  what  may  be  its  heredity,  its  previous  duration 
or  its  type.  Nothing  that  is  abnormal  about  the  patient,  and  that  can 
be  removed  or  remedied,  should  be  allowed  to  pass.  To  mention  all 
the  possible  abnormalities  would  require  an  enumeration  practically  of 
all  the  diseases,  medical  and  surgical,  to  which  the  human  body  is 
liable.  Every  organ,  every  tissue,  every  function  should  be  closely  in- 
terrogated and  if  found  to  be  wrong,  should  be  righted  as  far  as  it 
is  in  the  power  of  modern  science  to  do  so.  When  this  is  done  the  fits 
Avill  diminish  and  ameliorate  in  a  certain  proportion  of  cases.  This 
is  the  mirage,  however,  towards  which  many  sincere  and  skillful  in- 
vestigators have  been  beguiled  w^hen  announcing  to  the  world  that 
epilepsy  is  due  to  certain  organic  peripheral  defects  and  that  they  have 
cured  it  by  removing  those  defects. 

Operations  upon  the  eyes,  nose  and  sexual  organs  have  all  been 
heralded  as  cures  for  the  disease.  Sooner  or  later,  however,  the  fits 
have  returned  in   spite  of  the  operations,   showing  that  the  reputed 


THE    XEUROXIC    DISEASES  21 5 

cure  was  nothing  but  a  temporary  relief,  not  even  a  permanent  ameliora- 
tion. 

All  hope  of  curing  the  disease  by  thus  removing  mere  peripheral 
excitants  shows  a  lamentable  misconception  of  its  true  central  patho- 
g'enic  basis.  The  eye-strain,  the  nasal  polyp,  the  tapeworm,  the  phimo- 
sis, the  constipation,  or  any  other  abnormal  condition,  must  be  re- 
moved as  promptly  as  possible.  It  will  not  cure  the  disease  but  it  will 
remove  possibly  an  excitant  of  an  epileptic  central  nervous  system  and 
so  cause  a  diminution  in  the  number  and  severity  of  the  fits. 

The  basis  of  epilepsy  is  a  cortical  change.  If  there  is  no  change  in 
the  cortex  and  the  fits  are  but  a  sort  of  a  Round-Robin-Hood  reflex 
manifestation  from  a  peripheral  excitation,  I  regard  the  epileptiform 
phenomenon  in  such  a  state  of  affairs  as  physiological  rather  than 
pathological.  It  is  not  true  epilepsy  though  it  may  be  highly  epilep- 
tiform. 

It  is  obvious  that  the  proper  wearing  of  glasses,  the  excision  of 
old  cicatrices,  the  extraction  of  an  ulcerated  tooth,  will  put  a  stop  to 
the  reflex  convulsive  phenomenon.  Xay  more,  if  done  early  it  may 
thus  even  be  said  to  cure  epilepsy,  in  some  few  cases,  prophylactically, 
for  it  is  undoubtedly  true  that  the  continuation  of  such  a  severe  form 
of  reflex  action  does  sometimes  set  up  an  epileptic  habit  in  the  cor- 
tical cells,  which  may  go  on  to  the  development  of  the  typical  degen- 
erative condition  which  underlies  the  true  disease. 

It  is  never  a  trivial  matter  therefore  to  remove  these  various  ab- 
normalities in  epilepsy;  it  is  trivial  to  regard  the  amelioration  caused 
by  such  removal  as  a  cure  of  the  disease. 

Where  a  patient  can  best  be  treated  is  a  question  that  always  pre- 
sents itself.  This  cannot  be  answered  until  after  many  factors  have 
been  taken  into  consideration.  If  the  disease  is  of  a  light  form  and 
the  patient's  intelligence  is  good  he  may  get  along  well  enough  at  home. 
Cases  that  first  appear  in  adult  life,  after  the  mind  has  developed,  as 
a  rule  do  not  need  removal  from  home  so  much  as  those  that  appear 
in  childhood  and  in  which  the  mind  is  likely  to  be  most  seriously  af- 
fected. 

In  general  it  may  be  said  that  most  epileptics,  young  or  old,  are 
better  oft  away  from  their  old  haunts  and  companionships  where  they 
are  neglected,  continually  looked  upon  as  peculiar  and  are  able  to 
constantly  draw  invidious  comparisons  between  their  own  unfortunate 
state  and  that  of  their  friends  and  relatives.  Institutions  and  colonies, 
and  private  sanitaria,  when  properly  conducted,  afford  the  best  re- 
treat for  them.  Here  their  food,  exercise,  bathing,  work  and  amuse- 
ments can  be  regulated  and  systematized  while  they  themselves  can 
be  protected  from  doing  themselves  or  others  harm  if  an  insane  fit 
should  suddenly  overtake  them. 

If  insanity  complicates  the  case,  of  course  removal  to  an  asylum  is 
absolutely  imperative,  and  though  the  insanity  may  be  only  tempo- 
rary it  is  better  for  the  patient  to  remain  there  in  case  it  should  un- 
expectedly reappear.  Even  the  mentally  weak  epileptics  are  undoubt- 
edly better  off  in  an  institution. 

The  absolute  control  of  the  patient  by  the  physician  is  a  sine  qua 


2l6  THE    XEUROMC   DISEASES 

)wn  to  any  degree  of  success  in  the  treatment,  and  this  alone  estab- 
Hshes  the  superiority  of  institution  over  home  management. 

Colonies,  such  as  those  at  Bielefeld,  in  Germany;  Chalfont,  St. 
Peter,  near  London,  and  Craig  Colony,  at  Sonyea  in  New  York  State, 
are  growing  in  popular  and  scientific  estimation.  The  home-life,  the 
preserv^ation  of  his  individuality,  the  absence  of  the  competitions,  ex- 
citements, allurements  and  comparisons  incident  to  urban  and  subur- 
ban normal  life,  and  the  sympathetic  con-ipanionship  and  uniformity 
of  avocations  here  secured  cannot  but  exert  a  better  influence  upon  the 
patient.  His  invalidism  is  less  emphasized  in  the  midst  of  such  sur- 
roundings and  his  entire  mode  of  life  and  treatment  is  under  closer 
supervision.  He  is  educated  intellectually  and  physically,  trained  in 
the  use  of  tools,  set  to  do  attractive  tasks,  and  in  every  way  encour- 
aged to  regard  himself  as  a  useful  and  responsible  member  of  the  com- 
munity. This  is  wholesome  upon  the  mind  and  so  checks  one  of  the 
saddest  possibilities  of  epilepsy,  namely,  the  mental  deterioration. 

All  epileptics  need  outdoor  exercise.  This  is  forcibly  demon- 
strated, as  Spratling  says,  by  the  records  at  Craig  Colony,  showing  a 
less  aggregate  number  of  fits  in  summer  than  in  winter,  and  less  among 
men  than  among  women.  The  outdoor  exercise  must  be  systematic  and 
non-exhausting.  Gardening,  farming  and  tending  cattle  are  espe- 
cially commendable.  I\Iild,  unemotional  indoor  games  and  occupa- 
tions are  to  be  encouraged. 

Marriage,  for  obvious  reasons,  had  better  be  discouraged  among 
epileptics.  Alcohol,  tobacco  and  other  dissipations  can  be  given  up. 
Spratling  says  that  in  some  cases  he  has  known  smoking  to  bring  a 
calm  that  the  individual  stood  in  need  of. 

The  dietary  of  an  epileptic  needs  supervision  in  only  a  few  par- 
ticulars. It  should  be  simple  and  include  the  breadstufts,  milk,  but- 
ter, fruits  and  cereals.  Eggs  are  good  but  meats  should  be  indulged 
in  sparingly.  Seeded  berries,  cake,  pastrv,  condiments,  pork,  veal, 
ham  and  grease-fried  foods,  alcohol,  tea  and  coffee,  .should  be  avoided. 
Regular  meals  and  abundance  of  easily-digested  food  should  be  the 
rule.    The  stomach  must  not  be  overloaded. 

The  omission  of  sodium  chloride  from  the  diet  of  the  patient  is 
the  latest  suggestion  that  seems  to  have  proved  beneficial  in  a  large 
number  of  cases. 

Climatic,  hydrotherapcitfic  and  electrical  treatment  can  only  affect 
the  disease  indirectly  by  upbuilding  the  general  constitution. 

The  medicinal  treatment  of  epilepsy  is  very  old  and  consequently 
boasts  of  a  long  list  of  remedies.  Some  of  these  are  still  used,  though 
they  are  probably  without  influence  upon  the  disease.  Others  mod- 
ify the  disease  indirectly  either  by  acting  as  general  tonics,  suppress- 
ing the  nervous  excitability,  or  influencing  the  circulation.  We  have 
no  remedy  that  will  make  over  the  degenerated  cortical  cells  into  nor- 
mal healthy  organs.  We  can  only  affect  their  abnormal  function,  ap- 
parently not  their  histological  structure.  .  If,  however,  we  can  check 
their  excessive  expenditure  of  nerve  force,  we  may  be  able  to  put  them 
in  such  a  state  of  quietude  that  they  can  catch  up,  as  it  were,  in  their 
self-nutritive  processes  and  this  in  the  course  of  time  Vvill  restore  them 


THE    NEURONIC   DISEASES  21/ 

to  a  more  or  less  normal  condition  histologically.  It  is  only  within  re- 
cent years  that  the  medicinal  treatment  of  epilepsy  has  been  correctly 
appreciated,  put  upon  a  sound  basis  and  afforded  the  most  desirable 
results. 

As  we  are  ignorant  of  the  minute  cellular  changes  upon  which  the 
epileptic  phenomena  depend,  and  as  we  only  know  that  certain  medic- 
inal agents  seem  to  have  the  power  of  suppressing  these  phenomena, 
without  knowing  how  they  do  it,  their  administration  is  regulated  by 
the  changes  produced  by  them  on  the  fits.  In  other  words  the  medic- 
inal treatment  of  epilepsy  is  purely  a  symptomatic  treatment,  and 
the  chief  end  of  our  efforts  by  these  m.eans  is  the  suppression  or 
diminution  of  the  paroxysms. 

This  statement  of  course  does  not  apply  to  the  use  of  general  ton- 
ics like  iron  and  quinine,  nor  to  the  use  of  remedies  directed  against 
particular  constitutional  conditions  like  syphilis,  malaria,  alcoholism, 
and  other  forms  of  intoxication  and  infection.  And  it  will  have  to  be 
modified  if  in  the  future  it  should  be  discovered  that  toxaemia  plays 
the  chief  role  in  the  disease,  and  serotherapy  is  established  on  a  posi- 
tive scientific  basis. 

In  the  control  of  the  paroxysms  sometimes  immediate  measures 
are  wholly  or  partially  successful.  These  of  course  are  only  appli- 
cable when  there  is  a  distinct  aura  of  sufficient  duration.  Patients 
can  carry  about  with  them  the  small  glass  pearls,  each  containing  three 
minims  of  nitrite  of  amyl,  and  when  they  feel  an  attack  coming  on, 
can  quickly  break  one  in  the  handkerchief  and  inhale  the  vapor.  A 
small  bottle  containing  a  bit  of  cotton  saturated  with  the  nitrite  can 
be  quickly  uncorked  and  the  contents  inhaled.  It  is  supposed  that  this 
flushes  the  brain  with  a  rush  of  blood,  or  at  least  relaxes  the  vasomotor 
spasm  of  the  cerebral  ch'culation  upon  which  the  paroxysm  is  hypo- 
thetically  believed  by  som^e  to  depend.  At  all  events  it  is  so  often  ef- 
fective in  abating  attacks  that  it  is  wise  for  all  patients  to  carry  the 
drug  and  use  it  if  they  have  time  to  do  so. 

When  the  aura  begins  in  a  limb,  an  old  and  sometimes  success- 
ful manoeuvre  is  to  suddenly  constrict  the  limb  with  a  tight  band. 
Many  patients  wear  a  strap  continuously  and  so  arranged  that  they 
can  quickly  draw  it  tight  them.selves.  Strong  flexion,  extension  or 
traction  on  a  limb  may  be  tried. 

Cutaneous  stimulation  with  a  dash  of  cold  water,  tickling,  pinch- 
ing, rubbing  and  slappmg  is  also  sometimes  available.  Two  or  more 
epileptics  can  travel  together  and  serve  each  other  in  this  way. 

Chloral  hydrate  in  hypnotic  dosage,  or  a  teaspoonful  of  common 
salt,  may  abort  an  attack, 

According  to  Fancher  and  Spratling  a  few  cases  have  been  checked 
by  the  hypodermatic  injection  of  i-io  or  1-15  of  a  grain  of  apomor- 
phine.    Vomiting  will  probably  follow  but  that  often  occurs  in  epilepsy. 

Brown-Sequard,  Bravais,  Hirt  and  Buzzard  have  attempted  to 
abort  the  seizures  by  maintaining  a  permanent  blister  about  the  limb. 

It  is  always  to  be  remembered  that  many  patients  are  better  for 
having  a  seizure,  and  hence  it  is  not  always  desirable  to  check  it.     If 


2l8  THE    NEURONIC   DISEASES 

they  are  somnolent,  stupid,  subject  to  headache  and  distressed  in  feel- 
ing after  the  abortion  of  the  fit,  it  had  better  not  be  checked  next  time. 

In  all  cases  it  may  be  said  that  the  aborting-  of  attacks  does  not 
modify  the  disease,  and  is  only  commendable  on  the  grounds  of  per- 
sonal comfort  and  the  avoidance  of  the  possible  accidents.  These,  how- 
ever, are  reduced  to  a  minimum  by  having  the  patient  under  constant 
surveillance. 

When  the  attack  has  occurred  there  is  not  much  to  be  done,  ex- 
cept to  guard  against  accidents.  The  clothing  should  be  loosened,  a 
piece  of  cork  or  rolled-up  rag  should  be  placed  between  the  teeth  to 
prevent  biting  of  the  tongue,  the  general  attitude  should  be  arranged 
so  that  if  vomiting  occurs  food  will  not  slip  into  the  trachea,  and  the 
patient  placed  where  he  can  sleep  after  the  paroxysm  is  past. 

In  status  epilepticus  rectal  injections  of  chloral  hydrate,  forty- 
five  to  sixty  grains,  or  amylen  hydrate,  five  to  eight  grains,  should  be 
tried.  Morphine  is  generally  useless  though  it  may  be  used  in  combi- 
nations. 

The  following  emergency  formula  is  highly  recommended  for 
status  by  Clark : 

I^     Tr.  opii  deoderat.  m.  v. 

Potass,  bromid.  gr.  xxv. 

Chloral  hydrat.  gr.  xx. 

Liq.  morph.  sulph.  (U.  S.  3j. 

Sig. — One  dose ;  repeat  in  two  hours  if  necessary. 

If  these  remedies  fail  to  modify  the  attack,  bloodletting  should  be 
resorted  to.  The  condition  is  desperate  and  the  remedy  must  necessa- 
rily be  heroic. 

Of  all  the  remedies  employed  to  control  the  fits  the  bromides  still 
continue  to  enjoy  the  highest  favor.  They  were  introduced  as  anti- 
epileptic  remedies  by  Laycock  over  half  a  century  ago,  and  though 
they  have  been  much  abused  and  even  when  carefully  employed  do 
not  constitute  an  ideal  therapy,  they  are  the  best  medicinal  agents  that 
we  possess.  Their  mode  of  action  is  quite  unknown  and  their  ad- 
ministration must  always  be  empirical.  On  this  account  there  is  even 
to-day,  after  these  long  years  of  trial,  much  diversity  of  opinion  as 
to  how  they  should  be  used. 

As  drug  treatment  is  necessarily  so  predominant  in  the  home 
treatment  of  epilepsy,  the  abuse  of  the  bromides  is  observed  more  in 
private  than  in  institutional  practice.  As  a  rule  the  remedy  is  given 
in  too  large  quantities,  it  is  pushed  after  it  has  demonstrated  its  in- 
effectiveness, and  it  is  not  administered  in  proper  time  relationship  to 
the  expected  paroxysm.  Moreover,  when  it  is  found  to  be  effective 
and  well  borne  it  is  not  continued  long  enough. 

There  are  a  number  of  bromide  salts  that  are  available,  though  in 
my  own  experience,  as  well  as  in  that  of  others,  the  potassium  salt  is 
in  the  long  run  the  most  useful.     Some  physicians  prefer  the  use  of 


THE    XEUROXIC    DISEASES 


219 


a  single  salt,  others  a  combination  of  two  or  three  of  them.  The 
potassium,  sodium,  ammonium  and  lithium  bromides  may  be  used  in 
this  way,  the  relative  dosage  varying  according  to  the  idiosyncrasv  of 
the  patient  and  the  predilection  of  the  prescriber.  Strontium  bromide 
is  said  to  disturb  the  stomach  the  least.  Calcium  bromide,  gold  bro- 
mide, zinc  bromide,  bromium  and  camphor  monobromate  are  other 
eligible  preparations  that  may  be  tried  when  those  first  mentioned  fail. 
As  a  rule  these  will  fail,  too,  but  in  a  disease  that  is  so  obstinate  one 
is  glad  at  times  to  have  something  to  ring  the  changes  on. 

The  bromides  may  be  used  alone  or  in  combination  with  other 
remedies  to  be  mentioned. 

Two  cardinal  rules  are  to  be  observed  when  thev  are  resorted  to. 
The  one  is  to  use  them  in  the  best  way,  and  in  only  such  quantitv  as 
will  check  the  fit.  The  other  is  to  continue  them,  when  found  to  be 
-effective,  for  a  year  or  more  in  spite  of  the  absence  of  all  symptoms. 

The  average  case  takes  from  a  dram  to  a  dram  and  a  half  a  dav. 
This  may  be  administered  in  several  small  doses  or,  better  still,  in  one 
large  dose  timed  so  that  the  maximum,  effect  of  the  bromide  will  cor- 
respond with  the  hour  of  the  expected  fit. 

^^'hen  stopping  the  use  of  the  bromides  it  is  never  safe  to  with- 
draw them  all  at  once ;  this  has  occasionally  precipitated  a  condition 
■of  status. 

Xo  rule  can  be  set  down  for  the  administration  of  these  prepara- 
tions, as  the  greatest  success  is  obtained  in  studying  carefully  their 
effect  upon  each  individual  case. 

•Dilute  them  largely  with  water;  do  not  administer  them  within 
an  hour  before  or  after  meals:  give  them  to  the  point  of  tolerance: 
prepare  the  largest  dose  about  five  or  six  hours  before  the  expected 
iit,  whether  it  be  nocturnal  or  diurnal ,  continue  the  remedy  for  one  or 
two  years :  withdraw  it  gradually :  and  employ  it  with  the  expectation 
•of  the  best  results  in  grand  mal,  and  the  least  favorable  results  in  petit 
inal  and  psychic  epilepsy. 

Such  are  the  main  points  to  be  remembered. 

Certain  accidents  are  to  be  avoided  in  the  use  of  the  bromides.  Of 
these  the  gastric  disturbances  and  the  facial  acne  are  especially  unfor- 
tunate. Sometimes  these  can  be  avoided  by  the  administration  of 
iron  and  arsenic  during  the  course  of  the  bromides.  2\Iitchell  has  seen 
irritability,  melancholia  at  menstruation,  bad  temper,  suicidal  or  hom- 
icidal tendencies  and  temporary  delusions  produced  by  them.  They 
-do  undoubtedly  depress  the  mental  faculties  :  so  does  the  disease  for 
which  they  are  administered.  It  is  not  always  assumable,  therefore, 
that  every  case  of  mental  deterioration  during  a  course  of  bromism  is 
the  result  of  the  medicine. 

In  the  hypochlorization  method  of  Toulouse  and  Richet  the  pa- 
tient's food  is  salted  with  bromide  of  sodium  instead  of  chloride  of 
sodium.  It  is  said  that  ten  grains  of  the  salt  given  in  this  way  is 
equal  in  eft'ect  to  twentv  grains  given  in  the  usual  way.  The  method 
is  worth  trying  in  some  cases,  though  it  is  not  always  successful. 

Spratling   commends  highly     bromipin,   especially   in     feeble   or 


220  THE    NEURONIC  DISEASES 

asthenic  cases,  in  children,  and  for  hypodermic  use  in  status  epilepticus. 
For  ordinary  administration  he  recommends  the  following  formula : 

I^     Bromipin  qIv. 

Syrup,  simp.  §iv. 

Spts.  menth.  pip.  3iv. 

Mucil.  acacije  ad  o^'^'j- 

Sig. — One  to  one  and  a  half  ounces,  for  adults,  three  times  a  day^ 

after  meals. 

It  does  not  affect  the  gastro-intestinal  canal ;  does  not  produce 
acne;  and  does  not  cause  abscess  when  given  hypodermically. 

Opium  has  long  been  tried  in  the  treatment  of  epilepsy  but  it 
has  not  retained  popular  favor.  Lately  it  has  been  used  again  but  in. 
combination.  In  1893  Flechsig  formulated  a  treatment  with  opium 
and  the  bromides.  For  six  weeks  mild  opium  narcosis  is  maintained.. 
The  drug  is  then  suddenly  withdrawn  and  the  bromide  substituted  irt 
doses  of  120  to  130  grains  daily,  and  continued  for  two  months.  The 
latter  is  then  gradually  reduced  and  maintained  at  about  30  grains  a 
day. 

The  plan  is  of  doubtful  efficacy  and  its  dangers  are  not  insignifi- 
cant. In  my  own  experience,  though  limited,  it  was  not  superior  to 
the  use  of  the  bromides  alone. 

After  the  bromides  there  are  two  remedies  about  equally  divided 
in  popular  favor.  They  arc  atropine  and  borax.  Either  one  may  be 
given  in  combination  with  the  bromides.  Small  doses  are  tO'  be  em- 
ployed in  the  beginning,  and  gradually  increased  until  tolerance  is  ob- 
tained. Both  may  be  continued  for  a  long  time.  The  extract  of  bella- 
donna may  be  used  instead  of  the  alkaloid.  The  conjunctivitis  and 
eczema  that  are  liable  to  occur  after  the  prolonged  use  of  borax  are 
best  combated  with  arsenic.  Its  cumulative  tendency  seems  to  give 
rise  to  persistent  attacks  of  furunculosis  and  this  militates  somewhat 
against  its  use. 

The  bromides  have  also  been  used  in  conjunction  with  antipyrin^ 
digitalis,  adonis  vernalis  and  chloral  hydrate. 

Ethylene  bromide  in  doses  of  one  or  two  minims  two  or  three  times 
a  day.  in  emulsion  or  capsule,  seems  to  have  been  effective  in  a  number 
of  cases  in  controlling  the  fits. 

Amylene  hydrate,  in  from  a  half  to  two  dram  doses  daily,  was 
extensively  tried  by  Weber.  Only  five  per  cent,  of  the  cases  responded 
favorably  to  it,  and  these  were  disturbed  in  general  health  and  made 
drowsy,  sluggish  and  dyspeptic  by  it.  It  may  sometimes  act  better 
than  chloral  in  cases  of  status  epilepticus. 

Nitroglycerin  in  minute,  frequently  repeated  doses  may  act  happily 
in  senile  epilepsy  where  there  is  marked  arteriosclerosis. 

Zinc  is  a  historical  but  not  much  used  remedy  nowadays.  Ure- 
thane  in  doses  of  twenty  to  forty-five  grains  has  been  commended  by 
Jacobi  and  Spratling.  Chloretone  acts  somewhat  like  the  Flechsig 
treatment.  According  to  Weeks,  it  should  be  pushed  as  rapidly  as 
possible.     About  six  grains  three  times  a  day  is  the  proper  dose  for 


THE    XEUROXIC    DISEASES  221 

prolonged  usage.  Solanum  carolinense  (fluid  extract,  o^A  to  oj  t.  i.  d.). 
and  simulo  (tincture  oij  to  oiij  t.  i.  d.),  have  had  their  advocates.  Thev 
are  useful  sometimes  when  the  bromides  cannot  be  tolerated,  are  com- 
paratively harmless  and  are  therefore  always  open  to  trial.  Trional  has 
been  tested  and  found  to  be  useless.  Tlie  coal  tar  derivatives,  anti- 
pyrine,  phenacetine  and  acetanilid,  affect  the  heart  and  fail  to  affect 
the  epilepsy. 

In  a  small  proportion  of  cases  continuous  chloroform  narcosis 
may  be  a  dernier  ressort.  It  cannot  be  relied  upon,  however.  The 
■employment  of  electricity,  hydrctherapeutics  and  other  general  meas- 
ures, except  for  their  general  constitutional  effect,  shows  a  want  of 
appreciation  of  the  true  nature  of  epilepsy. 

The  valerianates,  aniline  sulphate,  silver  nitrate,  asafoetida,  calabar 
l)ean,  camphor,  cannabis  indica,  chloralamid,  conium,  copper-am- 
monio-sulphate.  duboisine,  gaduol,  hyoscyamine.  ignatia,  str\-chnia, 
lobelia,  paraldehyde,  phosphorus,  physostigma,  picrotoxin,  rue,  san- 
tonin, sodium  fluoride,  spermine,  stramonium  tincture,  sulphonal, 
stunbul  and  many  others  constitute  a  list  of  remedies  that  ma}-  be  tried 
when  the  usual  medicines  fail.  These  will  doubtless  fail,  too,  but  their 
administration  may  be  useful  for  the  constitutional,  tonic  or  psychic 
effect  while  other  more  general  measures  are  being  put  into  force. 

Bacterial  products,  serum  therapy  and  other  measures  to  produce 
immunity  and  to  combat  the  toxaemia  are  being  experimented  with  by 
those  who  believe  in  the  intoxication  and  autointoxication  theory  of 
the  disease.     So  far  the  results  have  not  been  very  encouraging. 

Surgery  for  the  relief  of  epilepsy  is  more  especially  applicable  in 
so-called  symptomatic  epilepsy.  Cranial  depressions,  spicule  of  bone, 
old  cicatrices,  cortical  cysts,  meningeal  thickenings  and  other  cranial 
and  cerebral  abnormalities  should  always  lead  to  the  question  of 
trephining.  The  draining  of  an  abscess  may  put  a  stop  to  the  disease. 
I  have  seen  the  fits  stopped  for  a  long  time  by  the  simple  operation  of 
trephining  in  a  case  of  multiple  abscess  discovered  during  the  operation. 

According  to  Sachs  and  Gerster  symptomatic  epilepsies  that  have 
•existed  for  more  than  three  years  do  not  offer  a  very  promising  out- 
look from  operative  procedure.  The  more  recent  the  injury  the  better 
the  prospect  for  ultimate  recovery  from  surgery. 

Surgical  measures  are  often  called  for  m  the  removal  of  some 
peripheral  source  of  irritation  that  may  be  keeping  up  a  reflex  type  of 
the  disease.  I  have  elsewhere  stated  that  all  such  excitants  must  be 
removed,  if  possible,  in  every  case. 

The  use  of  the  seton  in  the  nuchal  region,  the  ligation  of  the 
carotid  and  vertebral  arteries  and  the  extirpation  of  the  sympathetic 
■ganglia,  are  among  the  historical  and  curious  relics  of  the  surgical 
treatment  of  epilepsy. 

HE^IIC:^ANIA.     ]\IIGRAIXE. 

This  is  a  paroxysmal  neurosis,  periodical  and  epileptiform  in  char- 
acter, in  which  headache  and  other  special  sensory  symptoms  constitute 
the  prominent  feature.     If  it  were  a  mere  headache,  its  classification 


222  THE    NEURONIC   DISEASES 

would  fall  in  the  following"  section  and  be  subject  to  the  same  criticisnx 
made  there  in  regard  to  all  forms  of  cephalalgia.  Some  authorities 
regard  it  as  a  special  disease  entity.  In  deference  to  their  views  and  on 
account  of  the  uncertainty  of  our  knowledge  as  to  its  exact  pathology, 
it  may  be  wise  for  awhile  yet  to  devote  to  its  discussion  a  special  chap- 
ter. I  place  it  here,  however,  because,  as  I  will  show  later  on,  I  believe 
it  is  most  intimately  related  to  epilepsy,  is  possibly  a  sensory  epileptic 
equivalent  of  a  special  type  and  should  be  considered  under  the  general 
head  of  epilepsy. 

Etiology. — No  fact  is  more  patent  in  the  etiology  of  migraine  than 
that  it  is  an  inherited  trouble.  The  inheritance  may  run  through  severat 
generations  and  be  either  direct  or  indirect.  How  frequently  we  are 
told  by  the  victims  of  this  disease  that  their  father  or  grandfather  suf- 
fered from  similar  attacks  of  headache !  They  often  volunteer  the  in- 
formation that  they  have  a  brother  or  a  sister  who  is  also  afiflicted  with 
it.  The  maternal  ancestry  may  also  have  been  subject  to  it,  though 
it  has  seemed  to  me  that  direct  heredity  was  less  prominent  on  the 
maternal  than  on  the  paternal  side.  Gowers  asserts  that  in  more  than 
half  the  cases  distinct  heredity  can  be  traced  and  that  usually  it  is  direct. 
An  indirect  inheritance  is  not  unconimon  and  usually  consists  of  a 
strong  neuropathic  taint.  This  may  come  from  either  side  of  the  house 
and  may  have  sprung  out  of  ancestral  dissipation,  excessive  mental 
work  or  some  related  nervous  disease.  Epilepsy,  hysteria,  mild  psycho- 
ses, neuralgia,  gout,  asthma,  paroxysmal  cardiac  troubles  are  among- 
the  diseases  noted  in  the  family  history. 

Given  this  inherited  neuropathic  constitution,  it  is  obvious  how  the 
exciting  causes  of  migraine  may  be  both  numerous  and  varied. 

All  unwonted  strains,  whether  mental,  nervous  or  physical,  may 
start  up  an  attack.  A  great  emotion,  fright,  prolonged  mental  labor, 
anxiety  and  worr}^  will  cause  it.  One  of  the  worst  sufferers  I  ever 
treated  was  a  young  girl,  whose  father,  now  dead,  had  had  the  disease, 
who  was  attempting  to  finish  a  college  course  during  the  absence  of 
her  lover  to  whom  she  expected  soon  to  be  married,  and  with  the  con- 
tinual presence  of  her  mother,  who  was  an  ignorant,  self-opinionated, 
nagging  woman.  Only  the  strictest  seclusion  in  a  hospital  for  a  time 
saved  the  girl  from  what  almost  threatened  to  be  complete  mental 
breakdown. 

Peripheral  reiiex  excitants  may  provoke  an  exacerbation  of  the 
disease.  Masturbation,  coitus,  hypertrophy  of  the  nasal  mucous  mem- 
brane and  working  in  overheated  rooms  have  been  blamed  for  it. 

Autointoxication,  with  or  without  obstipation,  is  believed  by  many 
to  be  a  most  important  factor  in  the  etiology. 

Peripheral  diseases  and  deformities  may  well  play  a  role  in  exciting- 
it.  Eye-strain  in  one  predisposed  to  the  trouble  is  just  as  much  a  cause, 
no  more,  no  less,  than  might  be  disease  of  the  sexual  organs.  Ansemia, 
overlactation  and  other  depressing  influences  will  aggravate  it.  It 
has  occurred  in  connection  with  diabetes  and  chronic  nephritis. 

The  similarity  between  the  etiology  of  migraine  and  that  of  epilepsy 
is  ver\'  impressive.  It  is  an  inherited  neuropathic  condition,  a  high 
degree  of  nervous  instability  upon  which  an  innumerable  list  of  ex- , 


THE    NEURONIC   DISEASES  223 

citants,  chemical,  physical  and  functional,  operates  to  provoke  an 
exacerbation  or  paroxysm. 

Weir  Mitchell  has  lately  compared  the  atmospheric  storm  curve 
with  the  headache  curve  and  finds  a  relationship.  March  and  April  are 
the  worst  months,  October  and  February  the  best. 

Pathology  and  Pathogenesis. — There  are  no  discoverable  char- 
acteristic anatomical  changes  in  hemicrania.  This  fact  stands  as  an 
unanswerable  argument  against  all  theories  in  which  this  neurosis  is 
attributed  always  and  solely  to  a  reflex  irritation.  If  hemicrania  is 
due  to  eye-strain,  then  eye-strain  must  always  be  found,  with  the  ac- 
companying anatomical  defect,  in  all  cases  of  the  disease. 

As  a  matter  of  fact,  there  is  no  pathology  knowm.  A  neuropathic 
condition  of  the  central  nervous  system  is  assumed  on  account  of  the 
heredity  and  other  suggestive  phenomena,  while  the  exciting  anatomical 
and  physiological  causes  of  the  outbreaks  of  the  disease  are  both  obvi- 
ous and  numerous. 

Where  so  little  is  known,  theorizing  is  always  rife.  Of  all  the 
pathogenetic  explanations  of  the  disease,  two  only  are  worthy  of  special 
consideration.  The  first  is  that  hemicrania  is  but  a  form  of  epilepsy ; 
the  other  is  that  it  is  the  expression  of  a  vasomotor  disturbance  due 
to  disease  of  the  sympathetic  nervous  apparatus. 

It  seems  to  me  that  if  any  reliance  is  to  be  placed  upon  compari- 
sons at  all,  the  etiology,  symptoms,  course,  occasional  complications 
and  other  manifestations  associated  with  migraine  point  most  clearly 
to  its  relationship  with  epilepsy.  The  heredity  in  the  disease,  the  de- 
pendence of  the  outbreaks  upon  exciting  causes,  the  periodicity  that 
occurs  in  these  outbreaks,  their  onset,  progression,  sudden  termination 
and  sequela  are  so  strongly  epileptiform  that  if  they  are  not  epilepsy, 
no  two  phenomena  ever  came  so  near  being  alike  while  yet  being  unlike. 
The  only  dift'erence  between  epilepsy  and  hemicrania  is  that  the  former 
is  characterized  by  prominent  motor  symptoms,  while  the  latter  is 
almost  wholly  sensory.  This,  however,  is  only  an  apparent  and  not  a 
real  difference. 

In  epilepsy  of  the  petit  mal  and  psychic  type  motor  symptoms  are 
often  wanting,  while  in  hemicrania  it  sometimes  happens  that  slight 
motor  phenomena  can  be  observed.  To  be  sure,  the  mental  disturbance 
is  the  cardinal  feature  in  all  epilepsies ;  but  in  hemicrania  the  mind  is 
very  often  seriously  affected.  This  is  seen  in  the  amnesia,  aboulia, 
aphasia,  irritability,  want  of  attention  and  stupor,  which,  however, 
never  or  very  rarely  passes  into  the  complete  unconsciousness  observed 
in  epileptic  fits.  The  sensory  character  of  migraine  is,  if  anything, 
confirmatory  in  part  of  its  epileptic  nature  in  view  of  the  more  recent 
conception  of  the  pathogenesis  of  epilepsy.  The  latter  is  by  most 
modem  pathologists  now^  believed  to  be  primarily  a  sensory  disease. 
The  sensory  elements  of  the  cortex  have  been  found  to  show  certain 
chromatolytic  changes.  A  toxic  degenerative  condition  attacking  these 
sensory  elements  causes  them  to  manifest  the  early  signs,  aura,  etc., 
of  the  fit.  Their  close  connection  with  the  motor  elements  is  the 
explanation   of  the   severe   secondary   spasms  and   convulsions.      The 


224  THE    NEURONIC  DISEASES 

severity  and  wide  extent  of  the  nerve  storm  accounts  for  the  profound 
coma. 

In  hemicrania  a  somewhat  similar  succession  of  events  takes  place, 
but  milder  in  degree.  There  are  the  sensory  prodromic  intimations, 
then  the  nen^ous  explosion,  which,  however,  does  not  overflow  into  the 
motor  elements  to  the  same  extent  that  it  does  in  grand  mal,  and 
finally  the  sudden  cessation  with  more  or  less  lingering  sequelae. 

The  outward  exhibition  of  the  two  diseases  being  thus  so  much 
alike,  it  is  but  fair  to  assume  that  there  is  a  similarity  in  the  underlying 
pathology,  whatever  that  may  ultimately  prove  to  be.  In  epilepsy 
the  process  is  generally  accepted  to  be  located  in  the  cortex.  In  mi- 
graine it  is  probably  cortical  also. 

On  account  of  the  prominence  of  the  headache  and  of  the  gastric 
symptoms,  some  hold  that  the  maximum  foci  of  the  disturbance  are 
localized  in  the  primary  centers  or  ganglia  of  the  trigeminal  and 
pneumogastric  nen-es.  This  may  be  true,  but  on  account  of  the  eye 
symptoms,  mental  disturbances,  aphasia  and  occasional  motor  phe- 
nomena we  must  still  believe  that  the  neurosis  is  in  large  part,  if  not 
wholly,  a  cortical  trouble. 

One  way,  and  perhaps  the  best  way  for  the  present,  to  express  the 
relationship  between  the  two  diseases  is  to  say  that  migraine  is  an 
epileptic  equivalent. 

Under  the  head  of  epilepsy  will  be  found  a  discussion  of  these 
so-called  equivalents. 

Of  all  the  explanations  of  migraine,  the  one  that  allies  it  to  epilepsy 
is  to-day  the  most  generally  accepted.  It  has  the  support  of  Liveing, 
Gowers  and  many  others. 

The  other  popular  theory  of  the  disease  is  that  a  spasm  of  the 
cerebral  arteries  causes  it.  Whytt  and  Du  Bois  Reymond  were  the 
leading  sponsors  of  this  explanation.  Mollendorf  and  others,  on  the 
other  hand,  urged  that  vascular  dilatation  rather  than  contraction  was 
the  basis  of  the  trouble.  Many  writers,  like  Latham  and  Eulenburg, 
think  that  both  spasm  and  dilatation  of  the  blood  vessels  are  the  cause 
of  the  disease,  and,  with  most  followers  of  this  theory,  assign  the  pri- 
mary cause  of  the  vascular  trouble  to  the  sympathetic  nervous  system. 
Latham  thinks  that  the  early  symptoms  are  due  to  vascular  contrac- 
tion, the  later,  and  especially  the  headache,  to  dilatation.  Eulenburg 
and  others  make  two  leading  types  of  the  disease,  which  they  have 
denominated  the  sympathetico-tonic  and  sympathetico-parah'tic  re- 
spectively. 

The  weakness  of  this  vascular  theory  is  that  the  basis  for  it  con- 
sists in  the  mere  appearance  of  certain  accessible  arteries  during  an 
attack.  It  assumes  that  the  same  thing  is  occurring  in  the  intracranial 
that  is  observed  in  the  extracranial  circulation  ;  that  this  is  a  cause 
rather  than  an  effect  of  the  disease,  and  that  it  is  dependent  upon  some 
hypothetical  change  in  the  sympathetic  nervous  apparatus.  In  addition 
to  assuming  so  much,  the  theory  is  not  founded  upon  a  single  post 
mortem  finding  that  would  lend  it  color  or  support.  Furthermore,  it 
does  not  account  for  the  remarkable  similaritv  between  the   sfeneral 


THE    NEURONIC   DISEASES  225 

symptoroatology  and  etiology  of  migraine  and  epilepsy,  unless  it  is 
likewise  adopted  as  the  explanation  of  the  latter  disease. 

It  seems  to  me  clear  that  as  migraine  is  so  closely  related  to  epi- 
lepsy, all  theories  that  are  advanced  to  explain  the  former  disease 
must  be  employed  to  explain  the  latter.  This  the  vascular  theory  does 
not  do,  and  it  is  therefore  inadequate  to  explain  the  nature  of  migraine. 

Migraine  is  a  primary  neurosis,  of  which  the  sudden  vascular 
•derangement  is  one  of  the  manifestations. 

The  exact  primary  seat  of  the  neurotic  storm  is  not  yet  determined, 
though  most  of  the  indications  point  to  the  sensory  centers  of  the 
cerebral  cortex. 

Symptoms. — Very  many  cases  of  migraine  have  premonitions  of 
an  oncoming  attack.  In  others  the  onset  is  sudden  and  abrupt,  some- 
times awakening  the  patient  out  of  his  sleep  at  night.  The  premoni- 
tory symptoms  are  not  unlike  the  premonitory  signs  and  aurce  that 
precede  an  epileptic  fit.  For  a  day  or  two,  or  several  hours,  the  patient 
will  feel  tired,  listless  and  indifferent.  Somnolence  and  a  fullness  of 
the  head  are  complained  of.  Sometimes  there  is  unusual  mental  bril- 
liancy, with  a  surprising  activity  of  memory,  imagination  and  intel- 
lection. As  a  rule,  however,  the  apathetic  condition,  with  yawning, 
inability  to  fix  the  attention,  vertigo  and  depression  obtains.  An  ab- 
normal hunger  or  indifference  to  food,  with  slight  feeling  of  nausea  and 
cardiac  palpitation,  have  been  spoken  of  by  patients  before  the  onset  of 
the  headache.  Immediately  before  an  attack  other  patients  experience 
visual  disturbance,  as,  for  instance,  spots  flying  before  the  eyes,  flashes 
of  color,  rainbow  formations,  star-like  fortification  figures,  hallucina- 
tions of  animals  and  strange  creatures.  Sometimes  the  visual  field 
slowly  increases  or  decreases,  grows  dark  or  light,  becomes  dark  in 
.segments,  with  transient  hemianopsia  and  scotoma.  A  blurring  of  the 
vision  more  frequently  occurs.  Hipp  us  or  alternate  contraction  and 
dilatation  of  the  pupil  has  been  seen. 

The  other  special  senses  are  only  rarely  subject  to  these  aurse. 
Tinnitus  aurium,  parosmia,  numbness  of  the  mucous  membrane  of  the 
mouth,  have  been  noted. 

Paraesthesia  and,  more  rarely,  cramps  and  spasms  have  appeared 
in  the  upper  extremities  just  before  an  attack. 

Transient  aphasia,  more  particularly  of  the  amnesic  type,  has 
■sometimes  been  premonitory  of  the  headache. 

When  these  sensory  premonitory  manifestations  are  marked,  it 
seems  that  the  succeeding  headache  is  less  severe  and  less  definitely 
localized  than  when  they  are  slight  or  absent  entirely.  There  is  no 
absolute  rule  about  this,  however.  Some  patients  have  actually  had 
these  aurse  without  the  appearance  of  the  headache  at  all. 

An  attack  of  migraine  or  paroxysm  of  the  disease  presents  a  cer- 
tain constant  clinical  picture,  the  details  of  which  are  subject  to  much 
modification. 

Soon  after  the  appearance  of  the  premonitory  symptoms,  and 
sometimes  even  without  them,  a  headache  occurs  abruptly  or  gradually, 
steadily  increases  to  a  climax,  where  it  remiains  several  hours,  accom- 
panied by  certain  sensory,  motor  and  psychic  manifestations,  and  then 


226  IHE    XEUKOXIC   DISEASES 

rapidlv  disappears  with  usually  an  attack  of  vomiting,  leaving  the 
patient  exhausted,  sleepy  and  depressed. 

It  is  to  be  noted  that  the  attacks  are  more  or  less  periodical  and 
])aroxysmal:  that  they  pretty  closely  resemble  one  another  always  in 
the  same  patient ;  and^  that  they  are  separated  by  intervals  of  apparent 
])erfect  health. 

The  headache  is  their  prominent,  but  not  their  only,  symptom. 

They  are  often  provoked  by  overexertion,  indiscretions  in  eating, 
mental  excitement  and  unusual  use  of  the  eyes.  Sometimes  they  come 
apparentlv  unprovoked. 

Paroxxsmal  headache  wath  vomiting,  visual  disturbances  and  other 
less  constant  symptoms,  appearing  rather  abruptly,  rising  to  a  maxi- 
mum of  intensity,  remaining  there  a  certain  number  of  hours,  and  then 
abruptlv  vanishing,  constitutes  the  clinical  picture,  in  brief,  of  an  attack 
of  migraine. 

As  the  minutise  of  this  picture  are  subject  to  much  variation,  I 
Avill  now  discuss  them  a  little  more  in  detail. 

Though  it  has  given  the  name  to  the  disease  because  it  is  so 
constant  and  prominent,  the  headache  is  not  by  any  means  its  sole 
or  most  important  symptom.  In  rare  instances  it  is  entirely  absent, 
and  in  all  cases  the  patient  has  become  so  accustomed  to  it  that  though 
it  causes  him  the  most  discomfort,  it  does  not  alarm  him  so  much  as 
some  of  the  sensory,  motor  and  psychic  phenomena  that  accompany  it. 

This  is  to  be  remembered  both  on  account  of  the  proper  concep- 
tion of  the  disease  and  its    proper  management. 

Hitherto  in  the  profession,  and  even  yet  to  a  large  extent  among 
the  laity,  the  headache  has  been  regarded  as  the  cardinal  feature  of  the 
disease,  and  in  a  way  the  cause  of  all  its  other  manifestations. 

The  disappearance  of  the  cephalalgia  synchronously  with  an  at- 
tack of  vomiting  and  vertigo  has  fixed  the  impression  in  the  minds  of 
the  people  that  the  liver  is  somehow  the  cause  of  the  headache,  and 
that  if  the  vomiting  of  bile  can  only  be  induced,  the  headache  must  of 
necessity  vanish.  They,  therefore,  commonly  speak  of  migraine  as 
"bilious  sick  headache,"  totally  ignorant  of  the  fact  that  both  the  head- 
ache and  the  so-called  bilious  manifestations  are  synchronous 
phenomena  depending  upon  the  same  neurotic  process. 

In  a  general  way  it  may  be  said  that  the  more  pronounced  the 
cephalalgia  is  the  less  obvious  will  be  the  other  special  sensory  and 
motor  symptoms.  When  the  latter  are  marked,  the  headache  is  apt 
to  be  of  a  minor  degree  of  severity. 

The  character  of  migrainous  headache  is  quite  distinctive.  As  I 
have  intimated,  it  appears  rather  suddenly,  but  develops  gradually. 
Sometimes  it  bursts  forth  in  all  its  excruciating  intensity  at  the  very- 
beginning.  It  does  not  fluctuate,  but  continues  steadily,  after  it  has 
reached  its  climax,  for  a  day  usually — sometimes  only  a  few  hours,  at 
other  times  for  two  or  three  days — and  then  rapidly  vanishes.  It  is 
generally  a  unilateral  headache,  the  seat  of  its  maximum  intensity  be- 
ing in  the  temporal  region.  After  remaining  aw^hile  in  one  temple  it 
may  cease,  only  to  reappear  in  the  other  temple.  It  may  extend  from, 
one  temple  over  the  front  of  the  brow^  or  across  the  top  of  the  head  to 


THE    NEURONIC    DISEASES  22/ 

the  otlier  temple.  Not  infrequently  the  pain  starts  in  the  occipital 
region,  extends  forward  to  the  supraorbital  region,  or  down  the  neck, 
even  into  the  arm.  In  the  same  patient  it  usually  occupies  the  same 
locality  and  extends  in  the  same  general  direction  with  each  succeed- 
ing attack.  Occasionally  it  always  appears  in  one  way  during  a  cer- 
tain period  of  life,  and  in  another  way  during  another  period.  Its 
focaiization,  steadiness,  intensity  and  paroxysmal  character  are  among 
its  striking  qualities. 

The  pain  itself  is  of  a  burning,  boring  sort ;  more  often  just  a  dull, 
incessant,  sickening  ache.  At  first  it  may  seem  to  be  superficial,  but 
later  on  it  feels  deep  in  the  cranium.  Percussion  aggravates  it,  as 
well  as  light,  noise,  or  any  peripheral  irritation.  Mere  pressure  does 
not  increase  it,  but  rather  affords  some  relief.  Movement,  jars  and 
other  slight  disturbances  seem  to  awaken  it  to  renewed  intensity.  The 
patient  therefore  instinctively  seeks  a  couch  in  a  dark  and  silent  room 
and  is  irritable  with  those  who  disturb  him  even  with  their  good  offices. 
The  skin  of  the  head  may  be  hyperaesthetic,  and  while  the  pain  is  on 
all  the  nerves  of  the  body,  but  especially  the  fifth  nerve,  have  their 
sensibiUty  highly  exalted.  Hence  the  patient  is  in  a  wretched  state, 
limp,  irritable,  excited  or  stuporous,  and  indifferent  to  those  about  him 
and  tlieir  attentions.  Frequent  experiences  have  taught  many  of  the 
victims  of  this  disease  to  bear  it  in  patience  and  to  await  in  seclusion 
its  early  termination. 

There  are  all  degrees  of  the  headache,  though  as  a  symptom  it  is 
more  or  less  always  present.  It  may  continue  to^  be  the  chief  mani- 
festation of  the  disease  throughout  life,  or  it  may  suddenly  cease,  to 
be  replaced  by  some  other  neurosis.  Two  sisters  whom  I  saw  suffered 
all  their  lives  with  asthmatic  attacks,  except  one  of  them  who  twelve 
years  ago  began  having  attacks  of  migraine  in  place  of  those  of  the 
asthmatic  neurosis. 

It  sometimes  happens  that  the  headaches  stop  and  epileptic  seiz- 
ures begin. 

I  have  seen  the  headaches  alternate  with  hysterical  outbreaks,  and 
other  spasmodic  conditions. 

The  headaches  never  occur  alone,  a  fact  which  more  than  any- 
thing else  indicates  the  protean  and  extensive  nature  of  the  disease. 

Next  in  frequency  to  the  headache,  and  usually  accompanying  it, 
are  the  gastric  phenomena.  These  consist  of  anorexia,  acute  indiges- 
tion, nausea,  retching  and  vomiting.  That  not  one  of  these  is  in  direct 
relation  to  the  headache  is  shown  by  the  fact  that  the  latter  is  in  no 
way  modified  by  them  when  they  occur  early  in  its  course.  Distress  in 
Lhe^  stomach  may  precede  the  head  pain,  occur  when  it  is  at  its  height, 
or  appear  only  when  the  latter  is  beginning  to  wane.  Usually  there  is 
some  anorexia  and  nausea  from  the  beginning  of  the  attack,  and  then 
at  the  end  violent  retching  and  even  vomiting  of  bile  accompanies  the 
cessation  of  the  headache.  If  food  is  taken  it  fails  to  digest  and  comes 
up  with  the  retching.  This  symptom  causes  great  distress  and  prostra- 
tion sometimes  and  is  generally  the  terminal  manifestation  of  the  par- 
oxysm.   Sleep  and  quietude  follow  it. 


228  TPIE    NEURONIC  DISEASES 

In  some  cases  there  may  be  diarrhoea  and  polyuria  towards  the  end 
of  the  attack. 

In  about  half  of  the  cases  there  is  some  visual  disturbance.  This 
assumes  a  great  variety  of  forms  and  usually  indicates  trouble  in  the 
occipital  cortex.  When  both  eyes  are  affected,  the  phenomenon  usually 
occurs  in  similar  parts  of  the  visual  fields.  Complete  or  partial  hemi- 
anopsia may  occur  or  the  vision  in  one  or  both  eyes  may  be  blurred. 
Flashes  of  light,  star  formations,  highly  colored  zigzag  lines  or  fortifi- 
cation figures  are  not  uncommon.  Actual  hallucinations  of  animals 
have  been  observed.  Moving  phenomena  are  particularly  frequent. 
Spots  float  across  the  field  of  vision,  objects  approach  and  recede, 
diminish  and  grow  large,  or  become  alternately  brilliantly  luminous 
and  dark.  Central  scotomata  have  been  seen.  In  rare  instances  double 
vision  has  occurred. 

All  of  these  manifestations  may  appear  abruptly  or  come  on 
gradually ;  they  may  be  more  or  less  constant,  though  as  a  rule  they 
come  and  go  or  change  from  one  to  the  other  in  the  course  of  the 
attack. 

The  functional  character  of  these  troubles  and  their  dependence 
upon  the  higher  or  cortical  visual  centers  are  obvious.  With  the 
headache  and  stomach  troubles  they  complete  the  tripod  that  most 
frequently  makes  up  the  clinical  picture  of  an  attack  of  migraine.  The 
other  symptoms  to  be  mentioned  occur  much  more  irregularly  and  in- 
frequently than  these  three. 

General  sensation  is  affected  in  many  patients  in  such  a  way  as 
to  clearly  indicate  a  cortical  functional  trouble.  Unilateral  or  bilateral 
parsesthesia  and  even  aneesthesia  may  occur  in  the  arms,  rarely  in  the 
legs,  in  the  face,  mouth,  throat  and  neighboring  parts.  Numbness, 
tingling,  pins-and-needles,  a  feeling  as  of  water  flowing  over  the  skin, 
hot  and  cold,  are  the  more  common  cutaneous  disturbances  complained 
of.  As  with  the  aurse  of  epilepsy,  these  sensations  sometimes  travel 
up  the  arms  in  gradation  or  in  skips,  and  then  appear  in  the  foot  and 
travel  up  the  leg.  They  rarely  last  longer  than  a  few  minutes.  The 
tongue  and  fauces  sometimes  feel  numb  and  may  become  actually 
anaesthetic.  Parsesthesia  of  the  limbs  usually  precedes  in  time  parses- 
thesia  of  the  face  and  lips.  When  unilateral  it  is  of  the  hemiplegic 
type,  involving  the  same  side  in  the  face  and  limbs.  These  cutaneous 
disturbances  are  far  less  frequent  than  those  of  the  sight. 

In  very  rare  instances  the  other  special  senses  have  been  affected. 
Tinnitus  aurium,  parosmia  and  alterations  of  taste  are  possible,  but  not 
common.  Transient  deafness  in  one  ear,  hallucinations  of  hearing  and 
taste  and  other  bizarre  observations  have  been  recorded. 

The  motor  symptoms  are  never  prominent  and  are  usually  entire- 
ly unnoticeable.  Slight  weakness  of  the  hemiplegic  type  may  be  ob- 
served in  the  limbs,  or  they  may  exhibit  a  certain  degree  of  spasm. 
These  motor  manifestations,  when  present,  appear  on  the  opposite  side 
from  that  of  the  headache.  They  are  always  associated  with  sensory 
symptoms  and  are  exceedingly  transient  in  duration.  Cerebellar  inco- 
ordination was  obser\^ed  in  one  case. 

The  vasomotor  symptoms  are   much   more   commonlv   observed. 


THE    NEURONIC    DISEASES  229 

Usually  there  is  an  initial  spasm  of  the  facial  blood  vessels  with  pallor. 
This  may  continue  through  the  attack.  In  other  cases  it  is  replaced  by 
a  congested  and  flushed  condition.  Pupillary  clmnges,  unilateral  sweat- 
ing, osdema,  redness  of  the  coniunctivce  and  retardation  of  the  pulse  are 
some  of  the  occasional  observations.  These  phenomena  are  usually 
bilateral,  though  they  mav  be  one-sided.  They  point  clearly  to  implica- 
tion of  the  sympathetic  nerves,  but  are  neither  constant  enough  nor 
sufficiently  indicative  of  the  intracranial  circulation  to  found  a  theory 
of  the  disease  upon  the  sympathetic  nerve,  as  some  have  attempted 
to  do. 

Aphasia  of  the  amnesic  variety,  more  rarely  of  the  motor,  is  a 
symptom  liable  to  appear.  It  is  rarely  complete  and  in  a  case  observed 
by  Oppenheim  was  combined  with  agraphia.  Hemianopsia  may  be 
associated  with  the  aphasia.  Word-deafness,  aphasia,  etc.,  are  seen 
in  only  a  small  percentage  of  cases  in  which  the  cephalalgia  is  left- 
sided. 

Giddiness  and  vertigo,  with  loss  of  equilibrium  and  nausea,  are 
sometimes  present. 

More  or  less  psychosis  occurs  in  all  of  the  cases  and  it  is  not  en- 
tirely due  to  the  pain  and  distress  experienced  by  the  patient.  It  is  a 
part  of  the  paroxysmal  phenomena.  There  may  be  slight  excitement, 
irritability,  intellectual  brilliancy  just  before  the  onset.  More  often 
there  is  emotional  depression,  weakness  of  memory,  lack  of  power  of 
attention.  There  follows  in  some  cases  actual  stupor  or  confusion, 
or  transitory  insanity  with  marked  hallucinations.  There  is  never  com- 
plete unconsciousness,  but  a  state  of  double  consciousness  has  been 
seen.  The  memory  may  recall  far-off  events  with  extraordinary 
vividness. 

The  general  prostration  caused  by  an  attack  of  migraine  is  severe. 
Not  only  during  the  spell,  but  for  some  time  after  it,  the  patient  is 
dull,  apathetic  and  somnolent.  At  the  climax  of  the  paroxysm  some- 
thing seems  to  suddenly  give  way.  Vomiting  suddenly  occurs,  the 
headache  rapidly  dies  out,  ptyalism,  perspiration,  profuse  micturition 
occur  and  the  patient  passes  into  a  profound  sleep,  from  which  he 
usually  awakens  some  hours  later  refreshed  and  feeling  quite  well 
again. 

It  is  useless  to  attempt  to  establish  types  of  the  disease  out  of  the 
many  peculiar  forms  and  combinations  that  the  symptoms  assume  in 
different  cases.  The  disease  is  ahvays  the  same  and  mere  prominence 
of  this  or  that  symptom  does  not  alter  it. 

In  the  larger  numiber  of  cases  there  are  present  only  cephalalgia 
and  the  gastric  disturbance.  When  the  disease  occurs  m  children  there 
may  be  some  elevation  of  temperature,  even  to  102  or  103  degrees  F. 

The  sensory  and  other  manifestations  of  the  disease  may  rarely 
occur  without  the  hemicrania.  Eye  symptoms,  transient  aphasia, 
paresthesia  in  the  limbs  may  thus  appear  alone  or  in  alternate  attacks 
with  the  headache.  Gowers  cites  a  case  in  which  for  years  the  only 
symptom  was  a  visual  disturbance  like  that  which  usually  precedes  an 
attack  of  headache.      At  no  time  was   there  any  pain.     These   cases 


230 


THE    NEUROXIC   DISEASES 


are  exceedingly   rare,   but   should   be  carefully   studied   and   properly 
recognized. 

Some  of  these  cases  may  belong  to  the  class  of  hcmicmmal  equiva- 
lents spoken  of  by  Mobius.'  In  this  it  is  assumed  that  the  disease  is 
epileptiform  and  lias  equivalents  just  as  ordinary  epilepsy  has.  Among 
other  equivalents  noted  are  cardialgia,  severe  vertigo,  gastroxynsis, 
circumscribed  pains  of  a  severe  character  in  other  parts  of  the  body 
than  the  head,  and  attacks  of  hemiparesis. 

Temporary  mania,  mental  confusion,  dream  states  and  melancholia 
have  been  seen  in  place  of  a  migrainous  attack.  One  of  my  patients 
would  lock  herself  in  her  room,  refuse  food  for  days  and  do  other 
strange  things  that  led  her  own  family  to  declare  that  she  was  insane, 
and  to  suggest  her  confinement  in  an  asylum.  During  several  months' 
treatment  under  my  care  in  a  private  hospital  she  showed  no  signs  of 
insanity,  but  had  several  unusually  severe  outbursts  of  headache. 

Mobius  has  made  use  of  the  occasional  cases  of  constant  hemi- 
crania  to  support  the  epileptic  theory  of  the  disease,  calling  these  cases 
instances  of  status  heinicraiiicus  and  comparing  them  to  status  epi- 
lepticus. 

Among  the  affections  sometimes  associated  with  hemicrania  epi- 
lepsy stands  prominent.  Epileptiform  attacks  may  mingle  with  those 
of  headache  or  the  latter  may  cease  and  be  replaced  by  typical  epilepsy. , 
\A'riter's  cramp  and  other  occupation  neuroses,  as  well  as  convulsive 
tic  have  been  seen  conjointly  with  it.  Nearly  all  cases  are  somewhat 
either  neurasthenic  or  hysteric.  Both  of  these  latter  diseases  may  be 
developed  out  of  the  prolonged  strain  and  sufifering  caused  by  the 
hemicranial  attacks.  As  a  rule,  however.  ihey  are  the  product  of  the 
same  neuropathic  constitution  that  underlies  the  migraine.  The  im- 
portance of  this  fact  is  shown  when  one  mistakenly  attempts  to  treat 
a  migrainous  headache  under  the  erroneous  notion  that  it  is  but  a 
symptom  of  the  neurasthenia  or  hystero-neurasthenia  that  may  be 
present.  The  latter  may  improve,  but  the  hemicrania  will  probably 
remain.  Disappointment  will  be  then  the  portion  of  both  the  patient 
and  physician. 

Diagnosis. — In  fairly  typical  cases  the  diagnosis  of  migraine  is 
easy.  The  points  to  be  carefully  noted  are  the  heredity  back  of  the  dis- 
ease, the  provocation  of  the  attack  by  some  unwonted  strain,  the  pre- 
moniton,-  symptoms,  the  somewhat  abrupt  onset  of  the  unilateral  head- 
ache, dragging  in  its  train  more  or  less  marked  visual  and  gastric  dis- 
turbances, other  sensory  symptoms  and  even  certain  motor  and  vas- 
omotor manifestations. 

The  comparatively  brief  duration  of  the  attacks,  their  somewhat 
periodical  and  paroxysmal  character  and  their  sudden  termination 
with  severe  vomiting  should  be  carefulh-  taken  into  consideration  also. 
The  association  of  the  trouble  with  other  neuroses,  especially  epilepsy, 
is  quite  confirmator}'. 

However,  other  headaches  are  sometimes  unilateral,  paroxysmal, 
combined  with  other  symptoms  and  in  man}'  ways  may  be  confused 
with  hemicrania.  In  these  headaches  assistance  in  making  the  diagno- 
sis must  often  be  obtained   solely  from   the   other   symptoms   of   the 


THE    NEURONIC   DISEASES  23I 

disease  underlying  the  headache.  The  cephalalgia  that  often  accom- 
panies hysteria,  neurasthenia,  ursemic  poisoning,  eye-strain,  constipa- 
tion, etc.,  can  thus  be  easily  distinguished  aside  from  their  own  char- 
acteristic features. 

In  tumor  of  the  brain  the  appearance  of  the  fundus  of  the  eye, 
the  comparatively  constant  presence  of  the  pain,  the  absence  of  the 
prodromes  and  peculiar  visual  disturbances  of  migraine,  and,  when 
present,  the  localization  symptoms,  v/ill  help  to  establish  the  diagnosis. 
The  pulse  may  be  retarded  in  migraine  as  it  is  in  cerebral  neoplasm, 
but  in  the  former  disease  it  is  an  exceptional  symptom,  while  in  the 
latter  it  is  a  common  manifestation. 

On  account  of  the  elevation  of  the  temperature  migraine  in  child- 
hood may  be  mistaken  for  iw^ningitis  and  other  brain  diseases.  The 
paroxysmal  character  of  the  headache,  the  ancestral  history  and  the 
absence  of  the  usual  objective  signs  that  accompany  these  diseases 
will  guide  the  diagnosis  in  the  right  direction. 

Petit  mal  may  be  overlooked  as  a  case  of  hemicrania.  The  dis- 
tinction is  sometimes  a  difficult  one  to  make  on  account  of  the  appar- 
ently close  relationship  between  the  two  diseases.  In  epilepsy  the 
visual  aurse  are  not  as  prolonged  as  they  are  in  hemicrania,  the  psychic 
manifestations  are  somewhat  more  prominent  and  the  sensory  sympto^ms 
are  less  noticeable.  If  the  slightest  convulsion  occurs  the  diagnosis  of 
epilepsy  is  of  course  assured. 

Tic  douloiireux  appears  in  a  particular  nerve,  the  fifth,  and  has 
not  the  aurse,  the  eye  symptoms,  the  general  sensory  manifestations  of 
the  hemicrania. 

Prognosis. — As  inheritance  is  so  important  a  factor  in  its  etiology, 
migraine  must  be  looked  upon  largely  as  of  the  nature  of  a  congenital 
defect.  This,  of  course,  precludes  the  possibility  of  its  complete  eradi- 
cation. And  yet  it  may  cease  suddenly  at  any  time,  though  it  is  then 
likely  to  be  replaced  by  some  other  form  of  neurosis  or  even  psychosis. 
Most  cases,  however,  continue  having  their  paroxysms  during  all  their 
lives.  Cases  that  I  have  seen  change  have  always  been  about  the 
climacteric.  In  several  instances  I  have  seen  migraine  replace  some 
previous  neurosis  about  this  period. 

The  longer  the  disease  has  existed  the  smaller  is  the  hope  of  its 
disappearance  or  even  amelioration.  The  latter  in  many  cases  can  be 
brought  about  by  changing  the  patient's  mode  of  life,  environment  and 
removing  all  possible  causes  of  peripheral  irritation. 

Hemicrania  is  practically  incurable.  The  type  of  the  disease  in 
which  the  visual  phenomena  are  especially  prominent  sometimes  pre- 
cedes tabes  dorsalis  and  dementia  paralytica.  When  it  is  associated 
with  hysteria,  hystero-neurasthenia  and  other  grave  neuroses,  especially 
epilepsy,  the  outlook  is  very  unfavorable.  Amelioration  and  the  remote 
possibility  of  a  spontaneous  cessation  is  about  the  best  sort  of  comfort 
we  can  hold  out  to  these  patients. 

The  disease  is  decidedlv  chronic  and  in  no  way  jeopardizes  life.  Its 
greatest  danger,  though  that  is  not  frequent,  is  its  transition  into 
epilepsy  or  insanity. 


23^ 


THE    NEURONIC   DISEASES 


Treatment.— In  undertaking  the  treatment  of  a  case  of  hemi- 
crania,  the  first  requisite  is  to  remove  every  discoverable  excitant  of  an 
attack.'  Many  patients  have  discovered  this  fact  for  themselves  and 
when  presenting  themseh-es  to  the  physician  for  advice  declare  that 
they  have  carefullv  avoided  all  habits  and  acts  that  have  initiated  their 
attacks.  Nevertheless  it  is  always  well  to  interrogate  the  patient  closely 
in  regard  to  his  environment,  his  occupation,  his  dietary,  his  custom 
in  regard  to  sleeping,  bathing,  exercising,  in  regard  to  his  sexual  life, 
his  bowel  functions  and  his  brain  work.  Not  a  stone  should  be  left 
unturned  in  this  search.  Proper  corrections,  of  course,  should  be  made 
where  errors  and  excesses  are  found  in  the  habits  and  manner  of  living. 
As  migraine  is  in  many  cases  a  reflex  disease,  the  patient's  body  should 
be  thoroughlv  examined  for  physical  and  functional  defects.  The  eyes 
may  be  defective  in  one  case ;  the  nasal  passages  obstructed  in  another. 
An"  enlarged  tonsil  or  a  mastoiditis  may  be  causing  the  trouble. 
Angemia  may  be  present,  or  there  may  be  some  latent  renal  disease. 
The  very  multiplicity  of  the  exciting  causes  of  migraine,  and  their 
elusive  character  in  so  many  of  the  cases,  urge  upon  the  diagnostician 
unusual  care  and  thoroughness  in  his  search  for  them.  Their  removal, 
of  course,  is  a  sine  qua  -non  to  all  further  treatment  of  the  case.  When 
this  is  done  many  cases  will  undergo  marked  amelioration  and  some 
will  be  absolutely  cured. 

As  the  neuropathic  instability  frequently  continues  in  such  cases, 
other  existing  causes  may  arise  and  provoke  the  attacks  anew.  Those 
who  vainly  attribute  migraine  to  these  peripheral  causes  alone  do  not 
have  a  proper  conception  of  the  disease  and  are  disappointed  when 
there  is  a  return  of  the  headaches  in  some  of  the  cases  in  which  the 
supposed  existing  cause  has  been  carefully  removed. 

All  discoverable  causes  having  thus  been  removed  as  far  as  possi- 
ble, there  should  be  an  effort  made  to  combat  the  disease  by  continuous, 
prolonged,  constitutional  treatment. 

The  dietary  should  be  regulated  and  rendered  as  bland  and  nour- 
ishing as  possible.  A  purely  vegetarian  diet  has  modified  some  cases. 
Stimulants,  condiments,  fats  and  rich  pastry  had  better  be  avoided. 
Tea  and  coffee  are  sometimes  harmful.  Milk  diet  is  commendable, 
though  a  large  percentage  of  these  cases  declare  they  cannot  take 
milk.  I  have  found  this  to  be  due  largely  to  the  psychic  impression 
that  biliousness,  which  they  think  they  suffer  from  in  their  attacks, 
is  somehow  associated  with  the  ingestion  of  milk.  I  nevertheless  in- 
sist upon  their  taking  the  milk,  in  small,  frequent  quantities,  and  have 
more  than  once  overcome  the  prejudice. 

I  urge  these  patients  to  drink  abundantly  of  pure  water  at  all 
times.  As  constipation  is  not  uncommon,  some  natural  water  with 
cathartic  properties,  like  Carlsbad,  Hunyadi,  Friedreichshalle,  is  to 
be  used  more  or  less  regularly  before  breakfast.  Tlie  general  health 
should  be  built  up  if  necessary.  Arsenic  and  iron  and  other  tonics 
should  be  given  if  the  state  of  the  blood  and  organs  calls  for  them. 
Hydrotherapy,  mechanicotherapy,  massage,  gymnastics  and  electricity 
may  all  be  advantageously  employed  with  this  end  in  view.  A  change 
of  climate  and  a  sojourn  in  the  mountains,  or  by  the  seashore,  may 


THE    NEURONIC  DISEASES 


^Zi 


so  alter  the  general  state  of  ill-health  as  to  cause  a  marked  ameliora- 
tion in  the  migrainous  attacks. 

-  For  the  disease  of  hemicrania,  like  epilepsy,  we  have  no  specific 
medication.  The  prolonged  administration  of  some  remedies,  however, 
has  resulted  in  a  number  of  complete  and  partial  successes.  Of  these 
remedies  arsenic,  nitroglycerin  and  the  bromides  head  the  list.  In  my 
own  experience  arsenic  has  seemed  to  be  the  most  successful.  It  very 
often  fails,  however.  Any  form  of  arsenic  may  be  used,  though  arseni- 
ous  acid  is  perhaps  the  most  available.  Fowler's  solution  and  arseniat- 
ed  waters  may  be  used  alternately.  It  must  be  continued  for  a  long 
time,  with  proper  precautions  and  intervals  of  rest,  and  in  full  physio- 
logical dosage.  Iron  may  be  advantageously  combined  with  it  in  some 
cases. 

I  have  not  been  so  successful  with  nitroglycerin.  Gowers  praises 
this  remedy  highly.  It  is  to  be  given  for  long,  continuous  periods  in 
doses  of  I-200  to  1-150  of  a  grain  three  times  a  day,  after  meals.  Dur- 
ing the  paroxysms  it  should  be  stopped.  It  is  in  the  angiospastic  type 
of  the  disease  that  it  exerts  its  happiest  effects,  accomplishing  it,  as 
Gowers  says,  by  regularly  flushing  the  brain  with  new  blood  and  so 
increasing  its  general  nutrition. 

The  continuous  use  of  the  bromides  has  helped  some  cases,  but 
as  a  rule  they  are  not  satisfactory  remedies. 

In  spite  of  all  we  can  do  in  most  cases  the  headaches  persist  in 
returning.  In  such  instances  all  we  can  attempt  to  do  is  to  mitigate 
the  patient's  sufferings  when  the  attack  is  on,  or  is  about  to  begin. 

Many  patients  have  become  so  discouraged  at  the  futility  of  all 
medication  that  they  refuse  to  be  treated,  seek  a  dark,  quiet  room,  and 
await  patiently  the  cessation  of  the  paroxysm.  Nitrite  of  amyl  inhala- 
tions may  be  tried  in  the  beginning  of  an  attack.  A  cup  of  strong  coffee 
or  twenty  drops  of  chloroform  has  checked  it  somewhat.  Herter  rec- 
ommends that  the  stomach  be  washed  out  with  water  at  105  degrees  F., 
and  a  brisk  saline  cathartic  be  administered.  The  patient  should  keep 
a  recumbent  position  in  bed  and  a  firm  hot  or  cold  compress  applied 
to  the  head,  and  his  feet  placed  in  hot  mustard  water.  Menthol  may  be 
rubbed  over  the  temporal  or  frontal  regions ;  instillations  of  cocaine 
may  be  made  into  the  conjunctival  sac;  and  a  mustard  poultice  applied 
to  the  back  of  the  neck.  Electricity  does  no  good  and  morphine  must 
be  withheld  as  long  as  possible. 

The  drugs  that  are  employed  to  combat  the  headache  are  numer- 
ous. In  their  eft'ects  they  are  very  variable.  What  may  be  most  suc- 
cessful in  one  case,  or  in  one  paroxysm,  may  fail  utterly  in  another. 
Hence  it  is  wise  to  have  in  hand  a  number  of  agents  to  experiment 
with.  In  most  cases  a  thirty  or  forty  grain  dose  of  potassium  bromide, 
sometimes  with  tincture  of  cannabis  indica  or  tincture  of  hyoscyamus, 
repeated  every  two  or  three  hours,  gives  considerable  relief.  Chloral 
produces  sleep,  but  after  this  wears  off  the  pain  comes  back  in  all  its 
pristine  severity.  Even  morphine  sometimes  acts  this  way.  The  coal- 
tar  preparations,  antipyrine,  acetanilid  and  phenacetine,  enjoy  an  un- 
deserved popularity.  In  large  doses  they  are  apt  to  be  dangerously 
depressing,  and  in  small  doses  they  are  not  rapidly  effective.     In  mild 


234 


THE    NEURONIC   DISEASES 


aises,  however,  I  have  gotten  some  results  from  all  three,  administered 
in  small  frequently  repeated  doses.  Personally  I  prefer  phenacetine, 
giving  twenty  or  thirty  grains,  in  five-grain  doses,  every  quarter  or 
half  hour.  While  taking  this  remedy  the  patient  should  lie  down  and 
take  some  brandy  or  aromatic  spirits  of  ammonia.  A  few  grains  of 
caffeine  with  potassium  bromide  makes  an  excellent  combination  for 
some  cases.  Sodium  salicylate  in  thirty  or  forty  grains,  administered  in 
a  cup  of  strong  coffee,  sometimes  suppresses  pain.  Caffeine  may  be 
combined  judiciously  with  it.  Guarana  (paullinia  sorbilis)  is  similar 
to  and  not  much  better  than  caft'eine.  It  may  be  given  in  twenty  or 
thirty  grain  doses,  repeated  every  half  hour  for  three  or  four  times. 
The  dosage  of  the  alkaloid,  guaranine,  is  one  to  five  grains. 

Other  medicaments  worthy  of  a  trial  sometimes,  and  always  use- 
ful as  a  reserve  force  when  the  otliers  fail,  are  analgen  (5-15  grains), 
exalgen  (4  grains),  methylene  blue  (i^<  grains),  cytisin  (1-20  grain), 
migranin  (16  grains),  cannabis  indica,  nux  vomica,  ergot,  ammonium 
chloride,  neurodin  (15-25  grains),  quinine  valerianate,  thermodin  (15- 
20  grains),  triphenin  (15-20  grains),  valerian,  aconite  and  belladonna. 

The  drug  treatment  of  migraine  is  far  from  being  all  that  could 
be  desired.  If  cannabis  indica  in  full  dosage,  the  bromides  with 
hyoscyamus,  sodium  salicylate,  the  coal-tar  preparations  and  caffeine 
fail,  there  is  not  much  to  be  hoped  for  from  anything  else.  Hence  it 
is  best  to  persist,  even  in  the  face  of  possible  ultimate  failure,  with 
these  than  to  rapidly  change  from  one  drug  to  another  of  this  long  list 
of  uncertain  and  often  inert  preparations. 

As  a  last  resort  hypodermics  of  morphine  may  be  turned  to,  though 
occasionally  even  these  fail,  and  in  doing  so  may  save  the  patient  from 
the  greater  danger  of  the  drug  habit. 

The  seton  has  seemed  almost  to  have  produced  a  cure  in  a  few  cases. 
It  is  inserted  in  the  back  of  the  neck,  the  tape  is  changed  fortnightly 
and  the  wound  is  dressed  daily  with  one  boric  fomentation.  Watson, 
Cornish  and  others  commend  the  treatment  in  obstinate  cases.  It  prob- 
ably acts  by  counterirritation. 

HEADACHE. 
CEPHALALGIA.    CEPHAL^A. 

Headache  is  only  a  symptom  accompanying  many  diseased  states 
and  the  term  ought  to  be  regarded  in  the  same  way  that  paralysis  and 
apoplexy  are.  As  it  is  so  prominent  and  frequent  a  symptom,  as  it  is 
so  often  the  only  symptom  of  which  the  patient  complains,  and  as  its 
cause  in  a  certain  percentage  of  cases  is  quite  hidden,  it  rises  almost 
to  the  dignity  of  being  a  special  disease,  and  so  perhaps  in  a  work  on 
nervous  troubles  deserves  a  special  section.  In  a  book  covering  the 
entire  field  of  medicine  there  would  be  no  need  of  a  special  discussion 
of  headache,  for  anything  like  complete  consideration  of  it  would 
include  a  discussion  of  the  whole  field  of  medicine. 

Not  every  pain  about  the  head  is  included  under  the  specific  term 
headache.  By  it  is  meant  a  more  or  less  diffuse  soreness  and  pain  in 
and  about  the  vault  of  the  head.     Facial  pains  and  pains  following  the 


THE    NEURONIC   DISEASES  2^^ 

course  and  distribution  of  particular  nerves  are  regarded  as  neuralgic. 
The  laity  sometimes  use  the  term  "neuralgia""  when  referring  to  head- 
ache, but  for  the  sake  of  clearness  the  above  distinction  between  the 
terms  should,  for  the  present,  be  insisted  upon  by  the  profession. 

Headaches  are  pains  of  variable  intensity,  extent  and  duration  that 
occur  in  the  frontal,  occipital,  temporal  and  vertex  regions  Oif  the 
•cranium. 

Various  classifications  have  been  made  upon  the  basis  of  location, 
cause,  character  and  relationship  to  other  diseases.  All  of  these  classi- 
fications are  of  some  practical  value ;  none  of  them  are  complete  or 
■entirely  satisfactory.  The  best  are  undoubtedly  those  in  which  the 
causes  of  the  headache,  considered  on  broad  lines,  are  made  the 
foundation. 

Etiology. — As  I  have  said,  a  discussion  of  the  causation  of  head- 
ache would  cover  the  whole  field  of  medicine.  There  are  certain 
prominent  factors,  however,  that  may  be  profitably  dwelt  upon. 
Neurotics  and  people  in  a  condition  of  nervous  depression  furnish  the 
larger  number  of  victims  ;  hence  heredity,  in  the  form  of  neuropathic 
transmission,  plays  a  role.  Age,  occupation,  environment,  habits,  dis- 
sipations, mode  of  life,  all  enter  into  the  etiology  in  so  far  as  they 
cause  nervous  inadequacy.  Including  migraine  in  his  statistics,  Dana 
finds  that  headache  attacks  ten  to  fifteen  per  cent,  of  school  children, 
over  fifty  per  cent,  of  women,  and  about  twenty-five  per  cent,  of  men. 

The  age  at  which  the  special  varieties  of  headache  make  their  ap- 
pearance depends  upon  the  underlying  cause.  Early  adult  life  for 
both  sexes  seems  to  be  the  favorite  period  of  the  disease.  The  com- 
petition and  strain  of  urban  life ;  the  dissipation  and  self-indulgence  of 
wealth ;  the  mental  overexertion  in  bad  hygienic  surroundings ;  the 
barometric  and  climatic  changes  of  various  seasons  and  localities,  are 
all  elements  in  determining  the  frequency  of  headache. 

From  the  standpoint  of  etiology  the  following  types  of  headache 
may  be  noted : 

I.  Hccmic  and  Vasomotor.  The  brain  being  so  abundantly  sup- 
plied by  blood,  as  the  ultimate  seat  of  consciousness  and  all  painful 
sensations,  it  would  naturally  be  expected  to  be  affected  when  the 
integrity  of  the  blood  or  the  amount  of  its  supply  is  any  way  disturbed. 
Anzemic  and  congestive  headaches  are  therefore  very  real  and  not  at 
all  uncommon.  The  former  may  be  associated  with  chlorosis,  sudden 
and  severe  hemorrhage  or  the  deteriorated  condition  following  a  long, 
exhausting  disease.  Arteriosclerosis  may  cause  a  local  anaemia  with 
nutritive  depression,  though  Oppenheim  suggests  that  the  rigid  vessels 
may  irritate  the  meninges.  Both  active  and  passive  hypergemia  will 
raise  the  intracranial  blood  pressure  and  thus  provoke  a  cephalalgia. 
It  may  be  arterial  and  caused  by  sudden  emotional  excitement,  toxicity 
of  the  blood  from  alcohol,  tobacco,  coffee  and  traumatism ;  or,  on  the 
other  hand,  it  may  be  venous  and  associated  with  cardiac,  renal  and 
pulmonary  disease.  Faulty  position  and  tight  constriction  of  the  neck 
may  impede  the  circulation.  The  nutritive  value  of  the  blood  may  be 
greatly  diminished  by  the  presence  of  infectious  material.  Thus  under 
the  class  of  hgemic  headaches  we  must  enumerate  all  those  that  are 


236  THE    NEURONIC   DISEASES 

associated  with  such  diathetic  conditions  as  gout,  rheumatism,  diabetes^ 
uraemia ;  such  infectious  fevers  as  malaria,  influenza,  typhoid ;  and 
such  forms  of  autointoxication  as  have  their  origin  in  gastric  dis- 
orders, constipation,  hepatic  and  renal  insufficiency,  etc.  Thus  mechan- 
icallv,  nutritively  and  physiochemically  are  these  hsemic  and  vasomotor 
headaches  produced. 

2.  Toxic.  In  a  smaller  number  of  cases  certain  poisons  probably 
act  as  direct  irritants  upon  the  pain  mechanism,  causing  minute  func- 
tional disturbances  in  the  nervous  elements  that,  if  continued  long- 
enough,  may  go  on  to  actual  neurotic  degeneration.  In  these  intoxica- 
tions the  effect  of  the  poisons  on  the  histological  elements  is  probably 
partly  direct  and  primary  and  partly  indirect  and  secondary  by  way  of 
the  vasomotor  disturbance  \\hich  they  set  up.  An  alcoholic  headache,, 
for  instance,  may  be  both  a  purely  toxic  and  a  secondary  haemic  head- 
ache. 

Among  the  numerous  toxic  agents  which  we  regard  as  of  etio- 
logical importance  may  be  noted  alcohol,  tobacco,  coffee,  lead,  mor- 
phine, chloroform,  ether  and  others.  Foul  air  in  badly  heated  rooms  or 
from  defective  plumbing,  impure  water  and  tainted  food  may  be  dan- 
gerous on  account  of  their  toxicity  as  well  as  by  reason  of  depriving  the 
organism  of  its  normal  needs. 

3.  Refl'W.  The  reflex  causes  of  headache  are  numerous  and 
have  furnished  the  ground  for  many  a  sharp  battle  of  opinion.  It  is- 
perfectly  reasonable  that  peripheral  abnormalities  should  at  times  pro- 
voke central  disturbances,  but  it  is  absolutely  illogical  to  affirm  that 
all  central  disturbances  are  due  to  such  peripheral  conditions. 

Through  its  outstretching  processes,  the  seat  of  consciousness  is 
in  close  relationship  with  every  tissue  and  organ  of  the  body.  It  may 
well  happen,  therefore,  that  disease  of  any  one  of  these  outlying  struc- 
tures may  be  such  as  to  set  up  a  high  degree  of  distress  in  the  pain 
centers  of  the  brain.  To  enumerate  the  sources  of  reflex  irritation,  one 
would  have  to  give  a  complete  resume  of  anatomy,  physiology  and 
pathology.  Suffice  it  to  say  that  they  are  most  coinmonh-  found  in 
connection  with  the  eyes,  the  stomach,  the  sexual  organs,  the  nose  and 
the  ear.  Errors  of  refraction  and  accommodation ;  naso-pharyngeal 
hypertrophies,  tumors  and  inflammations :  sexual  excesses,  masturba- 
tion, uterine  diseases  and  menstrual  disorders ;  indigestion,  gastric 
catarrh,  intestinal  parasites^  etc.,  are  among  the  more  common  periph- 
eral reflex  causes  of  cephalalgia. 

4.  Xeuropathic.  Under  this  head  we  place  those  headaches  that 
accompany  epilepsy,  neurasthenia,  hysteria,  neuritis,  neuralgia,  chorea,. 
etc.  These  partake  of  the  etiology  of  the  disease  with  which  they  are 
associated.  In  my  opinion  most  of  them  are  toxic  or  autotoxic  in 
origin,  and  not  a  direct  expression  of  the  neuropath}-  in  the  way  that 
the  general  neurosis  is.  For  example,  neurasthenia  is  a  general  neu- 
rotic deterioration;  the  headache  that  accompanies  it  is  usually  the 
result  of  the  auto-intoxication  that  develops  from  the  functional  in- 
efficiency of  the  organs  of  assimilation  and  excretion.  The  pain  of 
hysteria  is  usually  the  result  of  a  psychic  or  physical  abnormal  reflex 
influence.     And  so  on  for  most  of  these  so-called  neuropathic  head- 


THE    NEURONIC  DISEASES 


^V 


caches.      Hemicrania,    though    discussed   b}-   itself   in    another    section, 
ialls  into  this  class,  being  related  to  epilepsy. 

5.  Organic.  By  organic  headaches  we  mean  those  that  are  set 
up  by  gross,  organic  lesions  easily  discovered  upon  post  mortem'  exam- 
ination, or  even  during  life,  and  tliat  may  or  may  not  be  amenable  to 
surgical  intervention.     Disease  of  the  bones  of  the  skull,  meningitis, 

-■cerebral  syphilis,  intracranial  neoplasms,  arteriosclerotic  productions  are 
some  of  these  organic  causes.  Under  their  respective  heads  the  symp- 
toms will  be  further  considered  in  detail. 

6.  Psychic.  Once  in  a  while  we  meet  cases  of  headache  which 
seem  to  have  been  brought  on  by  pure  psychic  influences,  and  are 
-certainly  sometimes  quickly  removed  by  suggestion  and  other  psychic 
means.  Sudden  emotion,  fright,  disappointment,  prolonged  intellectual 
action,  dread,  terror  and  other  depressing  psychic  influences  sometimes 
give  rise  to  headache.  In  a  few  cases  of  -masturbation  it  has  seemed 
to  me  that  the  headaches  and  other  symptoms  were  due  to  the  dread 
and  shame  and  fear  of  insanity,  more  than  to  the  mere  physical  stress. 
"With  Wundt  I  regard  the  mental  acts  as  processes  and  not  actual  en- 
tities. They  are  not  simple,  but  complex.  They  represent  the  inter- 
play of  certain  elementary  sensory  mipulses  in  and  among  one  another. 
If  this  interplay  is  suddenly  disturbed  or  shocked  it  reacts  injuriously 
upon  the  underlying  sensory  elements  and  causes  them  to  manifest 
pain.     These  cases,  however,  are  very  rare. 

Pathology  and  Pathogenesis. — It  is  somewhat  of  an  anomaly  to 
speak  of  the  pathology  of  a  symptom.  Only  diseases  have  a  patho- 
logical basis,  and  headache  is  not  a  disease.  And  yet  there  are  some 
facts  in  regard  to  the  pathogenesis  of  even  a  single  symptom  so  promi- 
nent and  unique  as  headache  sometimes  is  that  need  a  moment's  con- 
sideration. 

Apart  from  the  pathology'  of  the  underlying  general  abnormality 
upon  which  the  headache  depends,  there  is  absolutely  no  known  con- 
stant lesion  that  can  by  any  stretch  of  reasoning  be  distinctly  associat- 
ed with  the  latter.  Hsemic,  toxic,  reflex,  neuropathic  and  organic  head- 
aches reveal  nothing  beyond  the  usual  findings  of  these  respective  con- 
ditions which  may  be  singled  out  as  the  specific  source  of  the  head  pain. 
Various  theories  have  been  proposed  and  the  cephalalgia  has  been 
assigned  to  the  implication  of  the  fifth  nerve  or  the  nerves  of  the  dura 
inater,  the  nervi  nervorum,  the  primary  and  basal  ganglia  or  the 
cerebral  cortex.  One  thing  seems  to  be  certain,  however,  and  that  is 
that  true  cephalalgia  is  not  the  result  of  disease  in  the  peripheral  nerves 
and  their  primary  ganglia,  for  this  produces  the  true  neuralgias  in 
and  about  the  head.  The  headache  pain  is  too  diffuse  and  otherwise 
unique  to  be  a  mere  nerve  pain.  There  is  nothing  beyond  mere  guess- 
work to  assign  the  pain  to  the  dura  mater.  Well-known  primary  and 
secondary  diseases  of  this  or  the  other  membranes,  aside  from,  the  pres- 
sure which  their  thickening  may  exert  upon  the  cerebrum  or  related 
nerves,  do  not  provoke  true  headache.  The  head  pains  of  syphilitic 
and.  tubercular  meningitis  are  pressure  pains.  To  attribute  all  head- 
aches to  the  dura  mater  we  would  have  to  assume  that  in  all  head- 
aches the  dura  was  diseased  and  more  or  less  thickened.     This  would 


238  THE    NEURONIC   DISEASES 

be  an  unwarrantable  assumption,  especially  in  tbe  total  absence  of  all 
other  indications  of  meningeal  disease. 

The  localization  of  the  original  source  of  the  pain  in  the  basal 
ganglia,  especially  the  optic  thalamus,  was  strongly  argued  by  many 
at  one  time.  Our  more  recent  knowledge  of  the  physiological  functions 
of  the  basal  ganglia  is  not  favorable  to  this  view  and  it  never  was 
anything  more  than  a  gratuitous  hypothesis  without  experimental  or 
pathological  proof. 

The  only  view  that  has  a  shadow  of  a  positive  foundation  whereon 
to  rest  is  that  which  attributes  the  pain  directly  to  the  functional  or 
organic  disturbance  of  the  sensory  elements  of  the  cortex.  Migraine, 
of  course,  is  something  more  than  a  mere  headache.  It  is  a  disease  of 
the  sensory  cortex  closely  related  to  that  other  primarily  sensory  dis- 
ease— epilepsy.  It  has  many  symptoms,  but  its  leading  symptom,  the 
headache,  is  in  all  essential  respects  the  same  as  the  various  types  of 
headache  now  vmder  discussion.  Therefore  if  migraine  is  a  cerebral 
sensory  phenomenon,  why  not  the  cephalalgias  that  so  closely  imitate 
its  dominant  symptom,  the  headache?  In  their  immediate  causation 
the  same  toxic,  retlex  and  other  factors  play  a  significant  role.  In 
their  diffusiveness,  changeability  and  localization  they  are  not  unlike. 
Even  in  some  of  their  manifestations  other  than  the  mere  pain  they 
bear  a  remote  resemblance.  And  in  their  management  the  same  gen- 
eral specific  medication  obtains.  In  otlier  words,  let  the  cause  of  the 
trouble  be  what  it  will,  as  well  as  the  general  nature  of  the  disease  or 
its  collateral  symptoms,  the  headache,  every  indication  shows,  is  a 
functional  disturbance  of  the  sensory  cerebral  cortex. 

It  is  quite  impossible  to  account  for  the  location  of  certain  head- 
aches in  particular  parts  of  the  head.  Psychic  auto-suggestion  may 
have  something  to  do  with  it,  as,  for  instance,  the  localization  of  the 
ocular  reflex  headaches  just  above  the  eyes. 

The  location  of  the  irritative  lesion,  as  in  some  of  the  organic 
cases,  may  determine  the  location  of  the  headache.  In  most  of  the 
cases  there  is  no  sort  of  imaginable  way  by  which  the  concentration  of 
the  pain  upon  this  or  that  side  of  the  head,  in  front  or  on  top,  can  be 
accounted  for.  This  very  indefiniteness  is  an  argument  in  favor  of  its 
cerebral  origin,  it  seems  to  me,  for  in  this  respect  at  least  it  resembles 
the  psychoses,  which  are  positively  accepted  as  of  cortical  origin,  but 
without  a  more  definite  seat  yvithin  the  cortex.  Like  the  latter  it  is  a 
functional  trouble  of  the  sensory  cortex  more  or  less  in  toto,  rather 
than  of  special  centers  of  sensation  in  that  cortex. 

Symptoms. — Cephalalgia  is  a  diffuse,  changeable  soreness  or  pain 
of  the  head  or  various  parts  of  the  head.  It  may  be  superficial  and 
aggravated  by  slight  percussion.  Steady  pressure  often  relieves  it. 
Sometimes  it  is  deep,  concentrated  and  boring.  At  other  times  it 
resembles  a  paraesthesia  and  is  described  as  burning,  cutting,  pressing,, 
pulling,  sticking  like  pins  and  needles.  Usually  the  scalp  is  hyper- 
aesthetic. 

The  character  of  the  pain  and  its  action  under  different  conditions 
are  sometimes  dependent  upon  the  immediate  cause  of  it.  The  sam.e 
may  be  said  of  its  location.     For  instance,  anaemic  headaches  are  dull 


THE    NEURONIC   DISEASES.  239 

and  heavy,  are  not  particularly  severe  and  are  spread  more  or  less 
over  the  entire  scalp,  the  brow  or  sides  of  the  head.  The  recumbent 
position  usually  alleviates  them.  On  the  other  hand,  the  congestive 
headaches  are  full  and  throbbing-,  combined  with  vertigo  and  aural 
disturbances,  visual  phenomena  and  redness  of  the  face  and  con- 
junctivae.    The  recumbent  position  aggravates  these. 

The  location  of  the  headache  is  often  strongly  suggestive  of  its 
cause,  though  no  absolute  rules  can  here  be  laid  down.  The  larger 
number  of  the  head  pains  are  frontal ;  next  in  frequency  are  the  oc- 
cipital headaches.  Vertical  and  lateral  localization  of  the  pain  is  not 
uncommon  and  often  generalized  combinations  of  these  are  met  with. 
Pains  that  are  more  or  less  constant  and  are  localized  in  the  supra- 
orbital region  are  apt  to  be  due  to  ocular  defects  or  dyspepsia.  If  the 
pain  here  is  absent  in  the  morning  and  appears  in  the  afternoon  it  is 
due  to  eye-strain.  In  neurasthenia  I  have  often  noticed  that  the  patient 
will  get  up  with  a  slight  frontal  soreness,  which  will  disappear  for  a 
few  hours,  only  to  return  later  on  in  still  greater  severity.  Auto- 
intoxication headaches,  with  constipation,  are  dull  and  constant  over 
the  upper  part  of  the  brow.  Sharp,  boring,  burning  pain  on  the  vertex 
is  a  neuropathic  headache.  As  clavus  it  is  typical  of  hysteria;  as  a 
full,  compressing  or  lead-cap  feeling  it  is  probably  neurasthenic.  A 
steady,  duller  ache  on  the  top  of  the  head  should  cause  us  to  look  for 
anaemia,  uterine  disease,  possibly  stomach  or  bladder  trouble.  Occipital 
soreness  is  mostly  uterine  or  gastric  in  origin  and  is  often  accompanied 
by  nausea.  There  may  be  vertigo.  Temporal  headaches,  particularly 
if  they  are  unilateral,  keen  and  persistent,  are  neuralgic  or  migrainous. 

In  the  diagnosis  of  the  headaches  of  organic  origin,  say  from 
tumor,  exostosis  or  meningitis,  one  would  not  rely  alone  on  the  pain 
symptom.  In  every  case  a  most  thorough  search  ought  always  to  be 
made  for  collateral  symptoms.  These  will  often  interpret  most  con- 
clusively the  cause  and  nature  of  the  head  pain. 

The  persistency  of  the  headache  will  suggest  a  persistent  cause, 
like  caries  of  the  teeth,  tumor;  headaches  that  come  and  go  may  be 
merely  neurotic  or  indicate  their  dependence  upon  conditions  that  are 
subject  to  changes,  such  as  nerve  tire,  constipation,  gastric  activity  and 
quietude. 

Diagnosis. — The  mere  diagnosis  of  headache  is  no  diagnosis  at 
all.  The  underlying  cause  or  disease  that  provokes  the  pain  is  the 
ultimate  purpose  of  the  examination.  It  is  always  a  confession  of 
defeat,  unfortunately  sometimes  unavoidable,  to  write  a  prescription 
with  no  better  end  in  view  than  merely  to  suppress  the  pain.  Head- 
ache is  like  the  wreath  of  smoke  that  should  lead  at  once  to.  the  threat- 
ening fire.  The  latter  is  not  extinguished  by  blowing  away  the  smoke. 
Hence  of  all  the  symptoms  met  with  in  the  practice  of  medicine  none 
needs  a  more  careful  study.  I  am  convinced  that  in  making  a  diagnosis 
in  headache  the  errors  will  be  less  in  number  just  in  proportion  as  the 
examiner  keeps  his  mind  off  of  the  headache  itself  and  turns  his 
scrutiny  upon  the  collateral  symptoms  of  the  possible  disease  that  is 
causing  the  headache.  In  other  words,  let  him  minimize  as  much  as 
he  can  the  cephalalgia  in  the  drawing  up  of  the  clinical  picture  of  the 


240  THE    NEURONIC  DISEASES 

case  in  hand,  and  emphasize  all  the  other  symptoms  that  may  be  pres- 
ent. For  instance,  search  keenly  for  the  symptoms  of  neurasthenia,  if 
there  is  an  intimation  that  the  head  pain  is  neurasthenic  in  origin ; 
rather  dwell  upon  the  paraesthetic,  lead-cap  character  or  what-not  of 
the  headache.  Delay  not  with  the  dull,  aching,  diffuse  character  of  a 
possible  anaemic  headache,  but  make  a  blood  examination  and  deter- 
mine the  presence  of  anaemia.  Be  not  satisfied  with  a  supra-orbital 
headache  as  of  ocular  origin,  but  study  the  case  as  though  it  had  pre- 
sented itself  primarily  as  one  of  eye  trouble. 

In  the  books  and  in  practice  too  much  reliance  is  put  upon  the 
location  and  character  of  the  headache  as  indications  of  its  cause.  They 
can  only  offer  the  barest  sort  of  hints. 

So  variable  are  the  different  types  of  headache  that  one  may  some- 
times easily  be  mistaken  for  another.  Authors  lead  their  readers  into 
a  feeling  of  treacherous  self-security  by  telling  them  that  each  sort  of 
headache  has  its  own  marked  and  distinctive  characteristics.  The 
characteristics  are  quite  shadowy  and  scarcely  ever  more  than  barely 
suggestive.  Exceptions  are  all  too  frequent  to  the  general  rules  laid 
down  in  the  books.  The  only  safe  way  to  do  is  to  search  for  and 
diagnose  the  primary  disease  on  top  of  which  lurks  the  headache  that 
induced  the  patient  to  consult  the  physician. 

Prognosjs. — This  depends  so  absolutely  upon  the  underlying 
cause  that  nothing  further  need  here  be  said  about  it. 

Tre.\tment. — The  proper  treatment  of  headache  is  the  removal 
and  treatment  of  the  underlying  cause.  Anything  short  of  that  is  a 
mere  makeshift.  The  shops  are  full  of  so-called  headache  remedies, 
sure-cures  and  patent  nostrums.  A  physician  w'ho  treats  a  case  of 
headache  that  presents  itself  at  his  office  by  prescribing  a  pain-killer 
or  shot-gun  sedative  mixture,  without  attempting  to  find  out  and  re- 
move the  cause,  is  exercising  about  as  much  intellectual  acumen  as 
the  individual  himself  w^ould  do  if  he  had  first  gone  to  the  drug  store 
and  asked  for  one  of  the  much-lauded  headache  cures'.  '  The  laity  rec- 
ognize this  and  reason  to  themselves  justly  and  unanswerably  that 
there  is  nothing  gained,  but  something  saved,  by  not  consulting  such  a 
physician.  ]Much  of  the  rampant  quackery  and  counter-prescribing  of 
the  day  is  thus  fostered,  and  such  physicians  can  take  much  of  the 
blame  for  it  to  themselves. 

Every  case  of  headache  indicates  some  disease  of  more  or  less 
severity,  and  though  a  physician  may  at  first  attem.pt  to  give  the  pa- 
tient comfort  by  annulling  the  pain,  his  duty  and  his  reputation  both 
demand  that  he  insist  upon  the  patient  joining  him  in  regarding  his 
trouble  as  something  more  than  mere  head  pain,  and  in  allowing  him 
to  search  for  and  remedy  so  far  as  possible  the  disease  of  which  the 
headache  is  one  symptom.  Under  the  head  of  etiology  I  have  pointed 
out  some  of  the  more  prominent  of  these  troubles,  and  their  treatment 
must  be  sought  for  elsewhere.  I  will  mention  here  merely  some  of 
the  means  of  relief  to  be  employed  temporarily. 

If  the  headache  is  at  all  severe  it  is  well  to  minimize  as  much  as 
possible  all  sources  of  peripheral,  sensory  irritation.  The  patient 
should  occupy  a  dimly  lighted,  still  room,  comfortably  warm  and  with 


THE    XEUROXIC  DISEASES  24I 

free  ventilation.  The  clothing  must  be  loosened  and,  better  still,  re- 
moved entirely  in  some  cases.  The  cutaneous  sensation  should  be  kept 
as  quiet  as  the  visual  and  auditory.  A  warm  bath  is  sedative  in  this 
respect.  If  there  is  congestion  of  the  head,  mustard  pediiuvia  are 
useful,  but  they  must  be  employed  for  half  an  hour  at  least.  Except 
in  a  few  instances  of  occipital  headache  mustard  to  the  nape  of  the 
neck  is  irritating  and  not  equally  compensating.  In  extreme  cases 
two  or  three  leeches  behind  the  ears  may  have  to  be  resorted  to.  Dry 
cups  to  the  shoulders  and  upper  spine  have  helped  some  of  mv  cases. 
The  effect  was  partly  psychic,  I  am  sure.  Electricity  is  useless.  Gentle 
rubbing  and  stroking  of  the  head,  the  cold  water  coil,  the  ice  bags  or 
hot  cloths  to  the  brow  and  nucha  may  be  tried.  Rubbing  the  temples 
with  the  menthol  stick  or  a  twenty  per  cent,  solution  of  menthol,  or  a 
chloroform  liniment  is  sometimes  useful.  Only  alleviation,  however. 
can  be  hoped  fdr  from  all  such  external  applications.  The  stinging  of 
the  skin  diverts  the  attention  temporarily  from  the  cephalalgia.  In 
most  cases  much  more  can  be  anticipated  from  a  brisk  cathartic  given 
early.  Calomel,  salines,  jalap  powder,  elaterium  and  croton  oil  are 
available  for  this  purpose. 

There  are  many  remedies  that  m.ay  be  given,  but  their  effects  will 
vary  in  different  cases.  Phenacetine  has  been  the  most  generallv  useful 
in  my  experience.  A  ten  or  fifteen  grain  dose  is  given  at  once,  and  five 
grains  every  hour  or  half  hour  thereafter  until  about  fifteen  grains  more 
are  taken.  Then  I  continue  the  remedy  in  five-grain  doses  every  two, 
three  or  four  hours.  It  is  well  sometimes  to  give  a  little  brandy  or 
aromatic  spirits  of  ammonia  at  the  same  time,  and  to  insist  upon  the 
patient  retaining  the  recum.bent  position.  Antifebrin  and  antipyrine  may 
be  used  instead,  though  in  my  experience  they  have  threatened  collapse 
several  times.  An  excellent  pain  sedative  sometimes  is  a  thirty  or  fortv 
grain  dose  of  sodium  salicylate.  [Muriate  of  ammonia  in  doses  of  a 
dram  or  half  a  dram  is  recommended.  .Some  of  the  remedies  sug- 
gested under  the  head  of  hemicrania  may  be  tried.  Such  medicines  as 
aconite,  cannabis  indica,  nitromuriatic  acid,  digitalis,  belladonna,  col- 
chicum,  ignatia,  nitroglycerin,  sodium  bicarbonate  and  valerian  should 
be  thought  of  when  the  particular  conditions  present  call  for  them. 
Caffeine  alone,  or  with  full  doses  of  the  bromides,  is  available.  Hydro- 
•  bromic  acid,  aromatic  spirits  of  ammonia  and  valerian  have  assisted 
me  in  some  cases.  Butyl-chloral  hydrate,  camphor,  chloralamid,  ethy- 
lene bromide,  gelsemium,  guarana,  hyoscyamus,  kola  and  quinine  con- 
stitute an  experimental  list  Avhich  it  may  be  convenient  to  have  ready 
at  hand  when  the  case  is  obstinate.  As  a  last  resort  the  stronger  nar- 
cotics may  be  used.  Even  morphine  fails  sometimes  and  there  is 
always  the  danger  of  establishing  the  habit  in  these  cases. 

So  desperate  are  the  cases  sometimes  that  even  blood-letting  and 
the  introduction  of  a  seton  have  found  approval. 

In  no  trouble  is  the  physician's  skill  and  resources  put  to  a  more 
severe  test.  The  greater  these  are  the  happier  he  will  be.  He  should 
never  allow  himself  to  be  so  resourceful,  however,  as  to  thereby  be 
rendered  forgetful  of  the  fact  that  the  fundamental  treatment  of  head- 
ache is  first,  last  and  all  the  time  the  steady  and  persistent  treatment 


242  THE    NEURONIC  DISEASES 

of  the  underlying-  disease  or  defect  out  of  which  the  cephalalgia  is  but 
a  mere  by-product. 

THE  NEURALGIAS. 

The  term  )iciiralgia  means  literally  nerve  pain.  In  a  broad  sense 
every  pain  that  is  experienced  is  a  neuralgia.  In  this  way  the  laity 
still'speak  of  headache  sometimes  as  a  neuralgia.  In  neurology  we 
have  restricted  the  use  of  the  term  to  pains  that  can  be  delinitely  local- 
ized in  the  nerves  of  the  body.  Indefinite  and  diffuse  pains  and  mere 
psychic  distress  we  do  not  include  in  neuralgia. 

The  explanation  and  definition  of  pain  has  been  the  problem  of 
the  ages,  and  we  are  almost  as  far  from  its  solution  as  ever.  Pain 
is  a  phenomenon,  a  manifestation  merely.  It  is  not  a  thing  itself,  but 
merely  represents  the  activity  of  some  thing.  Just  what  this  thing 
is,  and  at  what  point  this  form  of  its  activity  ceases  tfl  be  normal  and 
becomes  abnormal,  is  the  still  unanswered  riddle.  The  localization  of 
the  phenomenon  we  call  pain  and  the  determination  of  its  relationship 
to  what  we  are  pleased  to  denominate  normality  would,  if  known, 
dispel  a  vast  amount  of  confusion  and  contradiction  in  regard  to  all 
neuralgia. 

I  will  endeavor  in  as  few'  words  as  possible  to  make  clear  the 
position  of  modern  neurology  in  regard  to  these  two  important  ques- 
tions, and  I  think  it  will  help  us  to  classify  and  comprehend  better 
the  specific  forms  of  neuralgia  now  about  to  be  considered. 

It  is  conceded  by  every  one  that  the  experience  of  pain  is  dependent 
upon  the  nervous  elements.  If  the  nervous  elements  of  the  body  could 
be  in  some  miraculous  way  dissolved  out  of  it,  without  in  the  least 
disturbing  the  bones,  muscles  and  other  tissues,  there  would  absolutely 
cease  to  be  all  pain  or  possibility  of  pain. 

In  what  part  of  the  nervous  system  does  this  function  of  the  pain 
sense  reside?  Both  experimental  and  pathological  observations  prove 
that  the  neurones,  the  true  nervous  elements,  the  cell-bodies  with  their 
processes,  constitute  its  seat.  The  neuroglia,  the  connective-tissue  and 
the  blood-vessels,  the  sustentacular  elements  interwoven  with  the  net- 
work of  neurones,  do  not  subserve  in  any  way  the  awakening  or  the 
transmission  of  the  pain  sense.  By  the  aid  of  certain  experimental 
and  pathogenetic  degenerative  processes  we  have  learned  pretty  ac-- 
curately  just  which  sets  of  neurones  it  is  that  are  sensory.  There  are 
so  many  different  forms  of  sensation,  such  as  touch,  temperature,  pain 
and  special  sense,  and  the  neurones  that  subserve  them  are  all  so  closely 
intermingled,  that  only  in  connection  with  one  or  two  of  the  special 
senses  are  we  able  to  say  just  what  sets  of  neurones  belong  to  each 
respective  form  of  sensation.  We  can  pick  out,  as  it  were,  the  visual  or 
the  auditory  neurones,  but  we  cannot  pick  out  the  pain-sense,  the  tactile 
and  the  temperature-sense  neurones.  We  can  only  speak,  then,  of 
general  sensory  neurones  and  special  sensory  neurones,  and  in  a  gross 
way  we  can  point  out  where  each  respective  set  is  to  be  found. 

When  we  examine,  by  staining  and  microscopic  methods,  these 
sensory  neurones  and  compare  them  with  w^hat  we  have  learned  to  be 
the  motor  neurones,  we  discover  that  apparently  there  is  no  essential 


THE    XEURONIC  DISEASES  243 

difference  in  their  intimate  structure.  1  say  apparently^  because  even 
yet  we  dare  not  assume  that  our  modern  means  of  investigation,  mar- 
velous as  they  are,  are  absolutely  perfect,  reliable  and  ultimate.  With 
our  present  means  of  investigation,  however,  we  make  bold  to  assert 
that  all  neurones  of  the  body,  sensory,  motor  and  trophic,  are,  except 
in  some  obviously  and  functionally  unimportant  particulars,  structurally 
alike.  This  assumption  is  strengthened  in  part,  as  I  have  pointed  out 
elsewhere,  by  the  fact  that  the  manifestations  of  nervous  activity 
are  revealed  to  us  not  in  the  nervous  elements  themselves,  but  in  their 
related  end  organs.  Motion  is  not,  strictly  speaking,  a  nervous,  but  a 
muscular  phenomenon.  Vision,  hearing  and  touch  are  manifestations 
or  experiences  evolved  by  special  extra-neural  apparatus  connected  in- 
timately with  similarly  constructed  nervous  elements. 

As  on  the  motor  side,  so  on  the  sensory,  then,  we  assume  that  the 
neurones  are  not  only  structurally  the  same,  but  functionally  the  same, 
and  that  their  apparent  differences  of  function  are  dependent  upon  the 
particular  end  organs  with  which  they  happen  to  be  connected. 

Though  the  proofs  from  the  laboratory  are  not  yet  absolutely  be- 
yond question,  they  are  so  strongly  in  favor  of  the  uniformity  of 
nervous  matter  everywhere,  both  in  structure  and  function,  that  it  has 
almost  become  an  axiom  iri  neurology  that  there  is  a  specific  nerve^ 
energy,  a  form  of  irritability  merel}^,  which  is  the  same  everywhere, 
but  which  is  revealed  in  various  ways  through  the  various  non-neural 
tissues  and  organs  with  which  the  nerve  elements  are  in  organic, 
functional  relationship.  If  this  is  so,  then  we  must  look  to  the  ends 
of  the  pain-sense  neurones  for  the  explanation  of  the  nature  of  pain. 
Unless  we  add  pain  as  an  additional  form  of  energy  in  the  nervous 
elements  to  the  one  universal  specific  nerve-energy,  irritability,  we 
must  account  for  the  pain,  just  as  we  do  for  motion,  for  secretion,  for 
vision,  for  hearing,  for  taste,  for  touch  and  so  forth,  by  the  presence 
of  some  extra-neural  mechanism.  If  it  be  so  added  as  merely  another 
form  of  neurility,  it  would  have  to  be  a  characteristic  of  motor  neu- 
rones too. 

Analogical  reasoning  bears  us  out,  therefore,  in  the  contention 
that  pain  as  a  specific  sense  is  the  result  of  nervous  irritability  working 
in  conjunction  with  some  sort  of  extra-neural  structure  or  mechanism. 

There  are  many  gross  observations  in  physiology  and  clinical  prac- 
tice that  lend  color  to  this  conception  of  the  nature  of  pain.  I  will 
now  refer  to  these  somewhat  in  detail,  as  they  will  have  to  do  with  the 
relationship  of  pain  to  what  we  are  pleased  to  call  normality,  and 
which  I  said  was  the  second  great  problem  to  be  solved  in  connection 
with  this  very  commonplace  phenomenon  called  pain. 

Having  shown  that  the  trend  of  modern  neurology  is  toward  af- 
firming positively  that  pain  is  not  a  neural  manifestation  per  se,  but  the 
expression  of  mere  neural  irritability,  responding  to  the  abnormal  work- 
ing of  some  extra-heural  tissue  or  mechanism,  it  behooves  us  to  point 
out  as  far  as  possible  w^here  and  what  that  extra-neural  mechanism  is. 

It  will  be  conceded  that  sensory,  like  motor  neuronic  irritability, 
needs  for  its  manifestation  an  external  stimulus.  It  will  doubtless  be 
also  conceded  that  for  its  proper  termination  into  what  we  call  pain, 


244  '^^^^    XEUROXIC   DISEASES  • 

and  not  into  some  other  form  of  sensation,  the  irritability  must  expend 
itself  upon  some  specific  organ  or  mechanism. 

The  stimulus  is  from  without  and  is  in  the  form  of  an  irritation. 
If  the  stimulus  can  originate  in  the  neurone  itself  and  provoke  thus  the 
specific  sense  of  pain  by  expending  itself  solely  within  the  neurone, 
apart  from  its  central  connections,  we  would  be  forced  to  go  back 
again  and  believe  that  the  evolution  of  pain  is  a  specific  form  of  nerve- 
energy. 

A  stimulus  may  come  from  a  degeneration  or  other  nutritional 
molecular  change  in  the  neurone,  or  in  a  part  of  it,  say  at  the  outer  end 
of  its  peripheral  process,  but  the  stimulus  will  have  to  pass  out  of  the 
neurone  in  some  way  to  provoke  pain  unless  we  believe  that  the  pro- 
duction of  pain  is  a  function  of  the  neurone,  which  vv'ould,  of  course, 
destroy  the  axiom  that  there  is  only  one  specific  form  of  nerve-energy, 
mere  irritability. 

Stimuli  we  find  may  be  conceived  of  as  extra-neuronic  and  intra- 
neuronic.  The  extra-neurcnic  forms  of  stimulation,  both  in  health 
and  in  disease,  are  of  common  observation  and  form  the  source  of  nine- 
tenths  of  our  pain  sensations.  The  intra-neuronic  forms  of  stimula- 
tion are  probably  best  evidenced  in  the  peripheral  degenerative  troubles 
in  the  sensory  nerves.  These  are  not  common,  though  they  may  be 
assumed  to  be  the  basis  of  some  of  the  pains  of  certain  general  and 
localized,  mild  or  severe,  degenerative  troubles,  like  pseudo-tabes  of 
the  Dejerine  type,  of  a  few  cases  of  so-called  peripheral  degenerative 
neuritis  from  alcohol,  arsenic,  etc..  and  possibly  from  some  forms  of 
neurosis  like  neurasthenia. 

These  peripheral  degenerations  are  not  uncommon,  but  it  is  always 
a  question  whether  they  are  primarily  degeneration  and  not  secondarily 
degeneration  from  a  compressing  inflammation,  new  growth  or  other 
lesion  in  their  close  proximity.  Granting  that  we  do  have  an  inherent 
peripheral  stimulus  in  this  occasional  primary  peripheral  degeneration 
in  the  neurone  that  subserves  normally  the  pain-sense,  we  have  an  ex- 
planation of  the  specific  primary  degenerative  neuralgias  referred  to 
in  the  books. 

This  stimulus  must  expend  itself  centrally  upon  some  special  cell, 
organ  or  mechanism  to  produce  the  specific  sense  which  we  call  pain. 
We  find  the  cell  bodies  of  the  sensory  neurones  scattered  all  the  way 
up  and  down  the  nervous  tracts.  This  I  have  pointed  out  in  the  earlier 
chapter  on  the  neurone  and  the  neuronic  architecture  of  the  nen^ous 
system. 

Are  the  central  sensory  cells  individually  the  pain-sense  centers? 
We  find  sensory  cells  in  the  posterior  root  ganglia,  in  the  posterior 
cornua,  in  the  bulbar  ganglia,  in  the  central  ganglia  of  the  brain  and 
in  the  cerebral  cortex.  W'hich  of  them  subserve  the  pain-sense ;  and 
were  we  able  to  determine  which,  would  the  cells  themselves  be  the 
mechanism  wherein  the  incoming  sensory  impulse  is  transformed  into 
a  pain-sense?  It  would  hardly  seem  so,  for  if  a  sensory  nerve  be  cut 
off  from  its  cutaneous  connections  and  the  proximal  end  of  it  be  irritat- 
ed, pain  is  experienced.  If  under  such  circumstances  the  transforma- 
tion of  this  afferent  impulse  into  the   specific  pain    sense  be   accom- 


THE   NEURONIC   DISEASES  245 

plished  by  the  individual  cell  to  which  the  impulse  has  centrally  arrived, 
apart  from  this  cell's  connection  with  all  other  cells,  we  will  again  be 
driven  to  attributing  to  these  cells  both  a  specific  structure  and  func- 
tion. We  will  then  have  to  relinquish  the  idea  again  that  nervous  ele- 
ments have  all  only  one  and  the  same  function,  the  manifestation  of 
irritability,  and  that  their  differences  of  function  depend  merely  upon 
their  connections.  This  will  not  be  necessary,  however,  it  seems  to  me, 
for  there  are  many  clinical  observations  that  go  to  show  most  sus- 
piciously that  the  sensory  cells  are  not  individually  the  centers  for  the 
transformation  of  mere  afferent  impulses  into  specific  pain  sensations. 
Chief  among  these  observations  are  the  following : 

1.  The  obliteration  of  consciousness  by  ether  narcosis  abolishes 
all  pain  sense,  without,  so  far  as  we  can  see,  abolishing  the  functions 
of  the  afferent  neurones  generally.  Of  course,  all  sensation  is  largely 
subjective  and  the  patient's  ego  being  for  the  time  in  abeyance,  there 
are  no  subjective  results  from  peripheral  stimulation.  Some  of  the 
reflexes  that  are  outside  of  the  sphere  of  consciousness  are  still  active ; 
for  example,  the  visceral  reflexes.  Here  the  sensory  cells  are  apparently 
still  intact  and  so  far  as  we  know  they  are  not  essentially  different  from 
the  cells  that  functionate  in  the  conscious   sphere. 

2.  In  the  same  line  of  proof  is  the  fact  that  memory  retains  spe- 
cific forms  of  sensation,  when  the  usual  sources  of  the  afferent  im- 
pulses are  removed,  as  is  seen  in  cases  of  amputation.  There  may  be 
some  question  as  to  whether  consciousness  is  co-extensive  with  the 
entire  nervous  apparatus  or  is  to  be  confined  solely  to  the  brain.  In 
regard  to  memory  there  is  no  such  question,  however.  Memory  is  a 
brain  function,  or  at  least  not  a  spinal  cord  function.  Most  de- 
structive diseases  of  the  cord  can  occur  without  the  slightest  weaken- 
ing of  the  memory.  In  the  amputations,  therefore,  in  which  memory 
retains  sensory  pictures,  it  would  be  demonstrated  that  the  functions 
of  the  cord  cells  and  brain  cells  are  dift'erent.  Cord  cells  don't  memor- 
ize, consciously  at  least;  cortical  cells  do.  As  the  cells  are  the  same 
functionally  and  histologically,  though,  we  must  search  for  another 
reason  for  the  difference  in  their  functions  in  this  respect.  It  is  to  be 
found  outside  of  the  cells — namely,  in  their  relationship  and  interplay 
with  other  cells.     It  is  in  the  mind. 

In  its  last  analysis,  then,  pain  is  a  pure  mental  manifestation.  It  is 
not  a  specific  form^  of  nerve-energy.  It  is  not  a  direct  product  of 
individual  cellular  activity.  It  is  dependent  upon  the  activity  of  certain 
cells  for  its  expression.  It  is  a  psychic  phenomenon,  with  all  the 
-variability  and  all  the  uncertainty  that  goes  with  a  complex  manifesta- 
tion of  a  complicated  physical  interplay  of  individual  physiological 
units,  such  as  the  mind  is. 

Pain  is  not  an  entity.  It  is  a  psychic  experience ;  one  of  what 
Wundt  well  calls  the  psychical  elements.  Being  dependent  for  its  pri- 
mary evolution  upon  the  activity  of  a  physical  basis,  it  assumes  a  phys- 
ical appearance  and  we  speak  in  common  parlance  of  physical  pain. 
On  the  other  hand,  being  a  psychical  element  and  partaking  of  all  the 
characteristics  of  mind,  w^e  speak  of  it  as  a  psychical  pain. 

There  can  obviously  not  be  two  kinds  of  pain  that  are  identical 


246  THE    NEURONIC   DISEASES 

and  yet  different  at  the  same  time.  The  difference  between  physical 
and  psychical  pain  is  one  merely  of  the  nature  of  the  stimulus  and  the 
underlying  physical  basis.  Like  the  distinction  between  colors,  which  is 
a  purely  psychic  or  cerebro-psychic  phenomenon,  and  which  we  project 
into  the  outer  world  by  attributing  the  colors  to  the  objects  or  sources 
of  the  visual  stimulation,  so  the  pain,  which  is  a  psychic  experience, 
is  projected  outward  and  we  say  that  the  pain  is  in  that  nerve  or  this 
organ,  whereas  the  latter  is  only  the  objective  source  of  the  stimula- 
tion. 

This  has  all  a  most  practical  bearing  and  if  the  general  truth  un- 
derlying it  is  fully  grasped,  it  will  not  be  difficult  to  realize  that  a 
psychic  pain,  such  as  may  occur  in  hysteria  and  other  psychoneuroses, 
is  as  much  of  a  reality  as  is  a  pain  caused  by  a  corn  on  the  toe.  In 
neither  case  is  the  pain  sense  per  se  different ;  in  either  case  it  is  a 
psychosis  due  to  different  sources  of  stimulation.  In  the  latter  case 
we  can  reach  the  source  of  stimulation  with  the  knife  and  salves ;  in 
the  former  case  there  is  a  disturbance  in  the  functional  interplay  of  the 
psychical  elements  of  such  a  nature  that  neither  surgery  nor  medicine 
can  reach,  but  only  psychic  measures  which  belong  to  the  same  sphere 
of  action,  the  psycho-netirotic,  that  the  disease  does. 

Extra-neural  stimuli  of  so-called  physical  pains  are  as  a  rule  very 
amenable  to  treatment,  and  their  prognosis  is  generally  favorable.  In- 
tra-neural  (neuronic)  stimuli  which  produce  both  the  so-called  physical 
and  mental  pains,  are  very  obstinate  to  treatment  and  possess  a  rela- 
tively hopeless  prognosis. 

As  the  pains  of  the  first  sort  were  the  most  obvious  and  the  first  to 
be  recognized  boldly,  and  as  the  particular  nerves  involved  in  the  extra- 
neural  lesion  were  clearly  and  easily  discoverable,  nerve  pains  came  to 
be  identified  with  individual  nerves  and  the  term  Neuralgia  acquired  a 
very  narrow  meaning.  So  fixed  is  this  meaning  now  that  it  would  be 
hazardous  in  the  extreme  to  use  it  in  any  broader  sense.  I  will  there- 
fore continue  to  employ  the  term  as  a  synonym  for  a  pain  that  can  be 
referred  to  some  particular  nerve  or  nerves.  As  these  nerves  are  sub- 
ject to  inflammation,  compression  and  destruction,  they  will  be  appro- 
priately discussed  under  their  own  individual  heads  in  the  section 
devoted  to  the  non-neuronic  affections  in  the  latter  part  of  this  book. 
Here,  however,  ought  to  be  noticed  those  neuralgias  which  are,  or  may 
be,  referred  to  particular  nerve  trunks,  but  which  reveal  no  discoverable 
changes  in  or  out  of  the  constituent  sensory  neurones,  which  are  of 
central  origin  and  which  therefore  partake  of  all  the  traits  of  a  true 
psychoneurosis. 

These  are  what  some  writers  mean  by  the  primary  or  essential 
neuralgias.  Like  all  similar  neuroses  they  have  a  neuropathic  heredity 
behind  most  of  them,  or  occur  as  a  part  of  a  general  neuropathic  state ; 
are  probably  the  expression  of  a  congenital,  nutritive  deterioration  of 
greater  or  less  degree  in  the  general  neuronic  elements  of  the  nervous 
system ;  are  of  doubtful,  often  hopeless,  prognosis ;  and  are  not  very 
amenable  to  treatment  except  through  general  tonics,  powerful  seda- 
tives, isolation,  disciplinary  and  psychic  measures,  by  which  they  may 
sometimes  be  considerably  helped,  but  not  cured. 


THE    XEUROXIC   DISEASES 


247 


Clinically  it  is  not  always  possible  to  differentiate  an  idiopathic 
neuralg-ia  from  the  pain  caused  by  neuritis,  reflex  irritation  or  neigh- 
boring disease.  This  is  because  both  may  be  of  such  a  slight  degree 
that  the  characteristic  symptoms  of  either  are  not  well  marked.  The 
difficulties  of  practice  should  not,  however,  be  allowed  to  interfere  if 
possible  with  the  accurate  presentation  of  the  known  facts  of  science. 
A  neuralgia  that  is  a  mere  reflex  pain  does  not  seem  to  me  to  be  prop- 
erly classified  as  a  disease,  though  it  is  proper  to  refer  to  it  in  a  work 
upon  nervous  disturbances,  just  as  we  there  also  refer  to  other  normal 
functions  of  the  nervous  system.  A  neuralgia,  for  instance,  that  is 
caused  by  a  cicatrix,  a  bad  tooth  or  loose  internal  organ,  I  would  call 
attention  to,  not  as  a  nervous  disease,  but  as  a  disease  overworking  a 
normal  ner^'ous  function.  It  is  to  be  corrected  by  removing  the  cause, 
but  it  is  certainly  not  a  "true  idiopathic"  neuralgia  in  the  sense  of 
being  a  disease  any  more  than  the  sudden  touching  of  a  hot  plate  or 
the  prick  of  a  pin  is  a  neuralgia  in  the  sense  of  being  a  disease. 

This  is  an  important  distinction,  for  practically  all  of  the  so-called 
reflex  neuralgias  are  of  this  character  and  need  no  treatment  other  than 
removal  of  the  source  of  the  reflex.  Every  nerve  pain  should  be  ex- 
haustively examined  for  a  possible  irritant  of  this  sort. 

This  leaves  then  only  the  inflamed  nen^es  to  be  differentiated  from 
the  idiopathic  pains. 

A  careful  consideration  of  the  pathological  condition  in  neuritis, 
and  the  absence  of  such  a  condition  in  primary  neuralgia,  will  help 
one  to  realize  the  diff'erence  in  the  clinical  presentation  of  the  two 
troubles.  The  former  is  locally  irritant  and  compressing :  the  disease 
process  is  not  uniform  throughout  the  entire  nerve  length ;  the  nearby 
motor  elements  are  im.plicated  in  the  damage,  along  with  the  sensory ; 
and  there  is  a  rather  sharp  limitation  of  all  the  sensory  and  motor 
signs  to  the  one  nerve  and  its  area  of  distribution. 

Idiopathic  neuralgia,  on  the  other  hand,  is  a  central  neurosis,  there- 
fore there  are  no  marked  local  manifestations :  the  nerve  is  sore,  to 
be  sure,  but  it  is  not  sharply  and  distinctly  locally  sore;  the  whole 
nerve  is  equally  sore.  The  pain  is  a  referred  pain.  I  recently  saw  a 
case  in  consultation  that  had  been  vigorously  treated  locally  with  mas- 
sage, electricity,  etc.,  as  an  instance  of  sciatica.  The  pains  were 
paroxysmal  and  complained  of  almost  entirely  in  the  foot  and  a  short 
way  up  the  leg.  Pressure  on  the  nerve  caused  soreness,  but  not  pain. 
I  diagnosed  intrapelvic  secondary  irritation,  which  proved  to  be  abun- 
dantly present  upon  further  examination  by  a  surgeon  of  ability. 

Idiopathic  neuralgia  has  no  motor  symptoms  except  what  may 
be  caused  in  a  general  way  by  the  pain  of  movement.  There  are  no 
electrical  reactions.  Xo  atrophy  appears  except  late  in  the  disease. 
The  paroxysmal  character  of  the  pain  indicates  its  idiopathic  nature, 
though  it  must  be  remembered  that  a  mobile  source  of  irritation  to  the 
nerve  may  cause  a  mere  reflex  pain  to  come  and  go  like  a  paroxysmal 
trouble.  A  tender  nerve  can,  of  course,  be  made  still  more  painful  by 
sudden  movements,  jars,  coughing  and  sneezing.  I  have  found  stretch- 
ing of  a  nerve  that  caused  marked  exacerbation  of  pain,  say  by  forcible 


248  THE    NEURONIC  DISEASES 

flexion  of  a  limb,  to  be  rather  indicative  of  a  neuritis  than  an  essential 
neuralgia. 

Early  motor,  other  sensory  symptoms  with  the  pain,  and  trophic 
manifestations  point  to  neuritis.  In  fact,  pain  and  only  pain  constitutes 
the  entire  clinical  picture  of  neuralgia. 

Late  trophic  symptoms  of  a  general  character,  like  falling  of  the 
hair,  etc.,  may  be  due  to  the  same  general  neuropathic  condition  of 
which  the  neuralgia  is  itself  one  evidence. 

Changeability  of  neuralgia  is  in  marked  contrast  with  the  fixity 
of  the  neuritis.  It  is  not  an  uncommon  thing  for  a  primary  neuralgia 
to  suddenly  transfer  itself  to  the  corresponding  nerve  on  the  opposite 
side  of  the  body,  or  to  some  other  remote  nerve.  Hypersesthesia  of  a 
slight  degree,  but  never  anaesthesia,  sometimes  occurs  late  in  the  area 
of  the  skin  innervated  by  the  affected  nerve.  The  pressure  points  of 
Valleix  are  as  a  rule  indicative  of  neuritis,  being  the  local  spots  in  the 
nerve  where  the  inflammatory  spots  are  most  exalted.  In  neuralgia, 
however,  they  may  indicate  where  the  sore  ner^^e  happens  to  pass  over 
a  bony  edge  or  prominence. 

Prolongation  of  the  pain  has  its  general  depressing  efi'ect  upon 
the  constitution,  though  it  must  be  remembered  that  primary  neuralgia 
is  mostly  observed  in  depressed,  cachectic  and  neuropathic  individuals. 
yUld  psychosis,  such  as  melancholia,  is  often  present.  Suicide  is 
thought  of  in  many  severe  cases. 

The  causes  of  primary  neuralgia  are  the  general  cachectic,  infective 
and  toxic  states.  Mental  shock  may  cause  it.  Debility  is  the  most 
frequent  cause.  It  is  doubtful  if  malaria  is  so  much  a  cause  as  it  is 
supposed  to  be.  Neuralgia  is  not  more  common  in  malarious  districts 
than  elsewhere.  One  must  not  confuse  the  neuralgia  of  the  general 
debilitated  state  induced  by  rheumatism,  gout,  Bright's  disease,  lead 
intoxication,  diabetes  or  exposure  with  the  neuritis  often  produced  by 
the  same  causes. 

Women  of  neuropathic  families  are  the  greatest  sufferers  from  the 
disease.  Children  and  the  aged  do  not  have  to  endure  it.  It  is  prac- 
tically unknown  before  fifteen  years  of  age. 

The  follow'ing  are  some  of  the  more  prominent  forms  of  idiopathic 
neuralgia  and  their  treatment : 

Tic  Douloureux.  Trigeiiiinal  Neuralgia.  Prosopalgia.  This  is 
a  frequent  form  of  idiopathic  neuralgia.  It  should  always  be  carefully 
distinguished  from  symptomatic  pains  in  the  fifth  nerve,  from  various 
lesions  and  sources  of  irritation  around  and  near  it.  The  latter  are  very 
common  and  w'ill  be  referred  to  again  under  the  head  of  special  dis- 
eases of  the  fifth  nerve.  In  tic  douloureux  the  patients  are  usually 
neuropaths  in  the  middle  period  of  life. 

All  branches  of  the  nerve  may  be  the  seat  of  the  pain  and  the 
trouble  may  be  unilateral  or  bilateral.  The  paroxysmal  and  intense 
character  of  the  pain  is  a  marked  feature  of  it.  Usually  it  is  limited  to 
one  branch  of  the  nerve  and  is  most  excruciating.  It  is  described  as  a 
feeling  like  a  boring  piece  of  hot  iron,  or  a  hot  knife  cutting  into  the 
face.  All  movement  is  avoided.  Tenderness  is  felt  and  even  twinges 
of  pain  in  neighboring  nerves.    From  the  cheek,  the  lips  and  side  of  the 


THE    NEURONIC  DISEASES 


249 


nose,  where  the  pain  is  usually  at  its  maximum,  it  seems  to  radiate 
into  the  teeth,  over  the  eye,  up  or  to  the  head  and  across  the  temple. 
The  face  becomes  red,  the  eyes  water,  the  flow  of  saliva  and  nasal 
mucus  increases.  The  agony  lasts  a  few  minutes  and  then  the  pain 
partially  recedes.  It  usually  returns  again  and  the  new  paroxysm  may, 
like  the  first,  be  started  by  some  simple  irritation  against  the  skin. 

Long  standing  cases  may  be '  accompanied  after  years  of  suffering 
by  premature  turning  gray  of  the  hair  and  in  rare  instances  facial 
hemiatrophy. 

The  disease  usually  involves  tlie  supra-maxillary  branch  on  one 
side.  The  supra-orbital  and  inframaxillary  branches  are  less  often  im- 
plicated. 

Changes  of  the  weather  sometimes  affect  the  pains  and  they  are 
worse  as  a  rule  in  winter  than  they  are  in  summer.  The  severe  forms 
of  these  neuralgias  that  sometimes  occur  in  the  aged  were  called 
epileptiform  by  Trousseau. 

In  the  diagnosis  of  tic  douloureux  every  possible  reflex  and  symp- 
tomatic pain  of  the  nerve  should  be  eliminated.  It  is  to  be  frankly 
admitted  that  this  cannot  always  be  done.  It  is  to  be  remembered, 
then,  that  pure  idiopathic  neuralgia  of  the  fifth  nerve  is  far  less  fre- 
quent than  any  of  the  other  forms.  One  should  always  be  on  the  alert 
to  recognize  at  any  time  symptoms  that  point  to  some  other  cranial 
disease  which  has  caused  the  pains.  If  the  patient  is  neuropathic,  if 
there  is  a  heredity,  direct  or  indirect,  behind  the  disease,  if  the  pains 
are  markedly  paroxysmal  and  severe,  almost  epileptiform  in  character, 
and  if  they  constitute  the  entire  clinical  presentation  in  the  case,  a 
diagnosis  of  tic.  douloureux  will  probably  be  correct. 

The  treatment  of  tic  douloureux  is  not  a  very  grateful  task.  It 
is  a  most  obstinate  trouble  and  often  resists  all  measures.  Sometimes  it 
ceases  all  at  once.    Would  that  we  could  always  take  the  credit  for  this. 

Ever}'  case  must  be  managed  along  general  lines  and  treated  for 
the  paroxysm.  The  whole  physical  and  mental  being  must  be  built  up. 
Change  of  scene,  change  of  thought  and  entire  change  of  environment 
may  be  necessar}'.  The  diet  must  be  abundant,  plain  and  nutritious. 
The  functions  of  the  body  must  be  systematically  attended  to.  Tonics 
like  iron,  quinine,  cod  liver  oil  and  hypophosphites,  and  especially 
arsenic,  may  be  judiciously  administered.  All  defects,  such  as  circula- 
tor}- weakness,  poor  blood,  insufflciency  of  the  kidneys,  ocular  anoma- 
lies, sluggish  liver,  must  receive  their  quota  of  attention.  In  some 
cases  general  treatment  along  these  lines  will  cause  the  paroxysms  to 
cease  entirely,  or,  what  is  more  likely,  to  remain  farther  apart  and  be 
less  severe. 

The  treatment  of  the  paroxysms  will  indeed  tax  the  physician's 
resources  to  the  uttermost.  It  is  discouraging  to  read  the  long  list 
of  remedies  that  are  recommended,  and  yet  that  generally  prove  inert. 
Still  something  must  be  done,  and  as  amelioration  does  sometimes  most 
unexpectedly  follow  the  administration  of  a  remedy,  we  must  go  on 
giving  them,  even  though  it  be  dike  a  forlorn  hope.  In  aged  persons 
nitroglvcerin,  gr.  i-ioo  every  three  or  four  hours,  has  been  effective. 
Ansemic   cases   mav   have   their   attacks   aborted  bv   an   inhalation   of 


250  THE    NEURONIC  DISEASES 

nitrite  of  am}l.  Sodium  sal!C}late  in  twenty  or  thirty  grain  doses  may 
be  successful.  Quinine,  arsenic,  gelsemium  and  potassium  iodide  in 
full  dosage  are  occasionally  available.  The  last  should  be  given  es- 
pecially if  there  is  the  slightest  history  of  syphilis  in  the  case.  Co- 
caine instillations  into  the  conjunctival  sac,  and  painting  of  the  nasal 
mucous  membrane  with  five  or  ten  per  cent,  solutions  may  afford  tem- 
porary relief. 

Butyl-chloral,  croton  chloral,  codeine,  narceine,  napellin,  neurodin. 
stramonium,  pyramidon,  atropine,  cannabis  indica  may  be  experimented 
with.  The  coal-tar  preparations  vvcre  useless  in  my  experience. 
Duquesnel's  aconitine  has  been  useful  in  some  of  my  cases. 

The  employment  of  morphine  must  be  instituted  with  extreme 
caution.  Dana  recommends  for  cases  not  over  four  or  five  years' 
standing  rest  in  bed  with  massive  doses  of  strychnine.  I  have  seen 
this  succeed  in  one  case.  The  drug  is  given  hypodermically  in  doses 
of  gr.  1-30  once  daily  and  gradually  increased  until  gr.  1-6  or  1-5  is 
reached.  This  is  kept  up  for  four  days,  and  then  gradually  reduced. 
Absolute  quiet  is  enjoined  in  bed.  After  a  month  iron  and  potas- 
sium iodide  are  exhibited.  The  treatment  can  be  repeated  with  less 
vigor. 

Certain  local  measures  sometimes  relieve  the  pain.  I  have  referred 
to  the  use  of  cocaine.  Local  freezing  with  a  methyl  chloride  spray,  or 
the  application  of  extreme  heat,  may  bring  relief  temporarily.  Schleich's 
subcutaneous  local  application  consists  of  a  solution  containing  cocaine 
gr.  j^,  morphine  gr.  %.,  sodium  chloride  gr.  iv^  and  water  5iij. 

Compression  of  the  carotid  arteries  may  be  tried. 

Electricity  is  often  beneficial,  but  it  may  have  to  be  used  in  various 
ways.  Oppenheim  cviriously  secured  temporary  good  results  with  a 
powerful  faradic  brush  applied  to  the  soles  of  the  feet.  This  was 
probably  a  psychic  result.  The  electricity  is  usually  directed  as  near 
as  possible  through  the  affected  nen^e,  or  it  may  be  applied  to  the 
cranium  or  to  the  sympathetic  nerve  in  the  neck.  Galvanic,  faradic, 
static  and  cataphoric  forms  may  all  be  employed.  Galvanization  of  the 
Gasserian  ganglion  is  the  most  generally  useful  method. 

Electrotherapy  so  often  fails  that  I  am  inclined  to  attribute  the 
supposed  cures  from  it  to  the  power  psychic  effect  usually  produces  on 
these  neuropathic  individuals. 

Operative  procedures  often  give  prolonged  temporary  relief,  but 
after  them,  just  as  in  spasmodic  tics,  the  trouble  comes  back.  The 
very  nature  of  the  trouble,  a  central  neurosis,  would  lead  me  to  expect 
that  sort  of  a  result.  However,  in  some  of  the  frightful  cases  a  tem- 
porary relief  of  several  months  amply  pays  for  the  risks  of  the  opera- 
tion. Neurectomy,  extraction  of  the  neiwe  and  intracranial  resection 
of  the  nerve  and  the  Gasserian  ganglion  are  the  procedures  resorted  to. 
Their  description  belongs  to  the  works  upon  surgery. 

Glossodynia  doubtless  should  be  classified  here. 

Occipital  Neuralgia.  As  a  pure  non-symptomatic  form  this  is  ex- 
ceedingly rare.  Usually  disease  in  the  upper  cervical  vertebrae,  or  their 
neighborhood,  and  hysteria,  are  the  causes  of  the  pains  in  the  upper  cer- 
vical nerves.    When  the  neuralgia  is  idiopathic,  unlike  the  other  forms 


TliE    NEURONIC   DISEASES  25 1 

here,  it  is  unilateral,  paroxysmal  and  intense.  Tender  points  are  elicited 
at- the  exits  of  the  nerves.  The  pains  may  alternate  with  those  of  tri- 
geminal neuralgia.    The  treatment  is  the  same. 

C ervico-hrachial  Neuralgia.  This  is  very  rare  idiopathically,  most 
cases  being  due  to  rheumatism  and  other  obvious  causes.  In  neuras- 
thenics and  hysterics  pains  shoot  around  the  shoulder  and  down  into 
the  arm  and  into  the  digits,  following  the  course  of  the  nerves,  particu- 
larly the  ulnar  nerve.  Most  of  the  cases  O'f  cervico-brachial  neuralgia 
that  I  have  seen  were  cases  of  neuritis.  The  diagnostician  must  be  on 
his  guard  in  regard  to  these  pains,  for  often  they  represent  meningeal 
and  other  organic  spinal  cord  lesions.  Their  treatment,  after  eliminat- 
ing all  sources  of  irritation  and  all  organic  disease,  is  the  same  as  for 
all  idiopathic  neuralgias. 

Intercostal  Neuralgia  and  Mastodynia.  This  is  second  in  impor- 
tance only  to  facial  tic  douloureux.  The  left  side  is  usually  afifected  and 
mostly  in  women.  Several  nerves  are  affected  at  the  same  time,  so 
that  the  pain  seems  to  be  in  the  side  of  the  thorax.  Sometimes  the 
radiation  of  the  pain  extends  to  the  inner  side  of  the  corresponding  arm. 
So  many  causes  produce  pains  around  the  body  that  one  must  be  most 
"keenly  on  the  alert  for  other  diseases  and  troubles  that  may  be  the 
cause  of  the  intercO'Stal  pains.  Always  remove  these  causes.  If  the 
pain  still  continues,  then  the  usual  measures  recommended  for  all 
idiopathic  neuralgias  are  to  be  employed.  In  mastodynia  the  neuralgia 
is  limited  to  the  nerves  that  go  to  the  breasts.  They  are  branches  of 
the  intercostal  nerves.  The  pains  are  paroxysmal  and  intense  and  seem 
to  spring  from  those  nerves  that  come  off  from  the  fourth  to  the  sixth 
intercostals.  The  skin  is  hypersesthetic  and  the  breast  tender.  Herpes, 
of  course,  does  not  occur  in  idiopathic  neuralgia,  only  in  neuritis.  The 
pressure  points  are  here  over  the  second  to^  the  sixth  spinous  processes. 
Women  of  middle  age  are  usually  affected ;  men  very  rarely.  Excit- 
ing causes  may  be  pregnancy,  lactation,  fissures,  trauma  and  mental 
excitement.    It  is  a  stubborn  neuralgia  and  the  treatment  is  difficult. 

Lumbar  Neuralgia.  True  essential  neuralgia  of  the  lumbar  nerves 
is  so  rare  that  it  may  be  almost  laid  down  as  an  axiom  that  pain  in 
them  means  neuritis  or  inflammatory  and  neoplastic  development  in 
and  about  the  pelvis. 

Sciatica  1  regard  practically  as  always  a  neuritis  or  a  mere  sec- 
ondary pain.  I  will  discuss  this  further  under  the  head  of  the  sciatic 
nerve. 

Pains  that  appear  in  the  lower  abdominal  region,  in  the  scrotum, 
along  the  perineum,  in  the  buttocks  and  down  the  thighs  will  almost 
surely  be  found  associated  with  some  pelvic  disease. 

Coccygeal  Neuralgia.  Coccydynia.  This  is  practically  a  woman's 
disease.  It  is  an  intractable  neuralgia  of  the  coccygeal  plexus  and 
interferes  with  sitting.  It  may  be  excited  by  walking  or  evacuation 
of  the  bowels.  It  is  sometimes  associated  with  a  local  inflammation, 
though  usually  it  seems  to  be  an  idiopathic  neuralgia.  Opiates  by 
suppository,  local  irritants  and  finally  operations  have  had  to  be  resorted 
to.  Electricity  has  often  here  proved  effective,  one  pole  being  placed 
over  the  coccyx  and  the  other  in  the  vagina. 


-0^ 


THE    NEURONIC  DISEASES 


Plantar  Xciiralgia.  Pododyiiia.  The  pain  here  is  in  the  heel  and 
sole  of  the  foot. 

J'isceral  Xeuralgins.  These  occur  in  neurasthenic  and  hysterical 
women,  especially  in  connection  with  the  heart  and  the  stomach.  They 
must  not  be  confused  with  the  crises  of  tabes  and  other  forms  of  symp- 
tomatic visceral  pains.  Pelvic  neuralgia  is  very  common  in  women. 
There  is  a  nephralgia  that  may  even  lead  to  operation  for  renal  calcu- 
lus. The  intestines,  the  liver,  the  spleen  may  possibly  be  the  seat  of 
pure  neuralgia,  but  if  so  it  is  very  rare.  These  pains  usually  mean 
some  organic  disease  and  had  better  always  be  regarded  in  that  light. 

Spermatic  neuralgia  is  a  very  rare  but  obstinate  affection. 

Uretkrodynia  is  a  rare  and  obstinate  trouble. 

ECLA^IPSIA. 

Convulsions  that  resemble  epileptic  fits,  that  tend  to  recur,  and  that 
are  dependent  upon  causes  outside  of  inherent  brain  changes,  are  now 
specifically  designated  by  the  term  eclampsia.  From  one  point  of 
view  they  may  be  looked  upon  as  a  sort  of  symptomatic  epilepsy,  but  as. 
they  are  always  acute  and  in  most  cases  cease  entirely  after  a  short 
time,  or  after  the  removal  of  the  cause,  it  is  well  to  use  another  name 
for  them  than  that  of  epilepsy. 

There  are  three  prominent  types  of  eclampsia  which  should  receive 
some  notice  in  a  volume  upon  neurolog}' — ^namely,  infantile  eclampsia 
(eclampsia  infantum  J ,  parturient  eclampsia  (eclampsia  parturioitium} 
and  ursemic  convulsions  ^eclampsia  urccmica). 

ECLA^IPSIA  IXFAXTU:^!. 

During  their  early  years  children  are  very  subject  to  convulsive 
seizures  upon  various  provocations.  It  has  been  suggested  that  this 
is  due  to  the  immature  and  undeveloped  condition  of  their  nervous 
apparatus,  especially  the  weak  condition  of  the  higher  inhibitor}-  cen- 
ters, a  reason  which  has  some  plausibility  in  it,  but  fails  to  account  for 
the  convulsions  of  childbed  and  ursemic  poisoning. 

Etiology. — The  causes  of  infantile  convulsions  are  numerous,, 
though  they  may  all  be  grouped  under  any  one  of  the  three  heads,. 
reiiex,  infectious  and  psychic.  Rickets  and  general  debilit}"  are  very 
important  factors  in  the  production  of  the  trouble.  Just  how  much  is 
to  be  attributed  to  the  cachexia  itself,  and  just  how  much  to  the  various 
disturbances  which  the  cachexia  leads  to,  it  is  not  easy  to  say.  Rickets 
occurs  chiefly  between  the  sixth  and  eighteenth  months  of  life.  It  is 
a  condition  that  fosters  or  represents  defective  development  just  at 
the  period  when  the  development  normally  is  most  active.  As  a  result 
it  leads  to  bad  dentition,  to  gastro-intestinal  irregularities  and  to  de- 
fective nutrition  generally.  A  rickety  child  as  a  rule  will  exhibit  a 
large  number  of  local  malformations  and  functional  abnormalities. 
These,  taken  in  conjunction  with  the  general  defective  nutrition,  con- 
stitute a  long  list  of  causes  of  infantile  convulsions.  The  laity  always 
think  of  worms  first  among  the  possible  causes,  but  they  are  not  such 


THE    XEUROXIC   DISEASES  253 

frequent  factors  as  auto-intoxication  from  gastro-intestinal  defects, 
the  distress  of  difficult  dentition,  overloading-  of  the  stomach,  especially 
with  indigestible  food,  profuse  diarrhoea,  etc.  Phimosis,  otitis  media, 
inguinal  hernia  and  other  sources  of  peripheral  reflex  of  an  abnormal 
character  acting  upon  a  badh'  nourished  and  undeveloped  brain,  mav 
all  be  counted  among  the  causes. 

Infectious  fevers  very  frequently  start  in  children  with  a  convul- 
sion. It  is  probably  of  the  same  nature  as  eclampsia  now  under  consid- 
eration, though  as  a  rule  it  is  not  regarded  as  the  same.  It  is  thus  seen 
in  scarlet  fever,  measles,  pneumonia,  etc.  As  a  symptom  of  brain  dis- 
ease, congestion,  inflammation,  hydrocephalus  or  meningitis  it  must  be 
remembered.  Natal  hemorrhage  may  induce  a  convulsion  immediately 
aiter  birth,  to  be  followed  later  on  b}'  all  the  usual  sequelae,  such  as 
hemiplegia,  epilepsy  and  mental  deterioration.  Alental  shock,  such  as 
fright,  night  terror,  fear  upon  being  suddenly  left  alone,  has  provoked 
convulsions. 

No  case  of  infantile  convulsions  should  be  regarded  lightly,  for  be- 
sides indicating  a  dangerously  susceptible,  possibly  cachectic,  constitu- 
tion, it  may  be  but  the  first  indication  of  genuine  epilepsy.  Out  of  1,450 
cases  of  epileps}"  Gowers  found  that  180  began  within  the  first  three 
years  of  life.  Osier  analyzed  460  cases  of  epilepsy  in  children  and 
found  that  in  187  the  fits  com.menced  within  the  first  three  years.  This 
is  the  period  of  life  in  which  eclampsia  occurs.  As  a  rule  epilepsia  con- 
tinues on  past  the  period,  whereas  eclampsia  ceases.  Such,  however, 
is  not  always  the  case.  Convulsions  have  occurred  in  infancy  and  epi- 
leptic fits  later  in  life.  It  would  be  desirable  to  know  just  what  is  the 
exact  relationship  between  epilepsy  and  eclampsia,  if  there  is  any.  It 
certainly  is  not  true  that  early  convulsions  produce  later  epilepsy. 
Hysteria  has  occurred  in  adults  who  had  convulsions  in  childhood.  It 
seems  more  likely,  therefore,  that  a  neuropathic  constitution  is  present, 
which  yields  easily  in  childhood  to  causes  that  provoke  a  convulsive 
seizure,  but  is  able  to  resist  the  greater  neurosis  until  a  later  age.  Epi- 
lepsy as  we  have  seen  occurs  in  infancy.  It  is  the  mj' staking  of  these 
cases  for  eclampsia  that  makes  every  case  of  the  latter  disease  a  mat- 
ter of  serious  consideration. 

Symptoms. — These  are  much  the  same  as  those  of  epilepsy.  Pre- 
monitions are  sometimes  seen  in  an  excessive  irritability,  with  facial 
changes,  slight  twitchings  about  the  mouth  and  rolling  of  the  eyes. 
Most  mothers  can  detect  an  oncoming  convulsion  when  others  see  noth- 
ing wrong.  The  attack  usually  appears  suddenly  with  fixation  of  the 
eyes,  pallor  of  the  lips  and  face,  stiffening  out  of  the  trunk  and  ex- 
tremities, rotation  of  the  head  and  disturbed  respiration.  The  fit  is 
epileptiform  in  every  respect,  except  in  its  severity.  In  a  minute  or 
so  the  spasm  relaxes,  not  to  appear  again  for  some  minutes  or  an  hour 
-or  so,  or  it  passes  into  a  clonic  condition  which  is  usually  slight  and  in- 
volves the  face,  eyes,  hands  and  feet.  In  other  cases,  a  moderate  tonic 
spasm,  interfering  somewhat  with  the  breathing,  may  continue  for 
tw^enty  or  thirty  minutes.  Sometimes  a  series  of  brief  convulsions  oc- 
curs with  partial  recover}-  only  in  the  intervals.  A  scream  accompanies 
some  of  the  attacks.     In  other  cases  onlv  screaming,  grinding  of  the 


254  '^HE    NEURONIC   DISEASES 

teeth  and  a  slight  bilateral  rigidity  are  observed.  These  convulsions 
are  to  be  distinguished  on  account  of  their  bilaterality  from  the  hemi- 
plegic  spasm  of  brain  lesions. 

Gradually  the  attack  subsides,  and  the  child  goes  to  sleep  in  a  state 
of  more  or  less  stupor.  In  fatal  cases  the  attacks  are  severe  and  run 
together  in  rapid  succession,  coma  being  present  as  the  child  dies. 
Death  is  particularly  to  be  dreaded  in  weak  children,  in  cases  with  great 
frequency  of  the  attacks  and  in  diarrhoeal  hydrocephaloids. 

Eclampsia  usually  ceases  after  a  time  never  to  recur.  If  the  con- 
vulsions continue  on  throughout  the  second,  third  and  fourth  years  they 
must  be  looked  upon  as  being  epileptic.  They  are  also  epileptic  if  they 
do  not  cease  after  the  removal  of  what  may  be  regarded  as  an  obvious 
possible  cause. 

Diagnosis. — The  chief  differential  diagnosis  always  to  be  made  is 
between  eclampsia,  epilepsy  and  organic  brain  disease.  The  first  comes 
on  suddenly  in  a  state  of  relative  good  health,  is  associated  with  some 
obvious  cause,  disappears  with  the  removal  of  the  'cause  and  does  not 
continue  or  recur  later  on.  The  second  continues  after  having  once 
appeared,  in  spite  of  the  removal  of  apparent  cause,  and  in  every  way- 
more  nearly  represents  a  true  epileptic  than  does  the  eclamptic  seiz- 
ure. The  third  reveals  characteristic  organic  symptoms,  one-sided 
spasms  that  are  more  or  less  permanent,  and  other  signs  of  intra- 
cranial hemorrhage,  meningitis,  etc.  Laryngismus  stridulus,  rickety 
spasms  and  rigidity,  and  the  hydrocephaloid  state  have  all  an  eclamptic 
appearance  but  need  not  be  considered  here  further. 

Prognosis. — This  is  always  serious.  Some  children  are  able  to 
pass  through  the  ordeal,  but  weak  and  debilitated  infants  usually  suc- 
cumb. Infant  mortality  is  largely  dependent  upon  eclampsia.  Febrile 
convulsions  are  not  very  serious  but  as  I  have  said  they  are  regarded 
by  some  as  not  exactly  the  same  as  eclampsia.  They  usually  occur  in 
more  robust  children.  Chronic  diarrhoea  with  eclampsia  usually  means 
death.  The  prognosis  also  takes  in  the  question  of  the  seizures  being 
those  of  genuine  epilepsy.  After  the  third  year  eclampsia  is  practically 
never  seen. 

Treatment. — Remove  causes  that  can  be  removed  and  treat  those, 
like  the  rickety  condition,  in  the  usual  way  with  syrup  of  the  iodide  of 
iron,  cod-liver  oil,  hypophosphites,  etc.  Every  mother  knows  the  value 
of  sudden  immersion  in  a  warm  bath.  Bromides,  chloral  and  chloroform 
inhalations  are  available  means  for  controlling  the  spasms.  Morphia 
hypodermically,  or  nitrite  of  amyl  may  have  to  be  tried  in  an  attack. 
Bromides  can  be  continued  afterwards. 

ECLAMPSIA  PARTURIENTIUM. 

Etiology. — Young  primiparge  are  the  most  frequent  subjects  of 
childbed  convulsions,  though  women  of  all  ages  and  with  any  preg- 
nancy may  have  them.  They  usually  occur  in  the  last  two  or  three 
months  of  pregnancy,  during  the  parturient  act  or  soon  after  it.  Many 
of  the  patients  are  epileptics  and  the  convulsion  is  only  one  of  their 
usual  fits.    Various  opinions  used  to  be  held  in  regard  to  the  real  cause 


THE    XEL'ROXIC   DISEASFS  255 

of  these  convulsions  such  as  reflex  irritation  in  the  womb,  sepsis  and 
cerebral  anemia  from  the  loss  of  blood.  All  authorities  agree  nowadays 
that  nephritis  is  the  cause  and  that  the  convulsion  is  reallv  ursemic.  It 
is  true  that  the  coma  of  ura^mic  eclampsia  is  usually  wanting  in  puer- 
peral eclampsia,  whereas  in  the  latter  some  credit  must  be  given  for 
the  reflex  influence  from  the  uterus  ;  the  statement  is  not  therefore 
weakened  that  both  ursemic  and  parturient  eclampsia  are  due  to  the 
same  cause  and  are  therefore  all  but  identical.  Albuminuria,  oedema, 
amaurosis  and  albuminuric  retinitis  ma}^  all  be  present  and  confirm  the 
etiology.  Infection  may  play  a  role  in  some  cases  from  a  specific 
bacillus. 

Symptoms. — These  resemble  an  epileptic  seizure  in  every  respect. 
In  addition  there  are  ursemic  manifestations  such  as  intense  headache, 
precordial  pain,  sudden  blindness  and  oedema.  The  fit  sometimes  in- 
cludes a  scream,  profound  com.a,  pallor,  biting  of  the  tongue,  fixation  or 
rolling  of  the  eyes,  and  violent  general  tonic  and  clonic  convulsions. 
The  temperature  often  rises,  the  pulse  becomes  weak  and  the  respira- 
tions assume  the  Cheyne-Stokes  character. 

Prognosis. — About  thirty  per  cent,  of  the  cases  die  in  coma,  in 
an  apoplectic  attack  or  from  the  sepsis.  Status  epilepticus  with  a  tem- 
perature of  109  degrees  has  destroyed  some  patients. 

Treatment. — To  hasten  the  deliverv%  and  how  best  to  do  it, 
are  questions  entirely  for  the  obstetrician.  A'enesection  that  used  to  be 
so  frequently  practiced  is  now  regarded  as  contraindicated.  It  weakens 
the  patient  merely,  without  modif}"ing  the  source  of  the  trouble  in  the 
kidneys.  Chloroform  inhalations,  morphine,  chloral  hydrate  in  full 
dosage,  venesection  with  transfusion,  diaphoresis  with  vapor  baths 
and  pilocarpine,  and  free  purgation  are  all  to  be  resorted  to  according 
as  the  demands  of  the  case  and  the  vigor  of  the  patient  will  indicate. 

ecla:\ipsia  uil^mica. 

The  cause  of  this  is  of  course  nephritis.  The  presence  of  the  kid- 
ney disease  is  determined  by  the  condition  of  the  urine,  albumin  and 
casts  being  generally  present,  by  the  hypertrophy  of  the  heart  and  by 
the  albuminuric  retinitis.  Just  what  is  the  mechanism  by  which  the 
state  of  blood  under  these  circumstances  causes  coma  and  epileptifonn 
seizures  is  not  entirely  clear. 

The  convulsions  usually  occur  suddenly  though  there  may  be 
some  headache,  restlessness,  visual  disturbances,  twitchings  of  the  mus- 
cles, even  a  comatose  state  and  visual  obscurity  just  before  their  onset. 
I  have  seen  such  symptoms  in  patients  in  whom  I  could  only  diagnose 
a  renal  insufficiency,  and  have  observed  them  disappear  with  the  free 
use  of  cathartics  and  diuretics.  They  certainly  suggested  a  remote  re- 
semblance to  uraemia  of  mild  degree. 

Alay  not  some  of  the  cardiac  irregularity,  the  pains,  the  general 
irritability,  the  fibrillary  muscular  twitchings  of  some  severe  cases  of  so- 
called  neurasthenia  be  due  to  slight  renal  trouble,  enough  to  provoke 
a  faint  degree  of  ursemic  intoxication  ? 

In  tvpical  uremic  convulsions  the  coma,  the   spasms,  tonic  and 


256  THE   NEURONIC  DISEASES 

clonic,  the  biting  of  the  teeth,  the  rolling  of  the  eyes  are  all  clearly 
epileptiform.  Nystagmus  is  sometimes  present.  The  pupils  are  gen- 
erally dilated  and  fail  to  react  to  light.  They  have  been  seen  contract- 
ed for  a  brief  spell  and  then  dilated.  Respiration  is  greatly  embarrassed 
and  right  after  the  fit  the  knee-jerk  is  gone.  Coma,  sleep  or  drowsi- 
ness may  all  follow  the  fit. 

Treatment. — Purgatives  and  hot  baths  should  be  used  when  an 
attack  is  threatened.  The  bowel  may  be  irrigated  with  water  at  a  tem- 
perature of  150  degrees  F.,  and  nitroglycerin  freely  used.  For  the  seiz- 
ure chloroform  inhalations  must  be  used,  and  morphine  and  chloral. 
Purgation,  diaphoresis,  with  hot  applications  and  pilocarpine,  and  mor- 
phine especially  for  the  delirium  are  about  all  that  can  be  done. 

TETANY.     TETANILLA. 

This  is  a  disease  characterized  by  tonic,  intermittent  or  continuous 
spasm  of  symmetrical  distribution  in  the  ends  of  the  extremities ;  by 
certain  indefinite  and  irregular  sensory  and  general  phenomena ;  and 
by  a  causation  that  points  strongly  in  the  direction  of  a  severe  intoxi- 
cation of  the  spinal  cord  or  lower  neurones.  Our  knowledge  of  its 
pathology  is  not  ample  enough  yet  to  enable  us  to  classify  the  disease 
definitely.  It  is  seen  but  rarely  in  this  country.  In  Europe  it  is  more 
common  and  in  some  places  of  Sweden  and  Austria  appears  to  be 
almost  endemic.  It  has  occurred  epidemically  in  the  spring  of  the  year. 
The  first  account  of  it  was  given  by  Steinheim  and  Dance,  but  it  was 
through  the  work  of  Trousseau  that  it  first  became  generally  known. 
Many  investigators  have  studied  it  carefully  since,  but  their  views  are 
still  unsettled  and  divergent.  It  has  been  called  pseudo-tetanus,  essen- 
tial contracture,  and  shoemaker's  spasm. 

Etiology. — Tetan}-  has  been  seen  in  every  period  of  life.  It  is 
most  frequent,  however,  in  early  childhood  and  in  early  adult  years.  Up 
to  the  age  of  about  twenty  males  are  far  more  subject  to  it  than  fe- 
males. After  twenty,  strange  to  say,  the  number  of  females  is  almost 
double  that  of  the  males.  This  argues  emphatically  against  an  occu- 
pation cause  for  the  disease  so  strongly  believed  in  by  many.  Children 
and  girls  are  physically  nearer  together  than  are  either  to  adult  males. 
After  fifty  the  males  begin  to  predominate  again.  Occupation  per  se 
is  hardly  a  cause  of  the  disease  though  it  is  said  that  forty-three  per 
cent,  of  the  cases  occurred  among  shoemakers  in  the  German  epidemics. 
The  chances  are  that  contact  with  some  poison  is  favored  by  the  hand- 
ling of  leather.  Certainly  the  disease  is  not  the  occupation  neurosis 
known  as  cobbler's  cramp. 

The  toxic,  infectious  origin  of  the  trouble  is  all  but  positively  sug- 
gested by  a  large  number  of  etiological  factors.  When  it  occurs  in 
women,  for  instance,  it  is  usually  about  the  particularly  exposed  periods 
of  pregnancy  and  lactation.  It  is  seen  in  connection  with  many  gastro- 
intestinal troubles,  so  that  a  gastric  tetany  is  often  spoken  of.  Diar- 
rhoea, intestinal  parasites,  constipation,  the  use  of  tainted  food  and 
pyloric  stenosis  with  dilatation  of  the  stomach  have  preceded  it  with 
suspicious  frequency.     One  woman  suffered  immediately  after  eating 


THE    XEURONIC  DISEASES  257 

some  grapes  and  drinking  soda  water.  Diarrhoea  is  a  particularly  com- 
mon antecedent  in  children.  Autointoxicatian  is  probably  the  explana- 
tion of  these  cases. 

It  is  fostered  by  all  depressing  influences  such  as  exposure  to  cold, 
fatigue,  acute  disease,  rachitis  and  other  diathetic  and  cachectic  con- 
ditions. Be  the  factor  what  it  may,  if  it  exhausts  and  debilitates  the 
constitution  in  general  it  favors  the  onset  of  tetany.  Some  of  the  gas- 
tric cases  have  been  supposed  to  be  reflex  in  character  because  the 
spasm  appeared  immediately  upon  the  introduction  of  the  stomach- 
pump.  Why  does  it  not  occur  m.ore  frequently  then  under  such  condi- 
tions, if  it  is  a  reflex  and  not  a  toxic  disease?  Cessation  of  the  spasm 
by  removal  of  intestinal  parasites  does  not  argiie  for  the  reflex  any  more 
than  it  does  for  the  toxic  hypothesis.  In  favor  of  the  latter  is  the  oft- 
observed  fact  that  extirpation  of  the  thyroid  gland  is  followed  by  it. 
It  was  seen  soon  after  the  injection  of  spermine.  Nephritic  disease,  the 
use  of  alcohol,  erg"otin  and  chloroform,  the  finding  of  toxic  substances 
in  both  the  stomach  and  the  urine,  are  data  enough  to  almost  establish 
the  toxic  origin  of  the  trouble. 

Among  the  infections  that  it  has  accompanied  may  be  enumerated 
typhoid,  scarlet  fever,  rheumatism,  measles,  diphtheria,  malaria,  influ- 
enza, pneumonia  and  smallpox.  Generally  the  spasm  appears  during 
the  convalescence  from  these  diseases. 

Whether  there  is  any  special  significance  in  the  rather  frequent 
association  of  hysteria  and  epilepsy  Avith  tetany  it  is  doubtful  to  sav. 
The  question  is  one  of  importance  from  the  standpoint  of  differential 
diagnosis  rather  than  of  etiology.  It  is  easily  conceivable  that  a  type 
of  constitution  that  tends  toward  the  instability  of  hysteria  and  epi- 
lepsy would  easily  yield  to  a  toxic  irritant  and  present  the  clinical  pic- 
ture of  tetany. 

Pathology  and  Pathogexesis. — Nothing  distinctive  in  the  way 
of  morbid  anatomy  has  been  found.  Some  poliomyelitic  changes  may 
or  may  not  be  due  to  the  reaction  upon  the  cord  of  the  violent  muscu- 
lar contractions.  The  same  changes  have  been  recorded  in  connection 
with  other  virulent  intoxications  involving  the  cord  and  lower  neu- 
rones, as  witness  acute  ascending  paralysis  of  the  Landr}-  type.  Hyperse- 
mia  and  small  hemorrhagic  foci  have  been  seen,  with  accumulation  of 
lymphoid  cells  about  the  capillaries,  and  even  minute  spots  of  myelitis. 
The  ganglion  cells  have  been  swollen  or  shrunken,  cloudy  and  softened 
and  full  of  vacuoles.  In  other  words  chromatolysis  has  been  present. 
The  spinal  membranes,  especially  in  the  cervical  region,  have  been  con- 
gested. All  of  these  occasional  findings  are  too  indefinite  to  establish  a 
fixed  patholog}"  upon,  but  when  we  compare  them  with  the  similar 
^findings  of  other  forms  of  severe  intoxication,  particularly  Landry's 
disease  and  some  cases  of  alcoholism,  we  are  impressed  with  the  fact 
that  if  tetany  be  indeed  a  functional  disease,  a  functional  disease  is  not 
always  one  without  any  organic  change  whatever.  Whether  the  spasms 
preceded  or  followed  the  few  organic  changes  that  have  been  observed 
is  immaterial  in  comparison  with  the  suspicious  fact  that  the  two  phe- 
nomena are  actually  associated  together.  The  association  alone  ren- 
ders ven-  shakv  the  rather  paradoxical  notion  that  functional  exhibi- 


258  TIJE   NEURONIC   DISEASES 

tions  can  be  existent  without  some  structural,  molecular  or  chemical, 
change. 

Until  we  get  more  positive  data,  it  may  be  well  to  still  speak  of 
tetany  as  a  functional  disease  and  classify  it  among  the  neuroses.  That 
the  trouble  is  probably  a  toxic  disturbance  of  the  nutrition  of  the  cells 
in  the  spinal  cornua  is  suggested  by  the  symmetrical  character  of  the 
symptoms  showing  a  central  seat  for  the  lesion,  by  the  prominence  of 
the  motor  manifestations  over  the  sensory,  by  the  similarity  of  the  clin- 
ical picture  in  some  respects  to  ergot  and  strychnine  poisoning,  and 
by  the  few  polioniAelitic  post  mortem  findings. 

The  subsequent  atrophy  in  the  spinal  cells  seen  in  some  rare  cases 
and  the  almost  total  absence  of  inflammator}^  signs,  suggest  that  the 
trouble  is  a  toxic  primary  neuronic  degeneration. 

Symptoms. — The  characteristic  symptom  of  tetany  is  the  muscular 
spasm.  There  may  be  sensory  phenomena  of  an  indefinite  character 
and  some  other  general  disturbances.    The  mind  is  never  afirected. 

There  may  be  premonitions  of  the  disease  but  they  are  not  com- 
mon. Usually  they  are  of  the  constitutional  and  sensory  type.  Among 
them  are  a  feeling  of  malaise,  apathy,  headache  with  nervous  vomiting, 
pains  in  the  back  and  down  the  limbs.  Sometimes  just  before  the  spasm 
appears,  various  parsesthesire  will  be  felt,  such  as  tingling,  pins-and- 
needles  sensation,  burning  and  numbness  in  the  extremities.  At  length 
the  upper  limbs,  particularly  the  fingers  and  hands,  more  rarely  the 
lower  limbs,  exhibit  a  condition  of  tonic  spasm.  Sometimes  the  feet 
are  afifected  at  the  same  time.  The  trunk  is  very  rarely  involved.  So 
characteristic  is  the  attitude  of  the  hands  that  the  disease  can  be  diag- 
nosed from  it  alone. 

It  is  to  be  noted  that  the  spasm  is  tonic  and  that  it  is  symmetrically 
distributed.  The  appearance  of  the  hand  is  much  like  that  of  one  writ- 
ing. The  ends  of  the  fingers  are  pressed  together  and  inclined  toward 
the  ulnar  side.  The  thumb  is  strongly  adducted  and  partially  tlexed 
beneath  the  index  finger.  The  palm  is  hollowed  and  the  wrist  is  some- 
what flexed.  The  condition  of  the  fingers  is  due  to  flexion  at  the 
metacarpo-phalangeal  joints  and  implication  of  the  interossei  muscles. 
Very  rarely  has  extension  of  the  wrist  and  fingers  been  observed.  In 
the  foot  the  ankle  joint  is  extended,  the  toes  flexed  and  overlapping, 
and  the  attitude  that  of  equino-varus.  The  knees  are  generally  extended 
though  they  may  be  flexed,  and  the  thighs  are  occasionally  adducted 
and  flexed. 

This  spasm  may  be  intermittent  every  few  minutes  or  hours  or 
days.  Sometimes  it  lasts  many  weeks.  It  can  be  provoked  by  irritation. 
The  muscles  are  and  feel  rigid.  Attempts  to  move  them  passively 
usually  cause  pain.  Of  course  their  condition  interferes  with  all  use 
of  the  hands  or  renders  the  movements  and  gait  awkward  and  difficult. 
The  strength  of  the  contractions  varies  between  wide  extremes.  It  may 
amount  to  a  slight  stiffening  or  an  immovable  tetanic  contracture.  In 
the  intervals  the  sensitiveness  of  the  parts,  and  even  the  paresthetic 
sensations,  usually  continue  somewhat.  They  rarely  disappear  entirely 
with,  or  as  promptly  as,  the  spasm. 

Other  muscles  besides  those  of  the  limbs  mav  be  involved.     In 


THE    NEURONIC   DISEASES 


259 


the  severe  cases  all  or  any  of  the  muscles  of  the  body  may  be  thrown 
into  a  state  of  rigidity.  Swallowing  and  respiration  may  be  interfered 
with.  The  ocular  muscles  have  been  affected  and  nystagmus  has  been 
noted. 

FIGURE  40. 


Position  of  the  hands   in   tetany.      (After   Oppenheim.) 

The  patient's  consciousness  is  not,  except  in  the  rarest  instances, 
altered. 

The  temperature  and  pulse  rate  during  the  attack  are  usually 
somewhat  elevated.  At  other  times  they  have  been  seen  to  be  sub- 
normal. 


26o  THE    XEUROXIC   DISEASES 

The  electrical  phowmoia  of  tetany  are  remarkable  and  some- 
times unique.  They  are  usually  referred  to  as  Erb's  sign.  There  is  an 
exalted  deg-ree  of  excitability  of  the  nerves  to  both  the  faradic  and 
galvanic  current.  With  the  latter  there  is  a  complete  reversal  of  the 
polar  reactions  to  a  remarkable  degree,  cathodal  closing  contraction 
equaling,  and  in  rare  instances  even  surpassing,  that  of  anodal  clos- 
ing. In  the  average  case,  only  a  weak  current  is  required  to  produce 
a  cathodal  closing  contraction.  The  current  that  would  be  needed  in 
health  to  cause  this  response,  produces  in  tetany  a  violent  tetanic  con- 
traction. Anodal  opening  tetanic  contractions  and  cathodal  opening 
tetanic  contractions  may  be  provoked.  The  latter  is  never  seen  in  any 
other  disease  than  this.  For  the  sake  of  brevity,  these  reactions  may 
be  represented  bv  and  compared  with  the  normal  formulje,  thus : 

Normal— CaCC,  An  CC.  CaOC,  AnOC. 
Tetany— AnCC,  AnOC.  CaCC  or  AnOC,  AnCC.  CaCC,  AnOTe. 

AnOTE  and  CaOTE  are  never  seen  in  any  other  disease  in  man. 

Along  with  this  electric  hyperexcitability  there  is  an  increase  of 
the  mechanical  irritability.  As  Chvostek's  sign  it  consists  of  a  vigor- 
ous contraction  of  the  muscles,  especially  those  of  the  face,  when  the 
related  nerve  is  slightly  tapped  or  irritated.  Trousseau's  sign  is  prob- 
ably due  to  the  same  mechanism.  It  consists  in  provoking  the  spasm 
by  compressing  the  nerve  trunks  or  bloodvessels  in  the  limb  in  such 
a  way  that  the  arteri?l  or  venous  blood  is  impeded.  Trousseau's  sign 
is  not  observed  in  any  other  disease,  though  Chvostek's  has  been  seen 
in  tuberculosis  and  simple  gastric  dilatation,  but  less  marked  than  in 
tetany. 

Increase  of  sensory  excitability  to  both  mechanical  and  electrical 
stimulation  is  known  as  Hoffmann's  sign.  That  the  sensory  nerves 
are  hyperassthetic  is  shown  by  the  radiating  parsesthesia  that  occurs 
in  their  areas  of  distribution  Avhen  they  are  compressed.  The  supra- 
orbital, ulnar  and  major  saphenous  nerves  are  available  for  this  test. 
Chvostek  noticed  the  phenomenon  in  connection  with  the  auditory 
nerves,  these  nerves  reacting  to  comparatively  weak  galvanic  currents, 
whereas  in  health  only  about  fifteen  per  cent,  of  cases  react  and  then 
only  to  strong  currents.  A  clang  is  observed  upon  anodal  closing, 
when  the  anode  is  held  still,  and  upon  anodal  opening. 

What  Bechterew  calls  the  reaction  of  excitation  is  the  progressive 
increase  of  the  mechanical  and  electrical  excitability  by  repeated  stim- 
ulation. 

Other  inconstant  symptoms  are  met  with.  The  association  with 
hysterical  and  epileptic  manifestations  has  alread}'  been  noticed. 
Myxoedema  and  exophthalmic  goitre  have  been  seen  with  it.  Even 
psychic  disorder  with  hallucinations  and  confusion  have  been  noted  as 
in  other  similar  toxic  diseases.  Some  of  the  vasomotor  and  trophic 
exhibitions  are  quite  prominent  at  times.  Hyperidrosis,  polyuria, 
albuminuria,  glycosuria,  cedema,  urticaria,  herpes,  pigmentation  and 
loss  of  hair  and  nails  have  all  been  recorded. 

There  is  nothing  of  moment  in  connection  with  the  reflexes.  Sev- 
eral times  the  knee-jerks  were  lost. 

Incipient  cataract,  believed  by  Peters  to  be  due  to  obstruction  of 


THE    XEUROXIC   DISEASES  261 

the  circulation  near  the  lens  from  spasm  of  the  ciliary  muscle,  mydria- 
sis and  pupillary  rigidity  are  among  the  occasional  ocular  symptoms. 

General  chilliness,  fugitive  pains,  nausea,  vomiting,  diarrhoea,  in- 
crease of  temperature  and  pulse  rate  are  seen  in  the  beginning  of  the 
trouble,  and  even  later,  and  are  probably  mere  evidences  of  the  general 
intoxication. 

Diagnosis. — The  clinical  picture  is  so  unique  in  fairly  typical  cases 
that  there  ought  to  be  no  difftculty  in  arriving  at  the  diagnosis.  The 
attitude,  the  intermittent  tonic  symmetrical  contractions  in  the  hands 
and  feet,  the  electrical  signs,  the  probable  history  of  infection  or  intoxi- 
cation, should  all  be  given  due  consideration.  Even  when  the  spasm 
appears  in  the  muscles  of  the  jaw,  trismus,  tetanus  can  be  differen- 
tiated by  the  fact  that  in  tetany  the  trismus  is  a  later  phenomenon,  the 
spasms  are  intermittent,  and  are  more  marked  in  the  extremities  than 
they  are  in  tetanus.  In  the  latter  the  extensors,  supinators  and  adduc- 
tors are  more  apt  to  be  affected ;  in  tetany  the  flexors,  pronators,  ab- 
ductors and  internal  rotators.  Tlie  finding  of  the  tetanus  bacillus 
clinches  the  diagnosis. 

Latent  tetany  of  childhood,  tetany-  without  spasm  but  with  parees- 
thesia,  Erb's  and  Chvostek's  signs,  and  even  a  pseudo-tetanus  of  in- 
fancy have  been  noted. 

The  differential  diagnosis  between  tetany  and  spinal  meningitis, 
hysteria,  epilepsy  and  torticollis  is  not  difficult  if  the  characteristic 
electrical  and  other  signs  of  the  former  are  conscientiously  sought  for 
and  the  symptoms  other  than  the  m.otor  are  inquired  carefully  into  in 
the  latter. 

Prognosis. — In  most  cases  the  prognosis  as  to  life  may  be  re- 
garded as  favorable.  Bad  signs  may  develop  suddenly,  however,  at 
any  time.  Therefore,  the  cases  are  always  serious.  The  accompani- 
ments of  the  disease  vary  the  prognosis.  Thus  in  cases  with  gastric 
dilatation,  in  those  in  which  a  goitre  has  been  cut  out,  in  those  sub- 
jects exhausted  and  debilitated  by  disease  and  where  respiratory  com- 
plications are  present,  it  is  grave.  Delivery  and  the  cessation  of  lacta- 
tion usually  terminate  these  forms  of  the  disease.  Infectious  and  intox- 
icating cases  frequently  run  a  mild  and  rapid  course  to  recovery.  Some- 
times the  recovery  is  tardy  and  relapses  are  not  to  be  unexpected,  es- 
pecially when  pregnancy  and  the  function  of  lactation  recur.  The 
course  of  the  entire  disease  may  be  from  a  fe^v  days  to  many  months, 
even,  without  remissions,  to  many  years. 

Treatment. — All  possible  causes  and  irritants  should  be  removed 
as  promptly  as  possible.  Intestinal  entozoa  should  be  gotten  rid  of,  the 
foetus  should  be  delivered,  tainted  food  should  be  washed  up.  The 
termination  of  the  pregnancy  in  the  pregnant  cases,  and  the  adminis- 
tration of  thyroid  extract  in  the  absence  of  the  thyroid  gland,  usually 
cause  a  disappearance  of  the  disease. 

For  the  rest,  we  must  depend  upon  rapid  elimination,  diaphoretic 
treatment  in  cases  following  cold,  and  the  use  of  nerve  sedatives.  Free 
diuresis,  catharsis,  and  diaphoresis  cannot  certainly  be  as  dangerous 
as  the  disease  itself  is.  Bloodletting  is  hardly  commendable,  or  the 
icebag  to  the  spine  either,  in  view  of  the  high  probability  of  the  dis- 


262  THE    NEURONIC   DISEASES 

ease  being  a  general  toxaemia.  The  stomach  pump  cannot  be  used 
and  in  all  manceuvres  the  danger  of  provoking  spasm  must  always 
be  remembered.  Warm  baths  and  warm  wet  packs  are  both  sedative 
and  eliminative. 

Of  the  sedatives  potassium  bromide  is  the  most  available.  It  must 
be  given  in  full  dosage,  30  to  60  grains,  three  times  a  day.  For  a 
severe  and  extensive  paroxysm  morphine  may  have  to  be  used.  It 
cannot  be  employed  continuously,  however,  for  obvious  reasons.  It 
is  in  the  continuous  cases  that  the  bromide  salt  is  applicable.  Hyoscin 
hydrobromate,  gr.  1-25,  hypodermically  every  hour,  until  full  medic- 
inal effect  is  obtained,  has  helped  in  some  cases.  Curare  and  curarine 
and  phosphorus  have  their  advocates.  Sanger  Brown  has  been  pleased 
with  the  use  of  chloral  and  chloroform  narcosis.  When  the  laryngeal 
and  respiratory  muscles  are  threatened,  chloroform  inhalations  are 
especially  to  be  recommended.  Administration,  of  course,  must  be 
careful,  especially  in  the  beginning".  Pilocarpine  subcutaneously  will 
also  temporarily  relax  the  muscles.  Look  out  for  exhaustion  and  do 
not  carry  the  use  of  either  chlorofrm  or  pilocarpine  too  far. 

One  wonders  how  electricity  had  ever  been  thought  of  as  a  thera- 
peutic agent  in  such  a  disease,  and  yet  a  stabile,  mild  galvanic  current 
has  the  approval  of  good  authority.  The  faradic  current  is  decidedly 
contraindicated. 

General  tonics  like  iron,  quinine  and  cod-liver  oil  should  be  given 
between  paroxysms,  especially  in  children. 

Moynihan  urges  the  early  adoption  of  surgical  measures  in  cases 
of  severe  gastric  tetany,  which  certainly  seems  reasonable  when  there 
is  a  mechanical  impediment  to  the  free  working  of  the  organ  from 
pyloric  stenosis. 

LOCALIZED  MYOSPASMS. 

A  spasm  is  a  symptom.  It  is  an  involuntary  and  abnormal  con- 
traction of  a  muscle,  due  to  disease.  It  arises  out  of  a  multitude  of 
conditions  involving  the  entire  neuro-muscular  apparatus. 

Spasms  may  be  classified  upon  an  anatomical  or  a  functional 
basis.  As  the  anatomy  and  functions  of  the  entire  neuro-muscular 
apparatus  are  very  extensive  and  complex  it  is  obvious  that  such  clas- 
sification must  prove  chaotic  and  confusing.  This  is  just 
the  condition  of  most  of  the  classifications  of  this  symptom 
at  the  present  day.  And  it  car,  hardly  be  expected  to  be 
improved  very  much  until  v.e  learn  '  more  of  the  patho- 
logical origin  of  the  trouble.  It  is  uesless  to  form  a  classification  with 
such  gross  anatomical  divisions  as  the  head,  the  neck,  the  trunk  and 
the  extremities  for  its  guiding  principle,  for  spasms  in  one  part  are 
very  generally  accompanied  by  spasms  in  another  part.  It  is  generally 
futile  to  classify  them  in  accordance  with  the  particular  nerves  involved, 
for  not  always  are  the  same  nerves  implicated  nor  is  the  spasm  always 
a  nerve  trouble.  In  the  production  of  a  muscular  contraction  many 
structures  are  concerned.  They  are  the  muscular  tissue  itself,  the 
neuraxone,  the  motor  neurone-cell  and  imder  most  circumstances  the 
related   sensory  neurone   with   all  its  peripheral  connections.     In  the 


THE    NEURONIC   DISEASES  263 

voluntary  and  semi-voluntary  muscular  contractions  the  centers  that 
subserve  volition  and  the  other  higher  psychic  acts  must  also  be  taken 
into  account.  Thus  it  is  clear  that  a  normal  muscular  contraction  is 
by  no  means  a  simple  affair.  Disorder  of  any  part  of  this  complicated 
mechanism  may  very  reasonably  provoke  a  disorder  of  the  resulting 
contraction  which  may  assume  the  character  of  an  over-contraction. 

Direct  irritation  and  withdrawal  of  inhibition  are  the  two  forms 
in  which  the  primary  disorder  occurs  out  of  which  the  spasm  is  evolved. 
The  irritation  may  be  in  the  muscular  or  the  nervous  part  of  the  mech- 
anism. Disease  of  the  brain  and  other  inhibitory  centers  may  cause 
certain  sensory-motor  mechanisms  to  be  set  free,  as  it  were,  tOi  func- 
tionate in  a  manner  far  in  excess  of  the  normal.  It  is  not  correct,  there- 
fore, to  say  that  spasm  is  a  symptom  of  spinal  cord  disease.  It  may 
be  a  symptom  of  disease  in  any  part  of  the  sensory-motor  neuro- 
muscular apparatus.  This  at  once  suggests  that  these  spasms  might 
be  classified  into  those  due  solely  to  muscular  disease  and  those  due 
to  nervous  disease.  The  latter  could  again  be  subclassified  into  those 
that  are  dependent  upon  lesions  in  the  motor,  the  sensory  or  the  cere- 
bral centers  that  subserve  psycho-motor-sensory  functions.  We 
already  use  this  classification  for  some  of  the  spasmodic  manifesta- 
tions and  were  we  in  possession  of  complete  data  m  regard  tO'  all  of  the 
diseases  in  which  they  appear  we  would  probably  find  that  this  classi- 
fication would  prove  the  best.  We  distinguish  even  now  between  the 
spasmodic  conditions  of  cerebral  irritation  and  cerebral  destruction. 
We  recognize  in  our  nosology  a  whole  host  of  sensory  reflex  spasms. 
We  acknowledge  that  psychic  spasm  may  occur  in  hysteria  and  allied 
states.  In  a  word  we  have  conceived  of  an  anatomical  basis  for  most 
of  the  spasmodic  conditions  that  we  meet  with.  For  want  of  a  better 
term  we  call  these  spasms  sometimes  symptoinatic,  which  means 
merely  that  we  are  fortunate  in  knowing  just  about  what  the  lesion  is 
that  is  causing  all  the  trouble.  These  spasms  being  but  symptoms  oi 
well  recognized  diseases  it  does  not  seem  to  me  necessary  to  describe 
or  refer  to  them  again  in  this  chapter.  They  will  be  found  treated  in 
detail  under  the  head  of  the  respective  diseases  wherein  they  appear. 

The  spasms  of  which  we  have  as  yet  no'  tlefinite  knowledge  m  re- 
gard to  their  pathogenesis  but  which  are  well  recognized  clinically  will 
be  considered  here. 

For  physiological  reasons  already  spoken  of,  it  will  be  assumed 
that  in  these  spasms  there  is  a  functional  disturbance  which  may  in- 
volve the  muscular  tissue  or  the  central  neurone-bodies.  The  term 
functional  has  a  broad  meaning  here.  It  may  be  allowed  to  indicate 
a  nutritional,  or  at  least,  a  physio-chemical,  change  of  some  sort  in 
these  elements  or  a  disturbed  innervation  among  them  whereby  they 
permit  of  unrestrained  activity  in  the  muscles. 

From  this  point  of  view  the  spasm  that  is  not  due  to  inherent  mus- 
cular disease  is  a  primary  neurosis.  In  these  spasms  heredity,  or  in 
other  words  the  neuropathic  constitution,  nutrition,  infection  and  trau- 
mata play  the  largest  etiological  role. 

These  spasms  may  be  at  times  excited  by  reflex  stimulation  but 
they  are  not  pure  reflex  spasms.     They  are  generally  accompanied  by 


264  fKE   NEURONIC  DISEASES 

Other  signs  of  a  neuropathic  state  and  very  often  by  another  distinct 
neurosis  Hke  hysteria  or  neurasthenia. 

In  taking  up  for  consideration  then  those  spasms  that  are  them- 
selves of  the  nature  of  pure  neuroses,  I  discard  all  those  that  are 
svmptomatic  of,  or  form  merely  a  part  of,  the  symptom-complex  of 
well-recognized  diseases  discussed  in  other  parts  of  this  book.  I  realize 
the  risk  I  am  running  in  possibly  including  here  some  spasmodic 
affections  that  may  be  merely  symptomatic,  but  the  uncertainty  of  our 
knowledge  as  to  their  real  nature  may  serve  as  m.y  apology  for  taking 
the  step. 

These  spasms  may  be  regarded  from  the  standpoint  of  their  clin- 
ical appearance,  which  is  useful  incidentally  for  purposes  of  descrip- 
tion but  which  should  never  have  been  adopted  as  a  basis  for  classi- 
fication as  it  unfortunately  too  often  has  been.  They  will  be  spoken  of 
as  tonic  and  clonic,  as  belonging  to  this  group  or  that  group  of  mus- 
cles, as  rapid  or  slow,  as  coordinated  or  incoordinated,  as  involving 
parts  of  the  muscles  or  the  whole  muscle. 

Walton  rightlv  urges  that  a  more  careful  use  of  terms  in  describ- 
ing these  spasms  should  be  insisted  upon.  By  way  of  illustration  he 
recommends  that  the  term  myoclonia  should  be  dropped  as  a  collective 
designation  for  unrelated  disorders,  in  which  I  heartily  agree  with 
him,  and  that  inyokyniia  should  be  limited  to  cases  showing,  without 
hereditary  or  congenital  history,  widespread  muscular  quivering  with- 
out indication  of  progressive  degeneration  of  the  nervous  system,  with- 
out constitutional  symptoms  and  without  signs  o-f  present  infection 
or  other  acute  disease.    And  so  on. 

It  is  not  possible  in  the  present  state  oi  our  knowledge  to  always 
separate  an  essential  myospasm  from  one  due  to  some  functional  or 
other  nervous  trouble,  any  more  than  it  is  possible  to  separate  an  es- 
sential progressive  muscular  atrophy  from  a  low  grade  chronic  anterior 
poliomyelitis.  It  is  not  improbable  that  we  will  come  to  believe,  as 
many  are  believing  in  regard  to  the  atrophy  and  anterior  horn  trou- 
ble, that  there  is  no  sharp  line  of  demarkation ;  that  functional  muscu- 
lar disturbance  is  always  more  or  less  accompanied  by  a  related  neural 
trouble. 

LOCALIZED  SPASMODIC  TIC.    TIC  CONVULSIF. 

A  quick,  sharp,  short,  electric-like,  painless  contraction  in  a  muscle 
or  group  of  muscles  is  known  as  a  spasmodic  tic.  It  may  occur  in  any 
muscle  of  the  body,  though  it  is  most  frequently  seen  in  the  facial  mus- 
cles, probably  because  they  are  the  most  active  and  intimately  con- 
nected with  mentalization  of  any  in  the  body. 

A  tic  may  consist  of  one  contraction.  Usually  there  are  several 
in  rapid  succession,  after  which  there  follows  a  period  of  quiescence. 

Sometimes  a  single  nerve  is  involved  or  even  single  branches  of 
a  nerve.  Very  often,  however,  a  number  of  nerves,  nearby  or  widely 
separated,  may  be  subject  to  the  trouble.  As  a  result  different  mus- 
cles, but  always  muscles  concerned  in  the  production  of  related  move- 
ments, are  contracted. 


THE    NEURONIC   DISEASES  265 

The  disease  is  a  chronic  disorder,  has  usually  a  neuropathic  his- 
tory behind  it,  and  occurs  frequently  in  association  with  hysteria,  epi- 
lepsy, and  other  neuroses  and  psychoses. 

A  nutritional  or  molecular  change  of  some  unknown  character  in 
the  nerve  nucleus  or  its  representative  center  in  the  cortex  is  assumed 
as  the  pathological  basis  of  the  trouble. 

These  localized  tics  are  often  miscalled  local  or  habit  chorea. 
They  have  nothing  in  common  with  the  latter  disease  and  the  manner 
of  the  muscular  movements  is  not  the  same. 

The  tics  should  always-  as  far  as  possible  be  sharply  differen- 
tiated from  mere  reflex  and  symptomatic  spasms  of  the  same  muscles. 

The  results  of  their  treatment  respectively  are  very  different.  The 
tics  are  not  very  amenable  to  treatment  and  in  their  management  dis- 
ciplinary and  psychotherapeutic  measures  have  a  large  share.  They 
represent  a  fundamental,  hereditary,  general  nervous  defect  or  the  neu- 
ronic, residual  change  after  the  operation  of  some  acute  cause  or  dis- 
ease. They  speak  always  for  more  or  less  central  degeneration  and 
are  therefore  apt  to  be  of  wide  distribution  or  concerned  with  mus- 
cles and  nerves  that  subserve  general  physiological  movements.  They 
may,  however,  implicate  individual  muscles  and  nerves. 

The  facial  tics  are  the  most  common  and  most  marked.  The  rea- 
son, as  I  have  said,  is  because  the  facial  reflexes  are  so  rapid  and  so 
closely  linked  with  mentalization.  The  psychogenic  origin  of  them  in 
many  instances  is  shown  in  the  way  that  they  suddenly  begin  after 
a  high  emotion  or  mental  s:hock.  Most  of  the  victims  are  more  or  less 
mentally  undergrade,  or  are  at  least  neuropathic.  A  vicious  habit  may 
evolve  the  trouble.  The  trouble  is  only  very  rarely  obtained  by  direct 
inheritance.  They  may  resemble  and  even  originate  as  an  occupation 
neurosis.  I  saw  such  a  tic  that  occurred  in  a  young  cornetist  with 
both  a  family  and  an  individual  pronounced  neuropathy.  Any  of  the 
muscles  of  the  face  may  be  affected,  and  the  symptom  may  be  bilat- 
eral, though  it  is  usually  unilateral.  Single  muscles  and  groups  of 
muscles  may  be  involved.  Perhaps  the  most  frequently  aifected  is 
the  orbicularis  palpebrarum  and  the  least  the  orbicularis  oris.  In 
fact  there  is  no  rule  and  every  possible  form  of  the  exhibition  may  be 
looked  for.  The  occipito-frontalis,  the  chin  muscles,  even  the  external 
auricular  muscles  have  each  been  seen  to  be  affected  by  themselves. 
Both  tonic  and  clonic  have  been  the  contractions,  though  the  latter 
are  the  more  usual.  Mental  and  physical  rest  diminish  the  jerks, 
wiiereas  excitement,  effort  and  voluntary  movements  increase  them. 
Cutaneous  irritation  usually  evokes  them.  Sometimes  they  can  be  par- 
tially controlled  by  the  Vv^ili.  These  spasms  do  not  impair  much  the 
ordinary  voluntary  movements  of  the  face,  and  as  a  rule  they  do  not 
cause  much  subjective  distress,  sometimes  not  any.  Hearing  phe- 
nomena may  occur  when  the  stapedius  muscle  is  affected.  The  velum 
palati  and  uvula  have  been  supposed  to  be  implicated,  though  these 
are  more  likely  to  be  due  to  some  gross  organic  lesion  which  may  be 
diagnosed  by  collateral  symptoms  .  There  are  no  sensory,  vasomotor, 
trophic  or  secretory  symptoms.  The  objective  signs,  except  the  con- 
tractions, are  all  negative  and  the  trouble  appears  to  be  a  pure  neurosis. 


266  THE   NEURONIC  DISEASES 

Of  course  every  case  of  facial  spasm  is  not  a  pure  tic.  Organic 
lesions  of  the  nerves  and  their  representative  centers  may  cause  facial 
spasm.  Such  cases  must  be  always  differentiated  and  in  every  case 
it  is  well  to  hunt  first  for  some  such  organic  cause.  Tic  patients  are 
often  the  victims  of  hysteria,  epilepsy,  hemicrania,  hystero-neuras- 
thenia  and  the  psychoses.  Stuttering  is  usually  a  form  of  tic,  though  it 
may  have  had  its  origin  in  a  vicious  habit.  Tic  may  be  spoken  of  as 
mimic  tic  but  it  is  entirely  wrong  to  name  it  chorea  as  is  so  often  done. 

Facial  tic  is  a  chronic,  sometimes  remittent  trouble,  with  a  gen- 
erally unfavorable  prognosis  as  to  cure.  Blepharospasm  holds  out  the 
most  hope  of  amelioration. 

No  treatment  but  general  tonic  and  disciplinary  treatment  will  do 
any  good.  I  have  seen  arsenic  cause  a  bad  blepharospasm  in  a  boy 
almost  entirely  to  disappear  for  a  time.  Bromides  may  help  some.  All 
other  remedies  usually  fail.  If  the  spasm  be  not  a  true  tic,  but  a  nerve 
reflex  or  symptomatic  trouble,  the  treatment  is  both  obvious  and  prom- 
ising. If  tic  douloureux  be  present  with  the  motor  tic  it  must  be 
treated  as  a  separate  condition. 

A  viasticatory  tic  is  sometimes  seen  that  involves  the  muscles  of 
mastication  supplied  by  the  motor  branch  of  the  fifth  nerve.  Trismus, 
hysterical,  rheumatic  and  reflex  spasms  of  the  lower  jaw  must  all 
be  carefully  differentiated.  The  reason  that  the  prognosis  of  most  of 
the  cases  of  masticatory  spasm  is  favorable  is  that  they  are  not  cases 
of  true  tic  but  are  due  to  inflammations  about  the  temporo-maxillary 
articulation,  to  diseased  teeth,  to  hysteria,  etc. 

What  is  said  of  masticatory  tic  is  true  of  occasionally  observed 
hypoglossal  tic.  The  tongue  here  shoots  rapidly  in  and  out  of  the 
mouth,  or  from  side  to  side.  The  spasm  is  generally  bilateral  but  a 
hemispasm  has  been  seen.  A  tremor  in  the  glossal  muscle  and  the 
spasm  of  some  neighboring  facial  muscles  have  accompanied  this  tic. 
Alternation  of  masticatory  and  hypoglossal  tic  is  a  curious  phenome- 
non. Sometimes  the  trouble  has  resembled  an  occupation  neurosis  com- 
ing on  upon  attempts  at  mastication,  cornet-playing,  etc. 

Tics  occur  in  the  muscles  of  the  trunk  and  of  the  extremities,  but 
they  are  rare.  Other  forms  of  spasm  such  as  occupation  neurosis,  re- 
flex, organic  and  symptomatic  spasms,  are  often  enough  seen  and 
must  be  clearly  separated,  both  on  account  of  the  prognosis  and  the 
treatment.  The  causes  of  the  spasms  here  that  are  not  of  the  nature 
of  true  tics  are  innumerable  and  consist  of  trauma,  local  irritations, 
overexertion,  varicose  veins,  and  intoxications.  Neurasthenia,  hys- 
teria, epilepsy,  chorea,  writer's  cramp  and  other  neuroses  may  be  pres- 
ent as  a  rule.  Spasms  of  the  trunk  and  limbs  therefore  are  not  un- 
favorable from  the  viewpoint  of  cure,  for  they  are  so  seldom  essential 
tics. 

Respiratory  tics  are  various,  always  troublesome  and  sometimes 
very  serious.  Singultus,  or  hiccough,  may  be  of  this  nature,  and  may 
or  may  not  prove  fatal.  It  is  usually  a  mere  reflex  trouble,  however, 
short  in  duration  and  not  alarming.  The  diaphragm  and  its  innerva- 
tion is  of  course  the  seat  of  the  phenomenon.  Yawning  and  sneezing 
are  scarcely  ever  of  such  a  character  as  to  be  regarded  in  the  light  of 


THE    NEURONIC   DISEASES 


267 


disease.  I  recently  treated  a  young  man,  with  a  syphilitic  history,  who 
suddenly  began  to  have  uncontrollable  yawning  spells  that  so  alarmed 
him  as  to  drive  him  to  seek  medical  advice.  Neurasthenic,  hysteric, 
epileptic  individuals  and  those  with  organic  brain  trouble,  meningitis, 
cerebellar  abscess  have  been  troubled  with  abnormal  yawning.  As  an 
aura  of  epilepsy  it  also  occurs.  A  snoring  spasm,  of  psychic  origin  has 
been  recorded.  A  coug-h  that  is  not  of  refiex  or  inflammatory  origin 
is  apt  to  be  hysterical. 

Counter-irritation,  internal  sedatives  and  electrization  of  the 
phrenic  nerve  are  the  chief  measures  that  we  possess  for  combating 
these  respiratory  spasms.  Fortunately  they  are  rarely  prolonged  or 
serious. 

Closely  related  to  the  localized  tics,  if  it  really  be  not  one  of  them, 
is  the  form  of  torticollis  known  as  spasmodic  ivryneck.  This  is  not 
the  same  as  congenital  torticollis  with  its  shortening  of  the  sterno- 
cleido-mastoid  muscles  due  to  obstetrical  injury  or  prenatal  atrophy ; 
nor  as  symptomatic  wryneck  with  its  rheumatic,  inflamed  muscle,  tu- 
mors, abscesses,  syphilitic  lesions  and  other  easily  discovered  causes ; 
TDor  as  spurious  wryneck  due  to  mild  caries  of  the  spine. 

Spasmodic  Torticollis  is  a  central  neurosis  and  is  associated  with 
the  hysterical,  neurasthenic  and  generally  psychopathic  constitution. 
The  muscles  supplied  by  the  spinal  accessory  nerve  are  the  ones  usu- 
ally, or  at  least  prominently  involved.  Other  muscles,  however,  and 
other  nerves  are  likely  to  be  implicated.  Heredity  exists  in  most  of 
the  cases  though  it  is  rarely  direct.  It  involves  more  especially  a  neuo- 
pathic  taint.  Women  are  much  more  subject  to  the  trouble  than  men. 
It  occurs  in  the  middle  period  of  life  and  often  follows  traumata  of 
various  sorts,  extreme  emotional  excitement  and  sometimes  no  appa- 
rent exciting  cause.     Stigmata  of  degeneracy  are  sometimes  seen. 

The  disease  is  a  central  neurosis  of  the  medulla,  more  probably 
of  the-  representative  centers  for  the  neck  muscles  in  the  cortex.  It 
is  a  degenerative  trouble  and  resembles  an  occupation  neurosis  in  being 
a  defect  in  the  coordinating  mechanism  for  the  movements  of  the 
neck.  In  this  form  of  the  disease  the  spasm  is  generally  of  the  clonic 
type,  tonic  spasms  being  more  characteristic  of  the  other  forms  of 
torticollis.  Irregular  impulses  are  sent  out  from  the  degenerating  and 
defective  centers  which  cause  the  muscles  supplied  by  particular  nerves 
to  undergo  irregular  and  intermittent  contractions. 

The  sterno-cleido-mastoid  muscle  is  the  leading  one  to  be  involved, 
but  others  are  very  often  implicated  with  it.  The  combinations  thus 
•effected  are  quite  numerous.  Some  of  them  have  received  special 
names  because  they  lead  to  special  movements  and  attitudes.  The  most 
common  combination  is  that  of  the  sterno-mastoid  and  trapezius  mus- 
cles. The  splenius,  scaleni  and  deep  cervical  muscles,  platysma  and 
omohyoid  all  may  be  affected. 

In  its  course  the  disease  passes  from  one  muscle  to  another. 

In  the  early  days  when  this  disease  was  not  differentiated  sharply 
"from  other  forms  of  torticollis,  especially  the  congenital  form,  tenotomy 
would  be  done  on  one  muscle  after  -another  as  they  contracted  after 
€ach  operation. 


268  THE   NEURONIC  DISEASES 

The  attitude  of  the  head  and  shoulders  will  of  course  depend  upon 
the  location  of  the  spasm.  When  only  one  sterno- mastoid  muscle  is 
affected  the  face  is  turned  towards  the  other  side,  the  mastoid  drawn 
down  and  the  chin  elevated.  Contraction  of  the  trapezius,  usually 
the  upper  part  only,  which  is  supplied  by  the  accessorius,  causes  the 
head  to  be  rotated  towards  the  side  of  the  muscles  aft'ected  and  drawn 
strong-ly  backwards.  An  alternation  of  contractions  between  the  sterno- 
mastoid  and  trapezius  muscles  causes  a  sort  of  circular  movement  of 
the  head  that  is  very  characteristic.  Other  movements  are  produced, 
when  other  muscles  such  as  the  complexus,  superior,  oblique  and. 
splenius  are  implicated.  In  most  cases  the  inferior  oblique,  recti  capitis, 
postici,  major  and  minor,  are  included  and  show  involvement  of  the- 
upper  cervical  nerves.    Less  frequently  the  contraction  is  bilateral. 

Retro-collic  spasm  is  a  drawing  of  the  head  directly  backwards- 
by  the  two  trapezii.     It  is  a  rare  condition. 

Spasmus  nutans,  salaam  spasms,  epilepsia  nutans,  the  nodding 
spasm  of  children,  is  occasionally  a  neurosis  of  the  eleventh  nerve- 
though  it  is  more  often  a  dentition  reflex  or  due  to  digestive  disorder,, 
basal  meningitis  and  gross  brain  disease.  It  may  be  associated  in 
such  cases  with  transient  loss  of  consciousness  and  thus  resemble  or 
be  accompanied  by  true  epilepsy.  Often  it  is  a  mere  habit  and  is  a 
veritable  tic.  It  is  revealed  in  a  rhythmical  nodding  or  oscillating  of 
the  head  of  various  degrees  of  rapidity,  even  up  to  fifty  and  sixty 
times  a  minute.  The  eye  and  facial  muscles  often  participate  in  the 
saham.  Nystagmus,  strabismus  and  blepharospasm  may  thus  be  a  part 
of  the  symptom-complexus. 

In  time  the  muscles  undergo  hypertrophy  in  some  cases.  An- 
atrophy  of  the  opposite  muscles,  as  observed  by  some,  is  probably  due 
to  neuritis  or  other  gross  damage.  The  same  may  be  said  of  the- 
pain  that  is  occasionally  present.  A  genuine  tic  does  not  have  pain 
with  it  but  the  muscles  may  feel  sore  and  ache.  The  spasms  as  a  rule 
cease  during  sleep  and  are  increased  by  mental  excitement  and  fatigue. 
They  are  clonic  and  recur  every  few  minutes  so  that  it  is  impossible 
to  keep  the  head  still  long.  In  typical  cases  there  are  no  objective- 
signs  of  organic,  motor  or  sensory  changes.  The  psychic  accompani- 
ments of  the  trouble  occasionally  include  mental  confusion,  delirium: 
and  melancholia. 

The  diagnosis  calls  for  a  sharp  differentiation  of  spasmodic  tor- 
ticollis from  the  other  forms.  The  shortness  of  the  sterno-cleido- 
mastoid  and  the  fixity  of  the  deformity  indicates  congenital  torticollis. 
Pain,  fever,  local  tenderness  belong  to  the  rheumatic  type  of  the  dis- 
ease. The  usual  signs  of  cp^ries  of  the  spines  will  aid  in  excluding  the- 
spurious  type.  All  forms  of  torticollis  should,  however,  be  most  min- 
utely examined  for  possible  reflex,  traumatic,  inflammatory  or  other- 
source  of  the  spasm.  They  must  be  excluded,  of  course,  before  a  diag- 
nosis of  spasmodic  wryneck  is  permxissible.  General  tic  and  paramyo- 
clonus may  first  appear  as  torticollis.  Facial  tic,  echolalia,  define  the 
former,  whereas  associated  spasm  ci  the  great  trunk  muscles,  bilateral 
in  distribution,  is  the  determining  feature  of  the  latter.  There  is  noth- 
ing choreic  about  torticollis  and  if  choreic  symptoms  are  present,  the 


■?HE    NEURONIC  DISEASES 


269 


patient  has  the  two  aftections  simultaneously,  just  as  he  may  have  tor- 
ticollis with  hysteria,  epilepsy  and  other  psychoneuroses. 

The  prognosis  and  treatment  follow  the  lines  of  that  of  all  the 
tics.  I  would  reiterate  and  urge  especially  again  here  that  a  most 
•careful  diagnosis  be  made  to  eliminate  all  possibility  of  the  disease  be- 
ing of  any  of  the  other  forms  than  the  spasmodic.  When  this  is  de- 
cided upon,  only  quiet  and  rest,  sedatk^es  and  psychotherapy  will  do 
any  good.  I  have,  like  most  of  my  confreres,  fallen  into  the  error  of 
recommending"  operative  procedures  but  I  have  learned  not  to  do  so 
any  more.  The  spasm  invariably  returned,  though  in  some  cases  there 
was  a  g-rateful  period  of  rest.  I  have  seen  it  immediately  reappear 
in  other  muscles.  I  have  not  been  so  unfortunate  as  to  have  seen  anv 
case  made  worse  by  operation,  though  such  observations  have  been 
made. 

Electricity  does  no  good  except  for  its  psychic  influence.  Re- 
lapses follow  it  and  cause  disappointment  and  mental  depression, 
which  are  bad  for  the  neurosis.  Apparatuses  to  hold  the  head  fixed  aie 
a  mere  useless  torture..  General  tonic  treatment,  change  of  climate, 
change  of  mental  stimulation,  change  of  general  regime  and  environ- 
ment with  such  occasional  sedation  as  bromides  and  opiates  can  give, 
are  as  effective  as  any  measures  we  can  institute.  The  cures  some- 
times reported  as  the  result  of  operative  and  other  mechanical  meas- 
ures are  doubtful  because  the  disease  itself  is  subject  to  remissions, 
and  because  most  of  such  cases  have  not  been  observed  long  enough 
after  the  reported  recovery. 

Of  course  the  therapeutic  story  is  an  entirely  different  one  for 
the  other  forms  of  torticollis.  Tenotomy  is  the  thing  tO'  do  in  con- 
genital torticollis.  Antirheumatics,  antiphlogistics,  counter-irritants  and 
later  on  electricity,  massage,  gymnastics,  fixation  apparatuses, 
setons,  nerve  stretching  and  nerve  resection  are  all  to^  be  employed  and 
with  a  legitimate  hope  of  success.  Here  as  elsewhere  essential  pri- 
mary neuronic  degenerative  troubles  are  beyond  the  power  of  medicine 
-except  so  far  as  the  latter  can  influence  their  nutrition.  The  extra- 
neuronic  troubles  that  irritate  and  damage  the  neurones  .secondarily 
are  amenable  to  treatment — all  except  the  damage  tO'  the  neurones. 

The  discussion  of  the  other  forms  O'f  torticollis  will  be  found  un- 
der the  head  of  diseases  of  the  special  nerves  (accessorius)  in  another 
part  of  the  book. 

GENERAL  TIC.     TIC  IMPULSIF. 

This  is  a  remarkable  psychoneurosis  originally  described  by 
Guinon  and  Gilles  de  la  Tourette  and  often  known  as  the  latter's  dis- 
ease. Other  names  that  have  been  given  to  it  are  maladie  des  tics  con- 
vulsifs,  maladie  des  tics  inipulsifs,  myospasia  impulsiva.  Gray  sug- 
.:gested  the  name  palmus.  Though  the  disease  is  confused  by  some  with 
chorea  it  is  really  a  psychoneurosis  more  nearly  related  to  hysteria 
than  to  anything  else.  Its  spasmodic  exhibitions  and  their  inherent 
neuronic  origin  make  the  discussion  of  the  trouble  in  place  here. 
When   Gilles    de    la    Tourette  first  described  the  affection  in  1885,  he 


270  THE   NEURONTC   DISEASES 

Stated  that  first  there  appeared  a  motor  incoordination  which  does  not 
affect  the  general  health  at  all  but  involves  the  face  and  upper  extremi- 
ties gradually,  the  latter  usually  one-sidedly.  Winking,  drawing  oi 
the  buccal  commissures  upward  and  outward,  contraction  of  the  mas- 
seters  with  grating  of  the  teeth,  projection  and  occasional  laceration, 
of  the  tongue  are  some  of  the  facial  manifestations.  The  neck  muscles 
become  involved  and  there  is  alternate  flexion  and  extension  of  the  head 
with  sometimes  inclination  to  one  side  or  the  other  by  the  sterno- 
mastoid  spasm.  In  the  upper  extremities  the  fingers  are  flexed  and 
extended  and  the  shoulders  raised  and  dropped.  Soon  the  lower  limbs 
participate  in  the  extraordinary  performance.  In  them  the  incoordi- 
nation is  more  extensive  and  involves  larger  masses  of  muscular  tissue. 
It  is  unilateral  or  bilateral.  The  foot  is  stamped  on  the  ground  or 
the  patient  stoops  over  and  suddenly  becomes  erect,  or  jumps  off 
of  the  floor.  The  movements  are  all  sudden,  rapid  and  serial.  During 
these  strange,  violent  antics,  the  inarticulate  cry,  like  the  sounds  "hem" 
and  "ah,"'  occurs  and  is  frequently  repeated.  Sometimes  the  sound 
is  articulate  and  loud  and  resembles  some  particular  word  in  each 
patient's  case.  Being  repeated  echo-like,  the  symptom  has  been  termed 
echolalia.  Oaths,  obscene  and  profane  epithets  are  often  emitted, 
coprolalia,  a  characteristic  which  Gilles  de  la  Tourette  thought  was 
pathognomonic.  Sometimes  a  gesture  made  to  or  before  him  will 
be  imitated  by  the  patient,  a  symptom  denominated  echokinesis;  or  he 
will  suddenly  and  involuntarily  give  voice  to  some  of  his  most  secret 
thoughts,  tic  de  pensee. 

Involuntary,  irregular,  violent  incoordinated  movements  of  par- 
ticular parts  of  the  body,  or  of  the  whole  of  the  body,  explosive  utter- 
ances, and  obsessions  or  fixed  ideas  constitute  the  clinical  complexus 
of  Gilles  de  la  Tourette's  disease. 

It  is  believed  that  the  French  authors  had  their  attention  drawn 
to  this  singular  hysterical  trouble  by  the  publication  of  Beard  in  i88q 
upon  "The  Jumpers  of  Maine,"  and  of  Hammond  upon  the  "Miryachit" 
or  Meriatschenje  of  Siberia  and  Kamchatka.  The  Malayan 
Latah  is  the  same  thing,  as  no  doubt  is  the  saltatory  spasm  of  Bam- 
berger, mentioned  under  hysteria. 

There  is  a  neuropathic  taint  behind  this  general  tic  and  it  is  most 
often  seen  in  children  between  the  ages  of  seven  and  fifteen.  In  rare 
instances  the  heredity  has  been  direct.  An  outburst  of  emotion,  a 
trauma  or  an  infectious  fever  has  been  in  some  cases  the  starting  point 
of  the  manifestation.  Being  a  hysterical  condition  the  patients  are 
aware  of  their  condition  but  they  cmnot  help  it.  In  fact  they  gladly 
yield  to  it  to  get  rid  of  the  irresistible  impulse.  It  is  a  lifelong-  affliction 
as  a  rule  though  not  absolutely  mcurable.  Remissions  occur  fre- 
quently. 

The  affection  must  be  differentiated  from  localized  spasmodic  tic, 
from  chorea,  from  hysterical  spasms  and  paramyoclonus.  A  careful 
consideration  of  its  complete  symptomatolog}'  will  make  the  differen- 
tial diagnosis  easy. 

Medicinal  treatment,  as  might  be  expected,  proves  to  be  futile. 
Chloroform  inhalations,  bromides,  chloral,  may  be  useful  during  the 


THE    NEURONIC   DISEASES  2/1 

attack  to  secure  temporary  respite.  The  same  general  treatment  used 
for  hysteria,  with  complete  isolation  as  a  prominent  feature  in  it,  is  to 
be  adopted  here. 

PARAMYOCLONUS  MULTIPLEX. 

This  is  a  rare  affection,  first  described  by  Friedreich.  He  gave  it 
the  above  name.  It  has  since  been  called,  however,  by  various  names, 
such  as  myoclonia  or  myoclonus  multiplex,  polyclonia,  convulsive 
tremor,  myospasia.  It  is  characterized  by  bilateral  clonic  spasms 
which  involve  whole  muscles  or  groups  of  muscles  that  belong  en- 
tirely to  the  trunk,  or  are  partly  attached  to  it.  We  know  so  little 
about  the  disease  that  it  is  difficult  to  give  it  a  positive  classification. 
Not  all  of  the  cases  that  have  been  described  as  paramyoclonus  multi- 
plex have  corresponded  exactly  with  the  clinical  picture  presented  by 
Friedreich's  case.  This  was  a  phthisical  man,  50  years  of  age,  who 
two  weeks  after  a  fright  felt  a  stift"ness  in  his  body  and  developed  a 
clonic  spasm,  ten  to  fifty  a  minute,  in  the  upper  arm  muscles  and  mus- 
cles of  the  thigh,  especially  the  quadriceps.  The  spasms  were  bilat- 
eral, were  lessened  by  voluntary  movements,  occasionally  ceased  for 
a  quarter  of  an  hour  and  were  absent  during  sleep.  Reflex  action  and 
myotatic  irritability  were  both  increased.  Galvanic  electricity  banished 
the  spasm  for  a  time  but  it  soon  returned.  There  were  no  findings  in 
the  muscles  or  the  spinal  cord.  Since  Friedreich  presented  and 
named  this  case  others  have  been  described  that  are  extremely  sug- 
gestive of  tic,  of  hysteria  and  of  electric  chorea.  As  has  well  been 
said  the  moment  we  diverge  from  the  clinical  picture  outlined  by  Fried- 
reich we  get  dose  resemblances  to  other  neuroses.  Because  some 
writers  have  freely  admitted  other  phenomena  under  the  name  para- 
myoclonus multiplex  we  find  it  extremely  difficult  to  know  just  where 
to  place  the  disease. 

Etiology. — Men  are  more  often  the  victims  of  the  trouble  than 
women.  It  occurs  chiefly  in  adults.  A  slight  hereditary  and  familial 
influence  seems  to  have  been  behind  some  cases.  Weiss  noted  the  trou- 
ble in  four  generations,  Gucci  in  three  generations.  Its  association 
with  hysteria,  neurasthenia,  epilepsy  and  other  famxilial  neuropathic 
tendencies  has  often  been  com.mented  upon.  It  has  followed  fright,  ex- 
treme emotion,  severe  strain,  traumata  and  infectious  disease. 

Pathology  and  Pathogenesis. — We  know  of  no  pathological 
changes.  The  disease  seems  to  be  a  violent  spinal  neurosis  of  some 
sort.  Further  than  this  we  cannot  go,  .and  even  this  is  but  a  tenta- 
tive statement.  There  are  probably  different  types  of  the  trouble  or 
it  may  be  but  a  symptom,  variously  modified,  of  other  well-known  dis- 
eases. It  is  certainly  difficult  to  give  the  disease  a  perfect  nosological 
independence.  Mobius  and  Striimpell  have  doubted  the  independence 
of  Friedreich's  own  form  of  the  trouble.  The  former  identifies  it  with 
chronic  chorea,  but  his  views  are  not  generally  accepted.  Raymond 
groups  it  with  electric  chorea,  with  which  Oppenheim  identifies  it. 
Others  believe  that  it  is  merely  a  form  of  hysteria  though  it  is  usually 
wanting  in  the  sensory,  but  has  revealed  some  of  the  psychic,  stigmata 
of  hysteria. 


272  THE   NEURONIC  DISEASES 

Symptoms. — Here  again  we  meet  with  a  confusing  diversity  of 
opinion.  Just  what  symptoms  should  be  inchided  under  the  name 
of  paramyoclonus  multiplex  has  not  yet  been  entirely  agreed  upon. 
There  is  no  dispute  about  the  location  of  the  spasm  bilaterally  in  the 
muscles  of  the  trunk  or  those  that  connect  the  trunk  with  the  limbs. 
It  is  not  accepted  that  the  symptoms  can  be  limited  to  the  limbs.  The 
spasm  may  begin  on  one  side  of 'the  trunk,  or  it  may  be  more  marked 
on  one  side  but  its  bilaterality  is  one  of  its  chief  characteristics.  The 
spasms  are  clonic  and  may  be  violent,  sharp  lightning-like,  throwing 
the  patient  off  his  chair  and  flexing  and  extending  the  body,  or  they 
may  be  so  fine,  delicate  and  tremor-like  that  they  scarcely  move  the 
part.  They  rarely  are  seen  in  the  face.  The  limbs  have  been  affected 
with  the  trunk.  The  movements  may  vary  from  thirty  to  a  hundred 
a  minute.  They  are  unsystematized,  are  symmetrical  on  both  sides 
of  the  body,  are  scattered  or  localized,  and  are  arrhythmical.  Single 
muscles  or  groups  of  muscles  may  be  involved.  Voluntary  movements 
repress  the  spasm,  whereas  excitement  and  emotion  increases  it.  They 
are  absent  in  sleep.  The  withdrawal  of  the  attention  causes  them  to 
diminish.  The  motor  phenomena  practically  completes  the  picture. 
The  reflexes  may  be  a  little  exaggerated  but  there  are  no  electrical 
changes,  no  mechanical  increase  of  irritability,  no  sensory  symptoms, 
no  paralyses,  atrophies  or  disturbance  of  general  nutrition.  There  are 
no  mental  symptoms  but  the  patients  have  often  shown  an  extreme 
susceptibility  to  suggestion. 

Diagnosis. — The  bilateral,  clonic,  unsystematized  spasm,  attack- 
ing only  the  trunk  and  muscles  distinguishes  this  disease.  It  has  some 
hysterical  resemblances  but  the  spasm  is  entirely  apart  from  the  will, 
the  muscles  involved  are  not  those  concerned  especially  in  the  produc- 
tion of  mental  purposive  acts  and  there  are  no  sensory  stigmata.  Con- 
vulsive tic  is  possibly  somewhat  more  of  an  hereditary  neuropathy. 
Chorea  is  less  localized  and  has  a  somewhat  different  etiology.  Never- 
theless it  must  be  frankly  admitted  that  no  sharp  lines  of  differen- 
tiation divide  these  various  neuroses.  We  may  still  have  to  do  what 
Raym'ond  has  done,  group  paramyoclonus  multiplex  with  electric 
chorea,  fibrillary  tremors,  non-painful  tic  of  the  face  and  general  con- 
vulsive tic,  name  the  group  the  myoclonias  and  regard  them  merely  as 
a  set  of  degenerate  manifestations. 

Prognosis. — ^This  is  grave.  The  disease  has  not  been  cured 
except  in  very  doubtful  cases.  It  may  run  on  for  months  or  years 
and  be  accompanied  by  relapses. 

Treatment. — The  bromides,  chloral  and  other  sedatives,  with 
tonics,  are  available.  Galvanism  is  worthy  of  a  trial.  Atropine,  hyos- 
cine,  and  arsenic  have  been  recommended.  Hydrotherapy  may  prove 
useful  both  as  tonic  and  sedative. 

OCCUPATION  NEUROSES. 

By  the  term  occupation  neurosis  is  meant  a  nervous  trouble  brought 
•3n  by  a  monotonous,  excessive  or  faulty  manner  of  using  the  muscles 
concerned  in  certain  special,  complicated  and  coordinated  movements 


THE    NEURONIC  DISEASES 


^72> 


and  shown  by  the  inabihty  to  perform  these  movements  without  the 
loss  of  other  movements  involving-  the  same  muscles.  If  the  use  of 
the  adjective /^M«c^/'ona/ be  applicable  at  all  to  disease,  it  certainly  is  ap- 
plicable to  this  disease  above  all  others.  An  occupation  neurosis  is  not 
only  functional  in  origin,  but  is  apparently  itself  nothing  but  a  disturbed 
function.  It  must  not  be  imagined  that  every  sort  of  inability  to  per- 
form muscular  movements  that  are  caused  by  occupations  are  to  be 
classified  under  the  head  of  this  neurosis.  Many  lines  of  work  involv- 
ing cramped  positions,  pressure  upon  particular  muscles  and  nerves, 
intoxication  as  with  lead,  or  direct  traumata  may  set  up  a  neuritis  or 
other  pathological  condition  that  will  decidedly  interfere  with  coor- 
dinated movements.  These  are  not  instances  of  the  disease  now  under 
consideration.  This  is  shown  in  various  ways,  but  in  none  more  em- 
phatically than  in  the  fact  that  the  prognosis  of  such  is  relatively  fav- 
orable, whereas  the  prognosis  of  the  occupation  neurosis  is  decidedly 
tmfavorable. 

As  the  disease  occurs  in  connection  with  a  great  number  and 
variety  of  occupations  chiefly  engaging  the  hands,  a  large  number  of 
names  have  been  given  to  it.  Writing  seems  to  provoke  it  more  than 
anything  else  and  it  has  more  particularly  been  studied  since  the  intro- 
duction of  the  use  of  the  steel  pen  in  the  early  part  of  the  last  cen- 
tury. It  is  commonly  called  therefore  zvrifer's  crajiip,  or  scrivener's 
palsy.  Occupation  spasm,  fatigue  neurosis,  coordinated  occupation 
neurosis,  professional  neurosis  are  so^me  of  its  synonyms.  An  inter- 
minable list  of  names  for  it  is  made  up  of  those  describing  the  partic- 
ular form  of  occupation  in  which  it  occurs,  as  for  example,  pianist's 
cramp,  telegrapher's  cramp,  milker's  spasm,  sewing  spasm,  etc.  Writ- 
er's cramp,  g-raphospasm,  mogigraphia,  in  a  word,  so-called  occupa- 
tion neurosis,  is  a  distinct  disease,  and  should  always  be  carefully  dififer- 
entiated  from  other  conditions  that  may  at  times  closely  resemble  it. 

Etiology. — The  etiology  has  soine  remarkable  features  about  it 
that  are  extremely  suggestive.  A  neuropathic  constitution  and  a  par- 
ticular occupation  strain  cover  the  main  points  in  regard  tO'  its  causa- 
tion. The  disease  is  rarely  seen  in  one  who  inherits  a  perfect  nervous 
constitution.  In  some  cases  there  is  a  distinct  nervous  heredity,  actual 
disease  having  appeared  in  the  immediate  ancestry ;  in  most  of  the 
cases  there  is  merely  a  transmission  of  a  neuropathic  predisposition. 
I  have  never  seen  a  case  in  which  I  could  not  trace  this  neuropathic 
inheritance  more  or  less  distinctly.  Neurasthenia,  hemicrania,  epilepsy, 
neuralgia,  convulsive  tic,  phobia,  and  tabes  have  been  seen  and  recorded 
in  association  with  it.  Worry  and  intemperance  that  are  said  to  predis- 
pose to  it  may  be  but  a  revelation  of  the  same  neuropathic  basis  upon 
which  it  likewise  rests.  The  artistic  temperament  is  generally  neu- 
rotic, and  this  neurosis  occurs  frequently  among  artists  when  they 
overwork  their  muscles  upon  musical  instruments.  Several  members 
of  the  same  family  have  been  stricken  with  the  trouble. 

The  influence  of  a  nervous  temperament  cannot  be  doubted.  Men 
are  more  frequently  affected  than  women  probably  because  they  are 
more  exposed  to  the  overexertion,  by  reason  of  business  life  that 
brings  it  on.    Thev  suffer  especially  from  the  motor  form  of  the  trou- 


274  iHE   XEUROXIC   DISEASES 

ble.  It  occurs  at  all  ages,  though  by  far  the  majority  of  cases  are  seen 
between  the  years  of  twenty  and  forty. 

That  there  is  something  behind  the  disease  of  a  constitutional 
nature  that  provokes  it  in  addition  to  the  mere  overuse  of  the  muscles 
is  shown  by  the  remarkable  fact  that  in  some  occupations  wherein 
women  predominate,  the  men  are  still  the  greater  sufferers.  For  ex- 
ample, Lewis  has  found  that  in  this  country  telegrapher's  cramp  was 
seen  in  only  four  women  out  of  forty-three  cases,  though  women  are 
employed  in  telegraphing  in  a  much  larger  proportion  to  men  than 
these  figures  would  represent. 

The  exciting  cause  of  the  disease  is  the  overuse  of  a  particular  set 
of  muscles.  This  is  perhaps  not  a  perfectly  accurate  w^ay  of  stating 
it.  As  these  same  muscles  respond  to  the  will  in  other  forms  of  move- 
ment than  that  which  brought  the  trouble  on,  it  should  be  stated  that 
an  excessive,  monotonotis  employment  of  a  particular  form  of  com- 
plicated, coordinated  movement  causes  it.  This  presents  the  affection 
in  an  entirely  different  light  and  begins  to  let  some  illumination  in  upon 
its  -manifest  connection  with  a  neuropathic  temperament.  It  is  the 
overuse  of  a  movement,  and  not  merely  of  the  muscles,  that  underlies 
the  trouble. 

^Movements  are  primarily  of  brain  or  mind  origin,  whereas  mere 
nerves  and  individual  muscles  are  represented  in  the  spinal  centers. 
This  etiological  fact  that  complicated,  coordinated  movements  rather 
than  mere  nerve  or  muscle  activity  is  the  cause  of  the  occupation  neuro- 
sis sharply  differentiates  this  disease  from  the  affections  that  simulate 
it  but  depend  upon  poliomyelitic  and  neuritic  changes. 

Not  every  kind  of  movement  provokes  it,  but  those  painfully  and 
slowly  acquired,  educated  movements,  that  are  highly  complicated  and 
require  an  extreme  degree  of  a  novel  form  of  coordination,  that  were 
and  are  purely  voluntary,  but  by  practice  have  grown  to  be  automatic, 
and  that  bring  into  play  an  unwonted,  antagonistic  set  of  muscles.  In 
writing,  playing  musical  instruments,  milking,  beating  a  drum,  manipu- 
lating a  telegraphic  key,  there  are  several  combined  acts  being  per- 
formed at  the  same  time  and  under  the  same  strain.  Not  only  is  firm 
prehension  exercised  by  some  muscles  while  others  at  the  same  mo- 
ment are  performing  the  required  movement,  but  both  are  under  an 
unusual  tension  that  at  first  consciously  and  later  unconsciously  gives 
unw^onted  exercise  to  the  cerebrum  and  the  central  coordinating  appa- 
ratus. In  writing,  for  instance,  the  pen  must  be  held  more  or  less 
firmly  and  it  must  be  properly  moved  by  both  fingers  and  the  arm. 
This  is  a  compound,  complicated  act  therefore.  It  means  a  remark- 
ably sharp  disassociation  of  the  movements  of  different  sets  of  mus- 
cles all  in  the  same  extremity  and  at  the  same  period  of  time.  This 
requires  an  extraordinary  adjustment '  of  function  between  different 
sets  of  motor  centers  in  the  cord  and  brain.  It  opens  up  new  path- 
ways of  inter-communication  between  these  centers  and  by  the  nature 
of  the  process  puts  these  new  pathways,  and  with  them  the  new  coor- 
dinating apparatus,  into  a  condition  of  severe  strain.  Exhaustion  takes 
place  and  though  the  associated  motor  centers  may  operate  and  cause 
the  muscles  to  contract  in  other  wavs  and  along:  other  coordinating 


THE    XEUROXIC   DISEASES 


275 


paths,  they  cannot  do  so  along  these  that  have  become  thus  wearied. 
That  the  mere  overuse  of  the  muscles  alone  is  not  the  cause  of 
the  trouble  is  shown  in  the  fact  that  neither  authors  nor  stenographers 
who  write  a  ver}-  great  deal  are  victims  to  any  great  extent.  Copyists 
and  those  who  use  a  cramped  hand  in  writing  and  pens  that  prevent 
a  free  movement  of  the  arm  are  th-e  great  sufferers.  Resting  the  hand 
on  the  little  finger  and  moving  the  pen  up  and  down  with  the  other 
fingers  while  the  arm  remains  comparatively  quiet  and  poised  seems 
to  be  a  particularly  dangerous  method.  Sharp  steel  pens  require  so 
much  more  stiffness  and  firmness  in  movement  than  do  soft,  loose 
quills  that  they  have  been  in  fact  justly  blamed  for  the  trouble.  The 
style  of  writing,  the  intensity  of  it  caused  by  hurry  to  get  through,  the 
instrument  employed  and  in  fact  everything  that  increases  the  demand 
upon  the  coordinating  apparatus  are  etiological  factors.  To  this  must 
be  added,  of  course,  the  monotonous  exercise. 

What  is  said  of  writing  applies  with  equal  force  to  all  other  occu- 
pation movements  from  which  the  disease  has  developed.  In  the  irreg- 
ular yet  carefully  regulated  movements  of  the  telegraphing  arm  and 
hand,  we  observe  a  strained  coordination  of  a  highly  complicated 
character.  The  pianist,  the  violinist,  the  flute-player,  the  milker,  the 
drummer,  the  cigar-roller,  the  seamstress,  the  tailor,  the  cobbler,  the 
dancer  and  others  are  usually  employed  in  an  occupation  that  upon  the 
face  of  it  shows  an  unusually  fine  coordination  between  various  com- 
bined and  antagonistic  groups  of  muscles.  At  first  this  coordination 
was  practiced  with  difficulty.  It  had  to  be  learned.  It  tends  to  becom.e 
automatic,  but  has  not  yet  reached  the  degree  of  complete  automatism. 
It  is  subject  to  weariness  and  to  depression  if  the  guiding  cerebral 
centers  are  vitiated  by  heredity  and  other  predisposing  factors.  Mo- 
notonous and  excessive  exercise  of  it  breaks  it  down. 

Local  inflammatory  conditions  in  the  hand,  injury,  wet  and  cold, 
albuminuria,  lead-poisoning  and  other  causes  of  neuritic  degenerative 
conditions  have  been  blamed  for  it,  though  it  is  a  question  whether 
these  cases  should  be  regarded  as  typical  instances  of  the  disease.  I 
am  sure  some  of  the  latter  are  but  cases  of  neuritic  incoordination, 
spasm  or  palsy  and  are  no  more  to  be  regarded  as  cases  of  occupation 
neurosis  than  the  ataxia  of  tabes  is  to  be  regarded  as  the  same  as  psy- 
chic vertigo. 

Emotion  is  an  etiological  factor. 

Pathology  and  Pathogexesis. — No  pathological  changes  have 
been  found  in  the  few  cases  that  have  been  examined  post-mortem.  It 
will  not  do,  however,  to  say  with  Oppenheim  that  none  will  probably 
ever  be  found  and  it  is  entirely  a  misconception  of  the  disease  to  attrib- 
ute it  to  the  neuritis  and  poliomyelitis  evidenced  in  some  supposed 
cases  of  the  disease  that  were  examined  pathologically.  It  is  undoubt- 
edly a  functional  trouble,  but  functional  troubles  must  necessaril}- 
spring  out  of  some  minute  nutritional  changes,  albeit  the  latter  are 
too  fine  for  our  modern  means  of  investigation.  Consider  for  a  moment 
the  etiology  of  this  strange  disease.  Note  how  a  tendency,  a  neuro- 
pathic tendency,  born  in  the  individual  or  fostered  by  his  environment, 
plays  a  leading  role  among  its  predisposing  causes.     Note  the  diseases 


2/6  THE    XKLUOXIC    DISEASES 

with  u  hich  it  has  been  associated  ;  neurasthenia,  functional  spasm,  epi- 
lepsy, heniicrania.  hay  fever,  neuralgia,  chorea  and  a  tendency  to  want 
of  all  self-restraint,  sobriety  and  regularity  that  go  with  a  strong 
and  healthy  mentality.  Obserye  its  frequent  association  with  emotional 
states,  with  wasting  diseases,  depressing  traumata  and  a  mode  of  life 
that  is  unhygienic  in  its  surroundings  and  duties.  The  background 
upon  which  the  disease  portrays  itself  is  suggestive  indeed  and  makes 
one  think  involuntarily  of  the  hysteroid  and  other  mild  psychoses  and 
subconscious,  cerebral  exhibitions. 

After  considering  the  etiology  of  the  disease,  observe  for  a  mo- 
ment how  it  reveals  itself.  It  is  preeminently  a  motor  i:rouble.  The 
disturbance  occurs  in  a  variety  of  movements  that  are  of  late  acquisi- 
tion, arc  educational,  are  striving  to  become  automatic  and  are  already 
partly  so,  and  are  the  result  of  a  most  complicated  a. id  refined  form  of 
coordination  that  is  too  coarse  to.  be  wholly  cerebral  ni  origin  and  yet 
not  coarse  enough  to  be  spinal,  but  just  of  such  a  character  to  be  sub- 
conscious, subpsychic,  like  some  of  the  phenomena  of  hysteria,  phrenas- 
thenia  and  other  forms  of  cerebro-psychosis  of  the  subconscious  order. 
Place  this  beside  the  fact  that  the  dise^ise  is  not  essentially  neural  or 
nuiscular  because  other  movements  can  be  readily  made  by  the  same 
nniscles,  as  witness  the  disabled  telegraph  operater  writing  with  great 
ease  and  fluency ;  beside  the  fact  that  none  of  the  usual  signs  of  mus- 
ctilar  or  neural  disease,  electrical  or  otherwise,  are  observed  in  typical 
cases :  and  finally,  besides  the  fact  that  the  prognosis  is  bad  and  the 
treatment  discouraging,  it  seems  to  me  we  have  enough  data  to  sug- 
gest that  the  trouble  is  essentially  central  in  origin,  is  a  subconscious 
cerebration  and  is  a  functional  weariness  or  exhaustion  of  the  coordi- 
nating apparatus. 

It  is  easy  to  understand  of  course  that  the  excessive  use  of  the' 
muscles  which  provoke  the  disease,  but  which  does  not  represent  it  in 
its  essential  nature,  for  it  is  not  muscle  exhaustion  so  much  as  it  is 
exhaustion  of  the  central  inhibitory,  coordinating  apparatus,  may  in  a 
reflective  manner  cause  atrophic  conditions  and  even  occasional  fugi- 
tive neuritic  and  poliomyelitic  changes  of  a  slight  character.  Exhaus- 
tion of  functional  coordination  with  certain  variable  secondary  changes 
of  a  grosser  nature  constitutes  then,  so  far  as  logic  can  demonstrate 
to  us  in  the  absence  of  more  positive  physical  findings,  the  pathogene- 
sis of  the  true  occupation  neurosis.  Here  again  it  is  shown  that  this 
disease  must  not  be  confounded  with  the  spasmodic  pareses  that  often 
sinnflate  it  but  that  owe  their  origin  to  some  limited  form  of  muscle 
or  nerve  disease  such  as  myositis,  neuritis,  poliomyelitis. 

Symptoms. — The  onset  of  the  trouble  is  always  gradual.  It  is 
first  noticed  that  the  use  of  the  hand  is  becoming  uncertain  and  be- 
yond the  delicate  control  of  the  will.  Xot  only  does  the  writing- 
seem  to  grow  more  difficult  but  it  begins  to  change  m  character.  There 
is  a  tremulousness  about  it.  a  little  jerkiness,  a  disinclination  to  pro- 
ceed in  the  old  regular  way.  Sometimes  a  feeling  of  soreness  or  weight 
or  slight  pain  is  felt  in  the  fingers,  up  the  arm  and  between  the  should- 
der  blades.     A  little  writing  mav  still  be  done  normally,  but  lengthv 


THE    XEUROXIC   DISE  \SES  2// 

use  of  the  pen  produces  a  feeling  of  extreme  tire  and  a  stiffness  and 
unnecessary  rigidity  in  holding. 

The  symptoms  of  the  fully  developed  disease  are  necessarily  varied 
because  the  many  occupations  in  which  this  neurosis  occurs  demand 
the  use  of  many  different  sets  of  muscles  and  nerves.  There  is  no 
fixed  clinical  picture  therefore  for  the  neurosis  in  general  though  there 
is  mere  or  less  of  a  definite  manifestation  in  each  special  occupation. 
There  are,  however,  three  well-recognized  types  of  the  trouble,  namelv, 
the  spasmodic,  the  paralytic  and  the  tremulous.  When  there  is  much 
pain  present,  the  type  is  referred  to  as  neuralgic.  So  much  more  prom- 
inent are  the  motor  symptoms  that  the  affection  may  well  be  looked 
upon  clinically  as  a  motor  neurosis. 

In  writer's  cramp  the  attempted  use  of  the  muscles  at  once  de- 
velops a  spasm.  They  become  stiff"  and  seize  the  pencil  and  the  move- 
ments are  awkward  and  uncontrollable.  Sometimes  other  muscles  than 
those  merely  necessary  to  perform  the  act  of  writing  participate  in  the 
spasm.  The  left  arm  has  thus  exhibited  an  associated  condition.  ]\Iore 
often  when  the  left  arm  is  employed  to  relieve  the  affected  right,  the 
latter  immediately  becomes  spasmodic.  A  lore  rarely  even  the  legs 
have  been  seen  to  be  spasmodic  when  onl}-  the  writing  with  the  right 
hand  provoked  the  trouble.  A  hemispasm  of  the  entire  body  has  been 
reported  and  suggests  strikingly  the  seat  of  the  primary  lesion.  The 
spasm  in  the  fingers  is  tonic  and  aff'ects  the  muscles  concerned  with 
the  performance  of  the  act.  Seme  authors  insist  that  the  latter  is  an 
essential  indication  of  the  disease,  but  Lewis  does  not.  The  flexors  of 
the  fingers,  more  rarely  the  extensors,  are  contracted.  The  thumb  and 
index  finger  are  especially  marked  by  the  spastic  weakness.  The  thumb 
may  be  controlled  and  pressed  firmly  into  the  palm  while  the  fingers 
are  forcibly  separated.  Sometimes  the  spasm  is  so  promiscuous  and 
spread  about  that  the  whole  hand  seems' to  be  in  a  state  of  riotous 
movement.  As  it  begins  to  appear  the  patient  changes  the  method  of 
holding  his  pen  and  thus  all  sorts  of  bizarre  and  even  ludicrous  posi- 
tions are  adopted  in  order  to  be  able  to  go  on  with  the  writing.  Per- 
sistence in  the  writing  even  with  the  new  attitude  causes  the  spasm 
to  appear  in  other  muscles  so  that  the  work  has  to  be  given  up  entirely. 
A  condition  almost  of  tetany  may  develop,  with  contraction  of  the  flex- 
ors of  the  wrist  as  well  as  of  the  fingers  upon  the  slightest  attempt  to 
use  the  muscles  for  writing  or  any  other  purpose.  ^Mitchell  described 
a  lock-spasm  in  which  the  contraction  of  the  fingers  and  hand  was 
so  violent  for  a  time  ^hat  the  latter  seemed  to  be  locked.  When  the 
spasm  wears  off  the  muscles  relax — feel  a  little  tired  and  weak.  In 
some  cases  there  is  during  the  spasmodic  condition  severe  pain  in  the 
muscles,  bones  and  joints.  A  significant  fact  is  that  the  more  the 
patient  worries  over  his  inability  and  the  more  frantic  his  efforts  are 
to  overcome  it,  the  worse  the  disturbance  is  both  motor  and  sensory. 

The  paralytic  form  of  the  disease  is  less  common  than  the  spastic. 
Like  the  latter  it  comes  on  gradually  and  has  other  symptoms  occa- 
sionally associated  with  it.  The  fingers,  hand  and  arm  are  subject  to 
a  feeling  of  intense  weariness  and  when  writing  is  attempted  they  re- 
main immobile  and  like  a  dead  weight  upon  the  table.     The  will  seems 


'2.y'6  THE    NEUlvOXIC   DISEASES 

to  have  lost  all  power  over  them.  Sometimes  this  paresis  follows  a 
spasm.  Paresis  in  one  muscle  with  spasm  in  another  has  been  seen. 
Rarely  a  paralytic  condition  is  followed  by  a  spasmodic.  The  result 
in  regard  to  the  occupation  is  the  same.  Inability,  awkwardness,  with 
strange  and  frantic  efforts  to  overcome  and  thwart  it  are  so  obvious  at 
times  that  the  attitude  alone  is  almost  sufficient  to  make  a  diagnosis 
upon.  In  the  paralytic  form  a  certain  degree  of  muscular  atrophy  is 
occasionally  noted.  It  is  unlike  the  wasting  of  the  progressive  form  of 
atrophy  in  the  fact  that  it  is  less  m  degree  and  it  is  amenable  to  re- 
covery. If  it  is  an  early  manifestation  and  is  accompanied  by  local 
pain  and  paraethesia,  neuritis  is  probably  the  cause  of  the  trouble  and 
not  the  neurosis  under  consideration.  A  mild,  localized,  permanent, 
late  atrophy  may  rarely  occur  as  the  result  of  secondary  damage  down 
to  the  central  cells  of  the  cord  by  the  severity  and  prolongation  of  the 
neurosis.  None  of  the  usual  objective  signs  can  be  elicited  by  exam- 
ination. When  electrical  reactions,  cutaneous  sensibility,  true  objec- 
tive paralysis,  tremor  or  ataxia  is  observed  the  disease  is  not  one  of 
occupation  neurosis  but  some  organic  trouble  of  peripheral  nerves  or 
cord.  Too  much  inportance  cannot  be  given  to  this  distinction,  for 
the  prognosis  and  treatment  depend  upon  it. 

It  is  very  rare  for  patients  to  complain  of  tremor  and  yet  in  some 
instances  an  irregular  tremulousness  has  been  observed.  One  must 
be  well  on  his  guard  not  to  mistake  dementia  paralytica  or  disseminated 
sclerosis,  which  sometimes  in  their  incipiency  reveal  only  a  tremor 
and  partial  inability  to  write,  for  this  disease.  As  an  exhaustion  mani- 
festation, tremor,  or  rather  trembling  or  unsteadiness,  may  well  be 
expected,  especially  in  the  forefinger  when  the  hand  is  at  rest.  An 
unusual  form  of  nystagmus  has  been  seen  among  miners  and  attributed 
by  Nieden  to  the  defective  illumination  of  the  mines  causing  eye-strain. 
The  neuralgic  forms  of  the  trouble  must  be  carefully  studied  in 
a  skeptical  frame  of  mind.  Authors  describe  all  sorts  of  painful  condi- 
tions that  are  clearly  due  to  neuritis.  One  writer  speaks  of  pain  over 
the  nerve  trunks  elicited  by  pressure,  of  hypersesthesia,  anaesthesia  and 
parsesthesia,  all  typical  of  a  distinct  neuritis.  What  is  the  logic  of 
having  two  descriptions  thus  of  the  same  disease  in  different  parts 
of  the  book?  If  this  author  regards  the  occupation  neurosis  as  an 
expression  of  a  neuritis  or  other  pathological  change,  it  can  and  should 
be  kept  under  the  symptomatology  merely  of  neuritis ;  if  the  occupation 
neurosis  is  not  a  distinct  disease  of  such  gross  organic  origin,  then 
these  symptoms  of  such  organic  disease  do  not  belong  to  it  and  should 
not  be  referred  to  except  as  an  evidence  of  a  complication.  Clearness  of 
distinction  and  logical  reasoning  are  in  neurology  as  in  every  science 
coequal  in  importance  to  the  mere  accumulation  of  facts  and  observa- 
tions. Complications  and  sequel?e  may  be  easily  understood  as  ac- 
companying an  occupation  neurosis.  Organic  gross  changes  and  in 
some  advanced  cases  even  undiscoverable  histopathological  changes  of 
a  nutritional  character  may  cause  various  vasomotor  and  trophic  symp- 
toms. These,  as  a  rule,  will  represent  neuritic  and  poliomyelitic  disease 
which  will  differentiate  the  trouble  at  once  from  an  occupation  neurosis. 
Diagnosis. — For  the  sake  of  clearness  we  must  in  this  disease 


THE    NEURONIC   DISEASES  2/9 

maintain  a  sharp  distinction  between  a  functional  and  an  organic 
trouble.  It  is  confusing,  unscientific  and  illogical  to  talk  about  a 
neurosis  being  a  functional  trouble  and  distinguished  from  organic, 
and  immediately  under  the  head  of  neurosis  begin  depicting  the  well- 
recognized  clinical  pictures  of  distinct  organic  diseases.  And  that  is 
just  what  the  older  writers  have  done  and  alas !  what  the  later  writers 
are  still  doing.  Neurology  cannot  hope  to  be  clear  to  the  general  reader 
When  its  followers  thus  wantonly  jumble  its  well-known  facts.  I  am 
not  criticising  the  difference  of  opinion  in  regard  to  the  real  nature 
of  the  occupation  neurosis,  for  I  admit  that  there  is  much  room  for  a 
difference  of  opinion,  but  I  am  criticising  the  method  of  calling  a  disease 
one  thing,  functional,  and  then  describing  it  with  the  symptomatology 
of  another  well-recognized  thing,  organic.  The  logical  contradiction, 
not  the  difiference  of  opinion  in  connection  with  the  disease,  is  the 
ground  for  my  criticism. 

I  have  perhaps  already  sufficiently  shown  that  in  my  opinion  an 
occupation  neurosis  is  not  a  neuritic  or  muscular  disease  itself,  though 
as  a  complication  or  a  sequel  it  may  have  accompanying  it  a  neuritic 
or  muscular  organic  trouble.  Its  etiology  and  its  symptomatology,  as 
I  have  previously  shown,  both  loudly  declare  that  it  is  a  disorder  of  the 
higher  conscious  or  subconscious  coordinating  mechanism.  Whether 
this  mechanism  resides  in  the  cortex,  basal  ganglia,  cerebellum,  medulla 
or  gray  matter  of  the  cord  we  cannot  say.  But  its  location  is  of  little 
consequence  in  comparison  with  the  fact  that  it  is  a  highly  compound, 
complicated  function  dependent  upon  the  play  of  one  source  of  nervous 
impulses  upon  another  source.  If  the  sources  of  these  impulses  them- 
selves are  organically  diseased,  we  may  have  spasms  and  pareses  with 
incoordination.  Such  diseases  will  be  recognized  as  well-known  organic 
lesions  of  the  brain,  cord  or  nerves.  On  the  other  hand,  the  mere 
functional  play  of  one  source  of  nnpulse  upon  another  source,  the  new, 
educated  function  as  it  were,  is  disturbed  and  exhausted.  This  is  a 
true  occupation  neurosis. 

There  are  many  diseases  in  which  m.uscular  weakness  and  dis- 
turbed coordination  with  spasm  are  seen  and  must  be  diflerentiated 
carefully  from  this  disease.  Every  sort  of  disorder  of  writing  is  not 
v^riter's  cramp.  The  former  is  seen  in  multiple  sclerosis,  in  high  tabes, 
in  dementia  parahlica,  in  paralysis  agitans,  in  hemiplegia,  in  chorea, 
in  progressive  muscular  atrophy  and  various  injuries  and  lesions  about 
the  hand  and  related  nerves.  The  difTerential  diagnosis  of  these  is 
easy  as  a  rule  and  involves  always  the  diagnosis  of  the  organic  or 
general  trouble. 

The  two  diseases  that  have  been  most  confused  with  writer's  cramp 
are  neuritis  and  poliomyelitis.  In  all  these  there  are  motor,  sensory 
and  other  exhibitions  that  lead  at  times  to  a  close  simulation  between 
them. 

Neuritis  has  very  often  been  mistaken  foran  occupation  neurosis  and 
vice  versa.  A  neuritis  certainly  interferes  with  complicated  movements 
and  it  may  spring  from  the  same  general  predisposing  and  exciting 
causes  in  some  instances  as  an  occupation  neurosis.  The  necessity 
for  a  clear  recognition  of  a  distinct  difference  between  the  two,  how- 


280  THE    NEURONIC    DISEASES 

ever,  is  indicated  in  the  opposite  character  of  the  prognosis  of  the 
two  diseases.  Neuritis  is  a  local,  distinct,  comparatively  permanent 
lesion  with  definite,  constant  symptoms.  In  nenritis  the  sensory  symp- 
toms are  in  great  evidence  often  and  are  always  more  or  less  present. 
They  certainly  hold  a  much  more  exalted  degree  of  prominence  in  re- 
lation to  the  motor  symptoms  here  than  they  do  to  the  motor  symptoms 
in  an  occupation  neurosis.  In  the  latter  we  often  have  muscular, 
crampy  pains,  general  soreness  and  widely  distributed  fugitive  aches, 
but  we  don't  have  the  localized  pains  upon  pressure  in  the  nerve  trunks, 
the  localized  spots  of  hypersesthesia  and  anaesthesia,  the  well-defined 
and  tmmistakable  parsesthesise  like  numbness,  tingling,  burning,  pins- 
and-needles  sensation  of  neuritis.  The  sensory  phenomena  of  the  latter 
are  prominently  cutaneous  and  objective;  those  of  the  former  are 
largely  muscular  and  subjective. 

Neuritis  suggests  clearly  an  organic,  well-defined  local  lesion  ;  an 
occupation  neurosis  has  a  sort  of  resemblance  to  neurasthenia  or 
hysteria.  It  is  in  the  motor  sphere  that  the  difference  between  a  neuritis 
and  an  occupation  neurosis  comes  out  most  clearly.  Incoordination,  it 
is  true,  is  prominent  in  both.  In  the  former  it  is  incidental,  in  the 
latter  it  is  all  but  the  entire  disease.  There  is  definite  weakness  and 
paralysis  in  individual  muscles,  so  that  for  no  sort  of  movement  can 
the  muscles  be  exercised  in  neuritis  ;  in  the  neurosis  there  is  only  ex- 
ceptionally paresis  and  then  only  as  a  result  of  prolonged  and  monot- 
onous exertion.  In  the  neurosis  the  muscles  may  be  powerless  to  move 
for  one  sort  of  movement,  but  apparently  little  afifected  for  the  per- 
formance of  another  sort  of  movement.  A  victim  of  pianist's  cramp 
may  be  able  to  write  normally :  an  affected  telegrapher  can  still  play 
the  piano ;  and  one  who  can  no  longer  write  may  still  be  able  to  draw 
with  the  greatest  facility.  \^"hen  the  trouble  involves  the  lower  ex- 
tremities other  movements  than  those  which  caused  it  can  usuallv  be 
well  performed.  This  argues  against  the  old  view  that  the  muscles 
themselves  are  diseased.  The  electrical  changes,  so  well  known  in 
neuritis,  the  reaction  of  degeneration,  are  not  seen  in  the  neurosis.  The 
presence  of  atrophic,  vasomotor  and  secretory  local  disturbances,  loss 
of  the  reflexes,  pareses  and  similar  manifestations  in  other  parts  of 
the  body  point  to  a  neuritis.  Neuritic  symptoms  are  bilateral,  when 
they  are  bilateral  at  all,  from  the  start.  In  the  neurosis,  an  attempt  to 
use  the  other  arm  may  set  up  bilaterally  the  same  trouble  in  it,  but  the 
disease  is  never  bilateral  from  the  beginning. 

As  I  have  said,  all  of  these  neuritic  manifestations  may  occur  in 
the  course  of  an  occupation  neurosis,  but  in  my  opinion  they  represent 
a  complicating  neuritis.  If  I  thought  the  disease  were  entirely  a  form 
of  neuritis,  it  would  be  referred  to  merely  as  a  symptom  of  this  disease 
described  elsewhere.  The  frequent  disappearance  of  the  neuritic  symp- 
toms while  the  incoordination  and  difliculty  in  writing  continue  shows 
also  that  a  neuritis  and  an  occupation  neurosis  are  not  the  same  thing. 

Polioinyelitic  symptouis  may  occur  also  in  the  course  of  an  occu- 
pation neurosis,  but  they  are  easily  differentiated.  In  poliomyelitis 
there  is  a  febrile  condition,  a  regressive  paralysis  finally  limiting  itself, 
along  with  rather  rapid  atrophy  in  particular  muscles.     Poliomyelitis 


THE    XEUROXIC   DISEASES  281 

occurs  most  frequently  in  the  legs  ;  the  neurosis  in  the  arms.  Spasm, 
pain  and  true  incoordination  are  wanting  in  poliomyelitis.  The  sore- 
ness of  the  muscles,  the  fatigue  symptom,  the  appearance  of  the  in- 
capacity upon  the  initiation  of  a  particular  form  of  complicated,  ac- 
quired movenient  are  also  absent  from  the  spinal  inflammatory  de- 
generative trouble. 

Tetan-v  has  been  mistaken  for  an  occupation  neurosis.  Tetany 
is.  provoked  by  any  sort  of  movement,  whereas  this  disease  has  its 
spasms  initiated  only  by  an  attempt  to  resume  the  occupation  that 
caused  it. 

The  "hcphcrstic  hemiplegia"  of  Dr.  Frank  Smith  seen  among 
Sheffield  smiths  is  declared  by  Gowers  to  have  been  cases  of  organic 
disease  of  the  hemisphere. 

Types  of  the  Disease  Based  upon  Occupation. — Practically  the 
trouble  is  always  of  the  same  nature  in  whatever  occupation  it  may 
have  been  acquired.  It  is-  useless  therefore  to  go  into  any  elaborate 
description  of  all  the  forms  of  the  disease  that  have  been  seen  and 
reported.  The  principal  feature  of  investigation  in  each  particular 
case  is  the  character  of  the  movement  that  has  brought  the  trouble 
on  and  the  particular  muscles  involved  in  the  elaboration  of  that  move- 
ment. The  whole  qtrestion  is  therefore  one  of  location  merely  and  of 
gross  anatomy.  This  investigation  will  have,  however,  rather  a  scien- 
tific interest  merely  than  a  therapeutic  one,  for  the  treatment  is  the 
same  in  all  cases.  It  may  be  of  value  diagnostically,  however,  if  the 
occupation  can  be  guessed  from. the  symptoms  of  the  disease  alone. 

Pianist's  cramp  is  chiefly  a  professional  disease  and  seems  to 
occur,  possibly  on  that  account,  more  among  women  than  men.  The 
spasmodic  and  neuralgic  varieties  of  the  disease,  more  particularly  the 
latter,  are  seen.  Precision  in  striking  the  key  and  prolonged  extension 
of  the  fingers  are  troublesome  manifestations.  Pains  are  often  felt  .in 
the  fingers,  up  the  arms,  in  and  about  the  shoulder  and  between  the 
shotflder  blades.  Gowers  mentions  a  case  that  had  pain  in  the  outer 
border  of  each  hand,  but  never  any  cramp  except  at  night.  Playing, 
of  course,  has  to  cease  as  soon  as  the  symptom  appears.  Paralytic  forms 
and  others  occur,  but  usually  pain  and  exhaustion  during  playing  repre- 
sent the  complexus  of  symptoms.  Violinists  may  be  affected  in  either 
or  in  both  hands.  In  Hute  players  the  left  hand  is  more  often  involved 
than  the  right.  In  a  young  cornetist  that  I  once  treated  who  had  failed 
to  get  much  improvement  from  many  previous  lines  of  treatment  and 
w^ho  improved,  but  I  cannot  say  recovered,  after  a  long  course  of  treat- 
ment with  me,  .the  lips  were  slightly  spasmodic  and  there  was  an  in- 
definite soreness  along  the  course  of  the  supraorbital  nerves.  He  was 
■  distinctly  a  neuropath,  but  exhibited  at  no  time  any  other  local  symp- 
tom. Aldrich  reports  a  case  in  a  trap-drummer  whose  duty  it  was 
to  beat  a  drum  by  the  operation  of  a  pedal  manipulated' with  the  right 
foot.  Cramping  pain  and  a  sense  of  exhaustion  seemed  to  be  located 
in  the  tibialis  anticus  and  peronei  muscles.  The  symptoms  appeared 
only  when  playing  or  when  walking  rapidly. 

I  once  had  at  my  clinic  for  a  long  time  what  seemed  to  be  a 
clear  case  of  the  disease  in  a  painter.     The  possibility  of  lead-intoxica- 


282  THE    NEURONIC   DISEASES 

tion  was  eliminated  by  tlie  absence  of  the  extensor  paralysis,  the  abdo- 
minal colic,  the  blue  line  along  the  teeth  and  other  well-known  signs 
of  saturnism  and  lead  neuritis.  He  could  move  his  arms  somewhat, 
but  there  was  no  spasm  and  only  soreness  in  them.  He  had  been  work- 
ing hard  and  continuously  for  a  long  time  on  a  steady  job  and  told 
me  he  had  scarcely  ever  rested  his  right  arm  by  using  his  left. 

To  blacksmiths  is  known  a  verv  painful  occupation  cramp  involv- 
ing especially  the  deltoid  and  biceps  muscles.  Seamstresses,  tailors 
and  others  who  do  sewing,  such  as  sail-makers,  carpet-weavers,  suffer 
at  times  from  the  disease.  Runge  believes  he  has  seen  it  in  zvaiters 
from  carrying  plates  and  glasses.  Cigarmakers  tcho  roll  cigars  all  day 
and  milkers  of  cows  have  the  cramp  sometimes.  Oppenheim  has  seen 
it  appear  in  barbers  ever}-  time  they  had  to  use  the  razor.  It  was 
spastic  in  character.  Lapidaries  are  not  free  from  the  neurosis.  A 
metal-chaser  has  suffered  from  it.  Among  the  other  numerous  trades 
that  at  rare  intervals  cause  it  may  be  mentioned  flower-makers,  turners, 
watchmakers,  knitters,  engravers  using  the  burin,  masons  handling  the 
trowel,  compositors,  enamelers,  shoemakers  and  money-counters.  A 
sawyer's  cramp  is  described  by  Poore. 

These  trade  neuroses,  so  to  speak,  are  not  as  frequent  by  any 
means  as  the  neuroses  caused  by  writing,  music  playing  and  telegraph- 
ing- 

Telegrapher's  cramp  seems  to  aft'ect  more  particularly  those  who 
use  the  ]\Iorse  system,  which  necessitates  an  up  and  down  movement 
of  the  key.  The  typewriter  may  produce  the  trouble  just  as  piano- 
playing  does. 

Stammering  and  stuttering  from  much  speaking  is  related  to  this 
disease,  so  is  the  painful  exhaustion  of  the  laryngeal  muscles  called 
mogiphonia  by  Frankel. 

A  dancer's  cramp  is  known  among  ballet  dancers. 

It  w^ould  seem  that  every  form  of  hum.an  occupation,  involving 
strained,  continuous  and  complicated,  coordinated  movements  is  liable 
to  provoke  this  neurosis.  Still  the  caution  must  be  repeated  not  to  con- 
found neuritis  with  its  degenerative  symptoms  and  which  lurks  behind 
the  occupation  palsies  with  this  neurosis. 

Prognosis. — Some  authors  affirm  that  the  prognosis  of  writer's 
cramp  is  variable.  It  is  if  the  symptom  alone  is  made  the  disease. 
If  the  trouble  is  confounded  with  a  neuritis  the  prognosis  naturally  will 
be  favorable,  for  that  is  the  prognosis  of  neuritis.  Of  the  disease  occu- 
pation neurosis,  as  I  conceive  it  and  have  endeavored  to  describe  it, 
the  prognosis  is  decidedly  unfavorable.  It  runs  parallel  with  the  sort  of 
prognoses  that  we  have  to  make  in  hysteria,  neurasthenia,  and  allied 
general  disorders.  Amelioration  occurs  after  periods  of  prolonged  rest. 
Absolute  cures  have  been  seen,  but  they  are  rare.  As  a 
rule  the  disease  continues  many  years  or  for  life,  relapsing  or 
rather  breaking  out  in  a  sort  of  exacerbation  every  time  the  original 
movements  that  caused  it  are  attempted.  There  is  danger  always  in 
using  the  other  hand,  as  writers  and  telegraphers  so  often  do,  for  it 
frequently  also  becomes  affected.    It  never  destroys  life. 

Treatment. — Prophylactic  treatment  is   of  great   moment.    The 


THE    NEURONIC   DISEASES  283 

instant  the  first  premonitions  of  the  trouble  appear  cessation  of  the 
-occupation  must  take  place.  All  writing  had  better  be  given  up  for  a 
-time.  The  prophylaxis  is  summed  up  in  the  ore  phrase,  avoid  all  stilt, 
cramped,  uncomfortable  attitudes,  style  of  writing  and  manner  of  hold- 
ing the  pen.  Place  the  body  at  the  desk  in  writing  so  that  an  easy, 
Joose  and  pliable  position  can  be  maintained.  Adopt  a  style  of  writ- 
ing that  is  large,  full,  round  and  flowing.  Use  soft  pens  in  thick 
■cork  handles.  It  is  good  to  vary  tlie  attitude  and  the  penholder  from 
time  to  time.  Whether  writing  or  telegraphing  the  entire  arm  should 
Test  on  the  table.  The  vertical  style  of  penmanship  is  said  to  be  less 
liable  to  produce  the  trouble  than  is  the  slanting.  Each  case  is  to  be 
-Studied  from  its  own  standpoint,  but  ease  of  attitude,  ease  of  mind, 
largeness  of  movement  and  frequent  relaxation,  are  among  the  im- 
portant preventive  measures  to  be  remembered.  The  rest  should  be 
absolute  and  not  merely  a  variation  of  exercise.  It  is  unwise  to  go 
from  much  writing,  for  instance,  immediately  to  piano-plaving.  The 
two  neuroses  have  been  seen  to  develop  thus  simultaneously  in  the 
.same  individual. 

When  the  trouble  has  fully  declared  itself,  only  absolute  and  pro- 
longed  rest  is  the  safe  plan  to  adopt.  Those  who  must  write  some  at 
all  hazards  may  be  guarded  somewhat  by  the  use  of  a  special  apparatus 
to  hold  the  pen  with.  These  are  very  numerous  and  consist  of  rings 
and  bracelets  for  several  fingers,  in  which  the  penholder  can  be  fastened. 
The  attitude  of  the  hand  is  decidedly  altered  while  the  writing  goes  on. 
All  instrument  makers  have  several  forms  of  apparatus  of  this  sort, 
specially  commendable  among  them  being  the  Alatthieu  finger  ring 
and  thumb  rest,  the  Xussbaum  finger  bracelet  and  others. 

There  is  no  drug  treatment  for  this  neurosis.  Of  course  the 
"neurasthenic  state  may  call  for  its  special  tonics.  The  ver\"  nature  of 
the  disease,  an  exhaustion  of  coordination,  precludes  any  hope  of  benefit 
irom  mere  medicinal  agents. 

Electric  treatment  is  also  ruled  out  by  the  nature  of  the  disease. 
tjalvanism  has  been  applied  to  the  cervical  cord  in  some  cases  with 
alleged  benefit.  As  everyone  knows  electricity  is  a  most  valuable  agent 
in  the  treatment  of  the  degenerative  neuritic  troubles,  both  galvanism 
and  faradism.  It  is  to  be  noted,  however,  that  these  who  claim  such 
•excellent  results  from  the  electric  treatment  of  writer's  cramp  do  not 
distinguish  sharply  between  the  pure  functional  occupation  neuroses 
and  the  neuritic  professional  palsies.  It  is  easy  to  understand  therefore 
Tiow  even  their  results  vary  so  extremely. 

Massage  and  gymnastics  afford  the  best  results.  The  former 
maintains  the  nutrition  while  the  muscles  and  nerve  centers  are  regain- 
ing their  tone  from  rest,  and  the  latter  changes  yet  engages  the  activities 
of  the  central  coordinating  apparatus.  Szuedish  movements  of  the 
Tiands  and  fingers  with  resistance  on  the  part  of  the  patient  are  particu- 
larly good.  The  fingers  and  wrist  are  flexed  and  extended,  adducted 
and  abducted.  The  pressure  must  be  regular,  the  seances  short  and 
the  practice  several  times  a  day.  Gentleness,  persistency  and  the  end 
to  be  attained,  the  restoration  of  wearied  muscles  and  exhausted  co- 
ordination, are  to  be  kept  clearly  in  mind. 


284  THE    NEURONIC    DISEASES 

Sngi;csfioii  and  psychic  treatment  has  some  influence,  as  psychosis 
enters  to  a  certain  extent  in  the  loss  of  the  coordinating  power. 

Tciwfoiiiv  and  nerve-stretching  are  mentioned  merely  to  provoke 
the  wonder  why  they  were  ever  thought  of. 

MYOTONIA  CONGEN  [TA. 

This  singular  affection  is  sometimes  called  Thomsen's  disease,, 
because  this  physician,  who  was  a  victim  of  it,  and  in  whose  family 
there  were  more  than  twenty  cases  in  live  generations,  gave  the  first 
complete  and  accurate  description  of  it.  Before  him  Sir  Charles  Bell, 
Benedict  and  Leyden  had  each  referred  to  it.  Since  the  prominence- 
which  Thomsen  conferred  upon  the  disease  it  has  been  quite  closely 
studied  by  Seeligmuller,  Westphal,  Mobius,  Erb,  Strumpell,  Vig- 
ouroux,  Hammond,  Dana,  Shaw  and  many  others.  It  is  not  a  common 
disease,  though  upwards  of  half  a  hundred  cases  perhaps  have  been 
reported.  It  is  more  frequently  observed  in  Germany  and  Scandinavia 
than  in  England,  France  or  America.  Its  exact  position  in  the  classifi- 
cation of  diseases  cannot  be  determined  for  reasons  noted  in  the  dis- 
cussion of  its  pathogenesis. 

Etiology. — The  predominant  feature  in  its  etiology  is  its  heredity 
and  occurrence  in  the  same  family.  A  few  isolated  cases  have  been 
observed  in  which  the  hereditary  influence  has  been  chiefly  neuropathic. 
Males  are  said  to  be  more  frequently  affected  with  it  than  females. 
The  disease  may  appear  in  early  childhood  about  the  period  of 
adolescence.  It  is  not  known  to  be  dependent  upon  any  exciting  causes 
for  its  outbreak,  though  as  it  appears  to  be  an  expression  of  defective 
development,  all  depressing  and  exhausting  surroundings  may  have 
something  to  do  with  hastening  its  appearance. 

Pathology  and  Pathogenesis. — So  few  cases  have  come  to 
autopsy  that  our  knowledge  in  regard  to  the  essential  basis  of  the 
trouble  is  far  from  being  adequate.  In  the  cases  of  Erb  and  others 
there  was  hypertrophy  of  the  muscular  fibers,  increase  of  the  sar- 
colemma  nuclei  and  an  overgrowth  of  interstitial  tissue.  The  fibers 
have  been  reported  as  being  diminished  in  size,  though  increased  in 
number.  All  of  the  muscles,  even  the  diaphragm,  have  exhibited  this 
change.  Dejerine  and  Sottas  have  confirmed  these  findings  and  added 
the  statement  that  in  their  case  the  brain,  cord  and  nerves  were  entirely 
normal.  In  some  cases  absolutely  no  changes  have  been  observed  either 
in  the  muscular  or  the  nervous  tissues. 

The  symptoms  of  the  disease,  taken  in  conjunction  with  these 
almost  negative  pathological  findings,  favor  the  hypothesis  that  it  is 
a  functional  trouble.  Most  writers  following  Leyden  have  described 
it  as  a  functional  disease  of  the  muscles,  not  including  it  at  all  under 
the  head  of  nervous  diseases.  This  is  extraordinary  in  view  of  the 
neurotic  and  psychic  relationships  of  the  disease.  And  yet  it  is  but 
fair  to  state  that  these  authors  look  upon  the  mental  deterioration  and 
the  nervous  manifestations  and  influences  often  observed  in  the  dis- 
ease as  of  the  nature  of  mere  complications.     The  same  developmental' 


THE    XEUROXIC  DISEASES  285 

inadequacy  that  affects  the  muscular  apparatus  affects  the  nervous  cen- 
ters. 

Other  authorities  classify  the  disease  with  the  dystrophies,  not 
merely  because  there  is  a  certain  similarity  in  some  of  the  clinical  fea- 
tures ^Yith  the  latter,  but  because  they  suspect  that  it,  as  well  as  the 
d}strophies,  are  remotely  dependent  upon  some  minute  central  change 
in  the  central  nervous  apparatus,  which  may  ultimately  show  that  the} 
are  closely  related  to  the  central  progressive  muscular  atrophies. 

A  third  group  ot  writers  are  mclmea  to  regard  the  trouble  as 
hysteroicl  m  origin,  though  not  m  any  sense  hysterical.  They  explain 
that  it  is  a  sort  of  psychosis,  a  psychic  incoordination,  a  connecting 
link  between  mental  and  bodily  ailments. 

The  absence  of  constant  and  distinctive  pathological  findings  fa- 
vors the  functional  character  of  the  disease.  The  hereditary  and  de- 
velopmental origin  of  the  disease,  its  chief  limitation  to  the  voluntar\ 
muscles,  its  close  relationship  to  the  volitional  faculty,  the  trequenc 
mental  defectiveness  and  the  absence  of  most  of  the  well-known  signs 
of  typical  organic  disease  of  the  brain  or  spinal  cord  lend  some  sup- 
port to  the  mental  theory. 

With  the  meagre  data  now  at  hand  nothing  definite  therefore  can 
be  said  in  regard  to  the  pathogenesis  of  this  remarkable  affection. 

Symptoms. — The  prime  symptom  of  Thomsen's  disease  is  an 
intentional  spasticity.  1  use  the  adjective  intentional  here  in  the  same 
sense  in  which  it  is  used  when  the  intentional  tremor  of  multiple  sclero- 
sis is  spoken  of. 

In  the  muscles  of  the  extremities  and  of  the  face  the  slightest  voli- 
tional moveinent  causes  a  slow,  firm,  irresistible  contraction.  This  may 
occur  at  any  time  when  the  patient  starts  to  use  the  particular  muscle  or 
set  of  muscles.  It  is  usually,  however,  most  prompt  and  severe  after  a 
period  of  rest.  With  a  powerful  exertion  of  the  will  the  contraction 
can  be  retarded  and  even  at  times  overcome.  Thus  it  is  seen  to  be  a 
volitional  phenomenon  in  part,  albeit  a  markedly  abnormal  one. 

Some  have  endeavored  to  explain  the  entire  disease  on  this  per- 
version of  the  volitional  muscular  function.  It  is  argued  tha-i  to  pro- 
duce a  desired  movement  the  volitional  faculty,  so-called,  must  exer- 
cise a  combined,  normal  control  over  every  muscle  of  the  body  and  its 
antagonist.  It  must  preserve  a  balance  between  the  two.  If  this 
balance  is  lost,  the  muscles  do  not  work  well  together,  action  and  over- 
action  causes  an  unnecessary  expenditure  of  force,  and  a  sort  of  pur- 
poseless movement.  As  one  author  has  put  it.  an  inhibition  of  volun- 
tary movements  due  to  a  muscular  rigidity  sets  in  during  the  action. 
Influences  like  increased  emotion  that  affect  the  will  affect  most  strik- 
ingly the  contractions.  Often  when  the  contraction  initiated  b}"  the 
will  is  once  started  it  cannot  be  stopped,  even  with  the  greatest  exertion. 
After  several  such  tonic  contractions  they  become  graduall}-  weaker 
and  finally  cease  altogether  from  exhaustion.  They  do  not  reappear 
until  another  voluntarv  movement  is  instituted  in  them. 

Warmth,  mental  qtiietude.  non-observation  of  self,  frequent  exer- 
cise of  the  involved  muscles  and  ingestion  of  a  small  amount  of  alcohol 
^vill  tend  to  diminish  the  severitv  of  the  contractions. 


286  THE   NEURONIC   DISEASES 

All  the  muscles  of  the  body  except  the  viscera  and  involuntary 
muscles  may  be  the  victims  of  the  disease.  Swallowing,  therefore^ 
may  be  difficult.  Speech  is  afifected.  Protrusion  of  the  tongue  may 
cause  it  to  be  caught  and  bitten  between  the  teeth.  In  grasping  an. 
object  the  hand  closes  like  a  vise.  The  act  of  walking  becomes  stiffs 
sluggish  and  irregular.  The  patient  may  even  fall  and  remain  rigid. 
The  ocular  and  laryngeal  mfuscles,  with  the  sphincters,  escape. 

In  repose  the  muscles  are  normal  to  the  touch ;  in  contraction  they 
are  hard  and  firm.  They  may  be  normal  in  size  or  slightly  enlarged 
or  diminished.  Sometimes  their  contour  is  abnormal  from  implication, 
of  a  part  of  a  muscle  group.  There  are  no  disturbances  of  the  re- 
flexes. 

In  .Erb's  so-called  myotonic  electrical  reaction  in  the  muscles  cer- 
tain changes  take  place  in  the  responses  to  the  galvanic  current,  those 
to  the  faradic  remaining  normal.  There  is  a  muscular  contraction 
of  long  duration.  The  muscles  show  an  increased  excitability  to  the 
direct  galvanic  current.  Only  contractions  upon  closure  are  obtained. 
Anodal  closing  contraction  is  usually  the  more  marked.  This  is- 
somewhat  of  a  reversal  of  the  normal  phenomena.  With  a  stabile 
galvanic  current  a  vermicular,  rhythmical,  wave-like  contraction  passes 
through  the  muscle  from  the  negative  to  the  positive  pole. 

The  contraction  in  the  muscles  may  be  started  by  any  form  of  ex- 
ternal irritation.  A  slight  tap  or  pressure  will  sometimes  bring  on  the 
slow,  worm-like  movement  in  them. 

Sensations  are  normal.  Only  a  slight  aching  pain  is  complained 
of  sometimes.  The  mind  as  a  rule  is  more  or  less  weak,  though  in 
some  instances  it  is  bright  and  clear.  Epilepsy,  hemicrania,  pseudo- 
hypertrophy, polyneuritis,  tetany  and  other  neural  complications  have 
been  observed  with  the  disease. 

Diagnosis. — The  diagnosis  is  not  difhcult  as  the  clinical  mani- 
festation is  so  unique.  Diseases  in  which  similar  spasms  occur  are  to 
be  differentiated  by  the  existence  of  other  symptoms  which  myotonia  is 
singularly  free  from. 

Prognosis. — The  prognosis  in  regard  to  life  is  excellent.  The 
disease  is  one  of  years  and  even  a  whole  lifetime.  It  is  not  pro- 
gressive in  the  true  sense  of  the  word.  Remissions  may  occur  during- 
its  course. 

Treatment. — There  is  no  treatment  that  will  prove  of  any  avaiL 
Gymnastics  and  constant  activity  helps  to  make  life  bearable  by  keep- 
ing down  the  severity  of  the  spasms. 

TITE  CHOREAS. 

The  term  chorea  is  from  a  Greek  word  meaning  a  dance,  and  is 
employed  to  indicate  certain  irregular,  involuntary,  incoordinated  mus- 
cular movements  observed  m  various  disease  states.  It  is  therefore  not 
a  distinct  pathological  entity  ;  it  is  merely  a  symptom.  This  fact  should 
be  carefully  kept  in  mind,  as  the  underlying  affection  of  which  the 
choreic  jerkings  form  one  symptom  is  the  indicator  for  the  proper 
treatment  to  be  employed,  and  not  the  choreic  movements  themselves. 


THE    NEURONIC   DISEASES  28/ 

The  separating  of  idiopathic  from  symptomatic  chorea,  as  some  authors 
attempt  to  do,  is  entirely  arbitrary  and  leads  only  to  confusion.  All 
the  choreas  are  symptomatic,  as  will  be  seen  in  the  further  discussion 
of  them.  Acute  minor  chorea,  the  type  of  them  all,  is  as  much  a  mere 
symptomatic  manifestation  of  an  underlying  toxaemia  or  other  disease 
as  are  the  choreas  of  hysteria,  pre-  and  post-hemiplegic  chorea,  the 
pandemic  choreas,  Huntingdon's  disease  and  the  choreic  phenomena 
associated  with  Friedreich's  disease  and  other  sclerotic  processes. 

ACUTE  MINOR  CHOREA. 

Acute  minor  chorea,  St.  Vitus'  dance,  or  Sydenham's  chorea,  is  a 
disease  of  the  central  nervous  system,  frequent  in  childhood,  charac- 
terized clinically  by  irregular,  involuntary,  incoordmated  muscular 
movements,  and  by  certain  less  obtrusive  sensory  and  mental  phenom- 
ena; and  pathologically  by  a  few  scattered,  circulatory,  intiammatory 
and  degenerative  findings. 

Etiology. — ^^Heredity  does  not  play  a  direct  role  in  acute  minor 
chorea ;  the  so-called  hereditary  chorea,  Huntingdon's  chorea,  is  an 
entirely  different  affection.  In  almost  one-sixth  of  the  cases  of  this 
disease,  however,  a  pronounced  neuropathic  taint  is  shown  to  run 
through  the  family.  The  child's  forebears  have  been  subject  to  epi- 
lepsy, insanity,  hysteria,  neurasthenia,  narcotic  poisoning  with  alcohol 
or  tobacco,  and  even  chorea  itself.  Race  exhibits  some  influence,  Jew- 
ish, German  and  Portuguese  children  being  especially  prone  to  the 
trouble.  According  to  Weir  Mitchell,  the  Negro  race  is  singulany 
free  from  it. 

Later  childhood  is  the  favorite  period  for  the  outbreak  of  St. 
Vitus'  dance ;  and  during  this  period  girls  are  more  frequently  affected 
than  boys,  in  the  proportion  almost  of  three  to  one.  Nine-tenths  of  the 
cases,  according  to  Cowers,  occur  between  the  ages  of  five  and  twenty. 
As  puberty  approaches  the  ratio  of  girls  to  boys  increases.  After 
twenty-five  years  of  age  the  disease  becomes  more  rare,  and  in  old  age 
it  is  very  rarely  seen  as  senile  chorea.  It  is  thus  a  disease  of  all  periods 
of  life,  but  especially  of  childhood,  with  a  slight  preponderance  in  the 
female. 

Ancemic,  neuropathic  and  irritable  children  are  often  the  victims 
of  chorea  and  becoming  hysterical,  they  sometimes  manifest  the  com- 
bination of  chorea  and  hysteria,  which  must  always  be  carefully  differ- 
entiated from  the  pure  hysterical  symptom  known  as  chorea  hysterica. 

The  relationship  between  chorea  minor,  acute  articular  rheumatism 
and  endocarditis  is  so  striking  as  to  call  for  more  than  a  passing  notice. 
It  is  estimated  that  approximately  one-quarter  of  the  cases  of  chorea 
give  a  history  of  acute  articular  rheumatism.  The  rheumatic  symp- 
toms usually  precede  the  choreic,  though  at  times  they  may  be  coinci- 
dent with  them,  or  even  follow  them.  The  rheumatic  history  is  not 
so  frequently  obtained  in  the  cases  of  early  childhood  as  it  is  in  the 
later  and  early  adult  cases.  Another  remarkable  coincidence  is  the 
frequent  appearance  of  endocarditis  with  chorea.  Cowers  affirms  that 
it  is  within  the  truth  to  say  that  in  on"e-half  of  the  cases  in  which  or- 


288  'I'Hli    NEURONIC   DISEASES 

ganic  tlisease  of  the  heart  exists  this  preceded  the  chorea.  Occasionally 
the  heart  lesion  develops  during  the  course  of  the  chorea.  So  promi- 
nent is  this  relationship  between  the  rheumatic  troubles  and  chorea 
that  many  authorities.  chieHy  among  the  English  and  French,  regard 
it  as  distinctly  causal.  German  and  American  authors  do  not  accept 
so  strongly  the  relationship  as  one  of  cause  and  effect. 

Many  explanations  have  been  offered  for  this  association  of  rheu- 
matism, endocarditis  and  chorea.  Some  say  that  chorea  is  merely 
rheumatism  of  the  central  nervous  system.  In  other  words,  chorea  is 
rheumatism,  or  rather  one  of  the  occasional  symptoms  of  the  general- 
ized trouble  known  as  rheumatism,  of  which  endocarditis  and  the 
articular  swellings  are  also  symptoms  and  complications.  The  absence 
of  any  distinct  climatic  influence  upon  the  development  of  chorea,  while 
on  the  other  hand  its  proneness  to  appear  in  the  spring  and  fall  seasons, 
when  it  is  known  that  rheumatism  is  most  frequent,  adds  weight  to  the 
suggestion  that  chorea  is  largely  a  rheumatic  symptom.  It  has  been 
argued  that  the  chorea  is  the  result  of  the  same  toxic  state  of  the 
blood  that  in  all  probability  provokes  the  endocardial  and  joint  inflam- 
mations. The  existence  of  a  specific  microorganism  ( Richter.  Berke- 
ley, Dana,  Meyer,  Pianese)  has  been  invoked,  after  some  observations 
and  experimentation,  to  account  for  the  toxaemia  which  institutes  the 
chorea,  and  not  a  few  believe  that  the  same  organism  will  be  found 
to  be  the  cause  of  the  rheumatism.  Such  a  view  receives  some  further 
support  from  the  fact  that  chorea  has  developed  during  and  after  well- 
recognized  infectious  diseases,  such  as  scarlet  fever,  typhoid,  measles, 
pertussis,  acute  pyaemia,  gonorrhoea,  syphilis,  puerperal  fever  and  even 
the  distemper. 

All  of  this  makes  of  rheumatic  chorea  merely  an  associated  mani- 
festation of  a  specific  form  of  intoxication.  It  has  this  in  its  favor, 
that  it  is  more  plausible  and  founded  upon  better  established  observa- 
tion than  is  the  older  view  that  minute  emboli  from  the  diseased  valves 
of  the  heart  are  floated  up  to  the  brain,  where  they  become  lodged  in 
the  finer  terminal  arteries,  and  produce  areas  of  cerebral  softening, 
which  in  turn  produce  the  motor  symptoms  of  irritation. 

Before  leaving  the  subject  of  the  relationship  of  rheumatism  to 
chorea,  let  me  warn  against  confounding  all  pains  associated  with 
chorea  with  rheumatic  pains.  Chorea  is  not  solely  a  motor  affection, 
but  not  unfrequently  shows  im.plication  of  the  sensory  apparatus  as 
well. 

It  is  a  well-attested  fact  that  a  severe  mental  shock  frequently 
results  in  an  attack  of  chorea ;  and  the  effect  of  mental  strain  in  school, 
worry,  and  otherwise,  is  undefinable.  Osier  says  that  the  prominent 
psychical  element  in  the  causation  of  chorea  is  certainly  one  of  the  most 
serious  objections  to  the  infectious  theory  of  the  disease,  since  there 
can  be  no  doubt  that  ordinary  chorea  may  rapidly  follow  a  fright  or  a 
sudden  emotion.  It  is  no  objection,  however,  it  seems  to  me,  but  rather 
a  confirmation  of  the  toxasmic  theor}^ 

It  is  beginning  to  be  well  recognized  now  by  alienists  that  changes 
in  the  blood,  either  of  a  toxic  character  or  at  least  affecting  its  metabolic 
function,  may  precede  or  follow  sudden  disturbances  of  mentalization. 


THE    NEURONIC  DISEASES  289 

The  chorea  from  simulation,  which  has  been  observed  endemically 
and  reported  from  boarding-schools,  etc.,  is  Hke  the  true  St.  Vitus' 
dance  epidemics  of  the  Middle  Ages.  It  is  hysteria  with  choreiform 
manifestations. 

The  occurrence  of  chorea  during  pregnancy  is  so  grave  a  circum- 
stance as  to  demand  a  moment's  consideration.  Some  think  it  i;s  i. 
reflex  chorea  and  is  to  be  regarded  in  the  same  light  as  chorea  irom 
other  peripheral  sources,  such  as  eye-strain,  accumulation  of  wax  in 
the  ears,  phimosis,  intestinal  parasites,  etc.  It  is  hard  to  imagine  how 
a  peripheral  mechanical  irritation  can  produce,  by  way  of'  a  reflex 
action,  so  unique  and  characteristic  a  symptom-complex  as  chorea  is. 
Reflex  action  as  a  cause  of  disease  has  been  heretofore  too  often  ap- 
pealed to;  and  in  view  of  many  experiments  and  observations  lately 
undertaken  had  better  be  dismissed  except  as  a  mere  slight  predispos- 
ing cause.  In  regard  to  the  chorea  of  pregnancy,  it  is  much  more  likely 
that  an  autotoxcBmia  is  in  some  way  responsible.  This  is  shown  by  the 
fact  that  the  chorea  may  appear  before,  during  or  after  the  pregnancy. 
The  severity  of  the  trouble  and  the  frequent  development  of  maniacal 
symptoms  are  also  rather  confirmatory. 

To  sum  up,  the  etiology  of  chorea,  though  varied  and  far  from 
being  established,  points  most  suggestively  to  an  infectious  trouble 
associated  with  an  unwonted  mental  strain,  the  underlying  toxins  af- 
fecting most  vehemently  the  upper  motor  neurones  and  to  a  certain 
extent  the  sensory  and  psychic  faculties,  in  that  period  of  life,  child- 
hood, and  under  that  peculiar  condition,  neuropathic,  when  they  are 
most  susceptible. 

Pathology  and  Pathogenesis. — If  we  are  contented  with  the 
view  that  chorea  is  merely  a  symptom  of  a  more  or  less  profound 
intoxication,  the  discrepancies  in  regard  to  the  pathological  findings 
Tnay  be  easily  accounted  for.  In  a  large  class  of  cases  there  are  no 
such  findings  and  the  disease  is  denominated  functional.  '^Unwonted 
susceptibility  on  the  part  of  particular  neurones  in  certain  children, 
or  the  character  of  the  causative  infection,  may  well  produce  changes 
that  will  disturb  the  functions  of  those  neurones  and  yet  elude  the 
power  of  our  modern  histological  methods  of  examination.  On  the 
other  hand,  this  infectious  state,  if  sufficiently  prolonged,  or  even  the 
reaction  caused  by  the  violence  of  the  disease  in  general,  may  lead  to 
such  scattered  lesions  as  are  sometimes  observed  at  the  autopsy. 
Of  the  latter  there  have  been  observed  intense  hypersemia  of  the  brain. 
Tiemorrhagic  and  inflammatory  foci,  spots  of  softening,  thromboses, 
emboli,  etc.,  in  the  meninges,  central  ganglia  and  in  the  area  sup- 
plied by  the  Sylvian  arteries.  Along  with  these  circulatory  findings 
must  be  mentioned  the  endocarditis,  valvular  disease  and  fatty  degen- 
eration of  the  heart. 

All  of  these  observations  are  inadequate  as  a  basis  for  establishing 
a  pathology  of  chorea,  and  thus  regarding  it  as  a  distinct,  uniform 
disease.  The  so-called  chorea  corpuscles  are  devoid  of  pathological 
interest  in  this  disease,  having  been  found  in  persons  dead  from  other 
causes   (Wallenberg). 

Symptoms. — The  most  obtrusive  symptom,  and  that  which  gives 


290  TH1<:    NliUKONlC   DISEASES 

the  name  to  this  affection,  is  the  iryegular,  involuntary,  incoordinated 
jerking  of  the  muscles.  As  it  is  the  upper  and  not  the  lower  neurones 
that  are  involved  primarily,  the  jerking  movements  are  not  limited  to 
individual  muscles,  but  rather  to  groups  of  muscles,  antagonistic  or 
otherwise,  that  subserve  generalized  movements.  Hence  the  head,  or 
the  arms,  or  the  legs,  or  special  parts  of  the  body,  like  the  tongue,  the 
lips  or  the  eyelids,  twitch  spasmodically.  In  other  words,  this 
symptom  involves  not  muscles,  but  rather  movements.  For  instance, 
the  head  will  every  few  seconds  jerk  to  the  left  or  to  the  right;  some- 
times it  will  be  drawn  backward  or  forward.  The  face  will  twist  first 
to  one  side,  then  to  the  other ;  the  lips  will  pucker  or  be  drawn  to 
one  side;  the  eyelids  will  rapidly  shut  and  open.  All  or  any  of  the 
movements  of  the  hand  and  arm  may  be  affected.  The  thumb  and 
fingers  will  snap  shut  and  then  open,  or  the  whole  hand  will  undergo 
a  series  of  supination  and  pronation  acts.  The  forearm  may  suddenly 
become  flexed  upon  the  arm  and  then  relaxed,  or  the  whole  arm  may 
be  manipulated  spasmodically  from  the  shoulder.  As  with  all  intra- 
cranial or  cerebral  troubles,  that  part  of  the  extremity  in  which  the 
finer  and  more  complicated  movements  take  place  normally  will  be 
more  affected  in  the  disease  state.  Hence  the  movements  of  the  face 
are  worse  as  a  rule  than  those  of  the  hand  and  forearm,  those  of  the 
hand  are  worse  than  those  of  the  entire  arm,  and  the  arms  are  worse 
than  the  legs.  The  trunk  muscles  usually  escape,  or  when  choreic 
movements  attack  them  the  disease  is  of  another  sort  than  the  one  I  am 
describing.  On  account  of  the  attitude  of  the  patient,  the  jerking  of 
the  feet  and  legs  is  not  so  noticeable  as  that  of  the  rest  of  the  body. 
When  the  patient  lies  down  or  rests  with  the  feet  off  the  ground  the 
leg  movements  become  more  obvious.  With  these  movements  ofttimes 
the  whole  body  will  be  thrown  violently  about. 

This  restlessness  or  incessant  jerking  may  involve  all  parts  of  the 
body  or  only  particular  parts.  It  may  therefore  be  confined  only  to  the 
head  or  to  one  arm  or  one  leg.  More  frequently  it  is  bilateral  in  char- 
acter, implicating  together  the  head,  the  two  eyes,  the  two  arms  or 
the  two  legs.  Occasionally  the  movements  confine  themselves  to  one 
side  or  the  other,  a  condition  known  as  hemichorea. 

The  motor  restlessness  which  comes  on  insidiously  is  peculiar  in 
chorea  and  the  symptom  is  not  likely  to  be  confounded  with  any  other 
form  of  spasm.  It  is  not  rhythmical  and  it  does  not  confine  itself  to 
any  one  muscle-group.  It  is  now  here,  now  there,  rotating  the  arm 
or  suddenly  abducting  and  adducting  it ;  then  the  legs  jerk  and  cause 
the  child  to  fall  or  at  least  to  assume  a  disturbed  gait.  The  entire  body 
will  turn  from  one  side  to  the  other.  The  eyes  will  twitch,  the  eyelids 
snap,  the  tongue  shoot  in  and  out.  The  speech  will  be  disjointed  and 
difficult,  and  in  extreme  cases  almost  incomprehensible. 

These  movements  are  all  involuntary  and  are  usually  increased 
when  under  observation.  The  patient  can  control  them  for  a  few 
seconds,  but  not  indefinitely.  They  occur  mostly  in  daytime  and  dur- 
ing wakefulness.  Sometimes  they  are  present  at  night,  during  sleep. 
They  are  generally  increased  by  associated  voluntary  movements, 
though  they  themselves  are  always  purposeless.     Their  constant  vari- 


THE    NEURONIC  DISEASES  29I 

ability  in  form,  direction  and  location  is  their  most  striking  character- 
istic. 

Respiration  is  affected  sometimes  in  so  far  as  it  is  a  voluntary 
process.  The  diaphragm  is  the  respiratory  muscle  most  involved.  The 
muscles  of  simple  phonation  generally  escape. 

The  violence  of  these  movements  varies  greatly  in  different  cases. 
In  some  patients  they  are  so  slight  as  to  be  scarcely  noticeable,  and  to 
be  elicited  in  examination  by  the  production  of  some  emotional  ex- 
citement only ;  while,  on  the  other  hand,  they  may  be  so  general  and 
terrific  as  to  give  rise  to  the  distressing  condition  known  as  muscular 
insanity  (folie  miaculairej ,  in  which  the  patient  hurls  himself  violently 
about,  leaps  up  and  down,  injures  himself,  bites  his  tongue  and  finds 
it  impossible  to  eat  or  get  a  moment's  sleep. 

Muscular  weakness  is  not  uncommon.  Sometimes  it  amounts  to 
a  mild  paresis.  The  paralytic  chorea  of  Todd  is  characterized  by  ex- 
treme paresis,  with  but  few  movements.  Rarely  after  the  attack  a 
permanent,  local  paralysis  or  weakness  remains. 

It  has  been  stated  by  some  that  the  disturbed  action  of  the  heart, 
sometimes  observed,  is  choreic.  This  is  scarcely  probable.  In  some 
of  the  cases  it  is  undoubtedly  one  of  the  signs  of  an  endocarditis.  The 
contractions  that  are  said  to  occur  in  the  papillary  muscles  are  not 
based  upon  adequate  demonstration. 

In  most  cases  the  above  symptoms  begin  insidiously  and  are  mild 
at  first.  Some  are  mild  throughout  the  entire  course  of  the  trouble. 
Another  class  of  cases  become  rapidly  violent  and  continue  so  until 
the  disease  reaches  its  climax  in  about  four  or  six  weeks.  Others  are 
so  frightful  as  to  resemble  acute  mania  of  a  most  active  type,  and 
still  others  exhibit  paralytic  rather  than  choreic  symptoms.  It  is  ob- 
vious, therefore,  that  chorea  as  a  symptom  may  vary  all  the  way  from 
mere  restlessness  or  slight  '"fidgets,"  for  which  the  child  is  too  often 
punished,  up  to  an  extreme  degree  of  muscular  activity  or  paresis 
with  mental  aberration.  There  is  no  good  reason,  however,  for  classi- 
fying these  various  degrees  of  the  trouble  into  the  distinct  types,  mild, 
severe,  paralytic,  maniacal,  etc.,  as  some  authors  do ;  for  as  the  chorea 
is  merely  one  manifestation  of  a  complex  symptom-group,  dependent 
I'pon  various  diffuse  lesions  of  a  more  or  less  infectious  origin,  the 
classification  might  be  carried  on  indefinitely,  since  no  two  cases  are 
ever  exactly  alike. 

So  prominent  are  the  motor  manifestations  that  many  other  symp- 
toms, almost  equally  important  at  times,  are  entirely  overlooked,  or  at 
least  not  sought  for.  Among  these  sensation  is  included.  Troussp:iu 
long  ago  used  to  declare  that  the  sensibility  of  the  skin  is  almost  con- 
stantly disordered,  and  yet  many  authors  to-day  affirm  that  the  sensa- 
tions are  never  affected.  I  have  found  present  not  only  formication, 
tingling  and  other  parcesthesice,  but  actual  pain  af  a  neurotic  origin. 
These  slight,  fugitive,  muscular  pains,  sometimes  sharp,  but  more  fre- 
quently dull  and  aching  in  character,  are,  I  am  convinced,  not  unfre- 
quently  mistaken  for  rheumatic  pains.  Headache  is  quite  a  frequent 
form  of  pain.  It  must  be  admitted  that  hypercesthesia  and  ancesthesia, 
hyperalgesia  and  analgesia,  and  all  the  intermediate  sensory  phenomena 


292  THE    NEURONIC   DISEASES 

may  occur  with  the  chorea.  In  all  probabilit}-  the  sensory  symptoms 
are  provoked  in  the  same  way,  and  probably  by  the  same  sort  of  lesions, 
as  are  the  motor  symptoms. 

Another  set  of  symptoms  too  often  passed  by  in  the  examination 
of  a  case  of  chorea  are  the  mentaL  There  is  rarely  a  case  in  which 
some  change  of  mentality  does  not  occur.  In  the  mild  cases  and  in 
the  beginning  of  nearly  all  the  cases  there  is  a  peevishness,  slight  irri- 
tability, heightened  emotionalism,  weakness  of  memory,  lack  of  con- 
centration and  power  of  attention.  These  symptoms  often  show  them- 
selves before  the  muscular  jactitations  attract  attention,  and  bring  down 
upon  the  child  the  anger  and  corrective  punishments  of  school-teacher 
and  parents.  The  other  extreme  of  the  mental  picture  seen  in  some 
rare  cases  includes  violent  delirium,  shouting,  singing,  incoherent  chat- 
ter and  all  of  the  usual  exhibitions  of  a  severe  acute  mania.  Accord- 
ing to  Fagge,  Dr.  Hills  of  the  Xorfolk  County  As}-lum  stated  that  more 
than  one  patient  suffering  from  chorea  had  been  sent  to  the  institution 
as  insane.  Such  errors  are  likely  to  continue  to  occur  so  long  as  chorea 
is  regarded  as  a  distinct,  substantive  disease,  and  not  as  a  mere  symp- 
tom which  may  be  present  in,  and  form  part  of,  or  at  least  be  associated 
with,  other  forms  of  mental  and  nervous  disease. 

The  chorea  may  be  the  chief  trouble  and  the  psychosis  a  complica- 
tion, or,  on  the  other  hand,  the  primary  trouble  may  be  mental  and 
the  choreiform  movements  may  be  the  passing  complications.  A 
careful  differentiation,  difiicult  to  make  at  times  it  must  be  confessed, 
will  be  the  only  means  of  positively  determining  into  which  category 
the  case  should  be  placed. 

The  most  severe  cases  of  the  maniacal  form  of  chorea  occur  in 
association  with  pregnancy.  Sometimes  they  last  for  several  weeks, 
the  mania  being  noisy  and  violent  for  a  time,  and  then  subsiding  into 
depression  or  apathy,  with  hallucinations,  ideas  of  persecution,  etc.,  or 
even  acute  paranoia. 

The  special  senses  are  usually  not  aft'ected  in  chorea.  In  some 
children  who.  as  a  rule,  are  of  the  neurotic  class,  and  therefore  would 
probablv  have  the  same  troubles  with  or  without  the  chorea,  there  is 
hvpermetropia,  astigmatism  and  muscular  insufficiencies.  The  fundi 
do  not  reveal  anything  particularly  abnormal,  although  optic  neuritis 
has  been  observed  in  a  few  cases.  The  pupils  not  unfrequently  are 
dilated,  but  they  react  promptly  both  to  light  and  accommodation. 
Irregularity  of  the  pupils  was  once  noted  by  Gowers.  the  larger  one 
being  on  the  side  opposite  to  the  limbs  most  affected. 

The  deep  reflexes  are  generally  normal,  but  occasional!}'  they  are 
diminished,  and  cases  have  been  recorded  wherein  they  have  been  ab- 
sent. This  symptom  should  not  be  given  much  stress,  as  the  deep  re- 
flexes are  variable  among  people  in  perfect  health. 

It  has  been  argued  by  some  that  the  joi)if  changes,  sometimes  seen 
in  choreic  cases  and  formerly  attributed  to  the  rheumatism,  are  true 
arthropathies  of  the  trophic  sort.  No  other  trophic  symptoms  of 
cerebro-spinal  origin  are  observed  in  chorea. 

According  to  Osier,  herpes  zoster  occasionally  occurs,  and  other 


THE    NEURONIC  DISEASP:S 


293 


skin  eruptions,  rheumatic  in  character,  such  as  erythema  nodosum  and 
urticaria  purpurica. 

As  a  rule  the  bodily  temperature  remains  normal.  A  slight  rise, 
however,  is  not  especially  exceptional.  In  maniacal  chorea  the  tempera- 
ture may  run  as  high  as  104  degrees.  Just  before  death  it  has  gone 
as  high  as  109  degrees.  These  elevated  temperatures  of  chorea,  even 
in  the  mild  cases,  are  usually  due  to  the  complications,  such  as  the 
joint  affections,  rheumatism  or  endocarditis.  With  die  rise  of  tem- 
perature there  will  usually  occur  an  increase  in  the  pulse  rate.  The 
rapid  pulse  rate  which  some  authors  assign  as  a  pure  choreic  symptom, 
indicating  chorea  of  the  heart  muscle,  is  not  necessarily  associated  with 
temperature.  It  is  not  due  to  chorea  of  the  heart,  but  is  merely  the 
irritable  pulse  characteristic  of  neurotic  children. 

In  marked  contradistinction  to  the  renal  function  of  hysteria,  the 
urine  of  chorea  is  generally  scanty  in  amount,  high-colored  and  con- 
centrated and  over-charged  with  phosphates  and  urea.  Albuminuria 
is  not  a  symptom  of  chorea,  though  it  may  be  present  when  kidney  dis- 
ease is  complicating  the  trouble.  In  chorea  nocturnal  enuresis  is  not 
unfrequent. 

Chorea  being  a  symptom  merely,  rather  than  a  disease,  it  follows 
that  it  has  numerous  complications.  Some  of  these  are  so  frequent  that 
they  have  been  elevated  by  some  authors  to  the  dignity  of  special  symp- 
toms. Such,  for  instance,  are  the  heart  complications.  Others,  I 
believe,  are  not  so  much  complications  of  chorea  as  that  the  choreic 
manifestations  are  but  additional  symptoms  of  the  diseases  sometimes 
spoken  of  as  the  complications.  This  is  illustrated  well  by  some  of  the 
so-called  rheumatic,  syphilitic  and  other  infectious  accompaniments,  the 
manias,  and  paralyses.  This  is  a  most  important  and  practical  distinc- 
tion to  bear  in  mind,  not  only  from  the  standpoint  of  diagnosis  and 
prognosis,  but  especially  from  that  of  therapeutics.  I  will  have  more 
to  say  about  it  under  the  head  of  diagnosis. 

While  at  a  loss  to  comprehend  how  the  cardiac  troubles,  important 
as  they  may  be,  are  to  be  considered  among  the  symptoms  of  chorea, 
I  will  grant  for  the  nonce  that  they  may  be  complications  and  will 
discuss  them  under  that  head.  It  is  my  own  belief  that  there  is  no 
direct  relationship  between  the  heart  manifestations  and  the  chorea, 
but  that  both  are  the  direct  result  of  the  underlying  toxic  state  of 
the  blood,  which  toxic  state  of  the  blood  sets  up  an  inflammation  in  the 
one  case  and  a  functional  neurosis  in  the  other. 

Endocarditis  is  the  most  important  heart  complication.  Pericarditis 
occurs  occasionally.  The  former  is  almost  invariably  of  the  simple  or 
warty  form,  according  to  Osier,  and  though  not  dangerous  in  itself, 
is  apt  to  produce  valvular  incompetency.  The  usual  sounds  and  signs 
of  this  heart  complication  are  present.  In  chorea,  however,  there  is  an 
accidental  heart  murmur  which  must  not  be  taken  as  indicative  of 
organic  disease.  It  is  anaemic  in  origin  and  is  heard  as  a  soft  systolic 
blowing  over  the  mitral  and  pulmonary  valves.  I  have  heard  a  good 
diagnostician  assert  that  in  his  experience  all  cases  of  chorea  exhibited 
heart  signs,  and  upon  the  strength  of  this  teach  that  chorea  is  always 
a  rheumatic  complication.     Of  the  140  patients  with  chorea  examined 


294  '^HE   NEURONIC   DISEASES 

two  years  later  by  Osier,  the  heart  was  found  normal  in  51,  disturbed 
functionally  in  17,  and  exhibiting  signs  of  organic  disease  in  72.  In 
my  own  study  of  100  cases,  about  forty-nine  per  cent  showed  heart 
trouble,  and  not  more  than  one-quarter  revealed  mitral   insufficiency. 

The  mistake  of  regarding  chorea  as  always  a  disease  with  heart 
trouble  as  a  complication  is  well  shown  in  the  attempt,  first  made  by 
Kirkes  and  afterwards  by  able  authorities,  of  explaining  the  neurosis 
on  the  ground  of  a  local  ischsemia  caused  by  the  presence  of  an  embolus 
washed  up  into  the  cerebral  circulation  from  the  diseased  valves  of  the 
heart.  It  is  true,  even  as  Oppenheim  says,  that  in  the  course  of  chorea 
such  an  embolus  takes  lodgment  and  produces  paralytic  symptoms.  A 
moment's  consideration  will  convince  any  one  that  such  a  cause  for  the 
chorea  most  emphatically  proves  that  the  choreic  jactitations  are  but 
a  symptom  of  a  much  more  extensive  trouble.  The  chorea  in  such  a 
case  is  of  the  pre-  or  post-hemiplegic  type,  and  is  but  one  of  the  symp- 
toms of  one  of  the  well-recognized  forms  of  cerebral  apoplexy.  The 
disease  is  not  chorea  with  embolic  obstruction  as  a  complication  ;  it  is 
cerebral  embolism  with  chorea  as  one  of  its  accidental  symptoms. 

Rheumatic  manifestations  in  the  joints,  as  well  as  generalized  acute 
articular  rheumatism,  are  sometimes  put  down  as  complications  of 
chorea,  and.  strange  to  say,  often  by  the  very  same  authors  who  argue 
that  chorea  is  the  direct  result  of  the  rheumatism.  It  seems  to  me  that 
this  ready  interchangeability  of  two  such  sets  of  phenomena  as  acute 
articular  rheumatism  and  chorea  minor  is  proof  sufficient  that  both 
are  but  symptom-complexes,  coincident  and  alike  dependent  upon  infec- 
tion. This  is  further  supported  by  the  occasional,  though  rare,  asso- 
ciation of  simple  neuritis. 

Among  the  psychoses  and  neuroses  associated  with  chorea  should 
be  mentioned  the  maniacal  manifestations,  mild  and  severe,  as  already 
mentioned,  hysteria  and  epilepsy.  I  recently  saw  a  case  of  severe  acute 
delirium  of  childhood,  caused  by  some  playmates  throwing  some  earth- 
worms down  his  back,  in  which  there  were  for  several  weeks  gradually- 
fading  frightful  hallucinations  with  choreic  jactitations.  The  chorea 
vanished  before  the  hallucinations  had  entirely  disappeared.  Here 
again  the  mere  symptomatic  character  of  the  choreic  jactitations  was 
made  obvious  and  the  impossibility  of  referring  to  the  psychosis  as  a 
complication  of  the  chorea  or  z'ice  versa.  Convulsive  attacks,  cataleptic 
in  character,  persistent  spasms  almost  like  typical  hemiplegia,  and  even 
paralysis,  are  all  seen  sometimes  in  association  with  chorea.  As  many 
of  these  are  of  hysterical  or  organic  origin,  they  should  more  probably 
be  regarded  as  separate  diseases  in  which  the  choreic  phenomena  play 
merely  an  accompanying  role. 

Diagnosis. — In  a  simple,  uncomplicated  case  the  diagnosis  of 
chorea  is  easy.  The  jactitations  are  characteristically  irregular,  involun- 
tary and  incoordinate.  As  the  term  chorea,  however,  refers  only  to 
the  muscular  movements,  the  disease,  if  it  is  to  be  regarded  as  a  dis- 
ease, is  scarcely  ever  uncomplicated.  It  is  these  complications  or  asso- 
ciated symptoms  that  sometimes  render  the  differential  diagnosis  diffi- 
cult. So  far  as  the  jactitations  are  concerned,  it  would  seem  hardly 
possible  to  confuse  the  choreic  movements   with   the   slow,   wax-like 


THE    XEUROXIC   DISEASES  295 

movements  of  athetosis,  the  rhythmical,  somewhat  more  controllable 
movements  of  hysteria,  the  intentional  movements  of  multiple  sclerosis, 
or  the  peculiar  tremor  of  paralysis  agitans,  etc.  The  distinction  be- 
tween them  will  be  pointed  out  under  the  head  of  these  respective  dis- 
eases. This  distinction  has  only  to  be  made,  as  a  rule,  in  adults,  as 
these  latter  diseases  do  not  occur  in  childhood. 

There  is  a  disease  of  childhood,  the  choreic  athetotic  form  of 
cerebral  infantile  palsy,  which  may  at  times  give  much  trouble.  The 
muscular  rigidity,  particiilarly  in  the  legs,  associative  movements  and 
the  athetoid  nature  of  the  twitchings  will,  if  carefully  sought  for, 
be  generally  found  and  will  indicate  the  cerebral  palsy. 

Chorea  has  been  mistaken  for  ataxia,  especially  when  limited  to 
the  lower  part  of  the  body,  and  thus  altering  the  gait.  Oppenheim  saw 
such  a  case  in  a  boy  three  years  old  and  was  not  led  to  make  a  diagnosis 
of  chorea  until  he  had  observed  the  involuntary  movements   in  rest. 

A  general  tic  may  be  mistaken  for  chorea,  or  vice  versa.  The 
differentiation  will  be  discussed  under  the  head  of  the  tics. 

Cases  of  Friedreich's  ataxia  were  wont  formerly  to  be  reported  as 
chorea.  The  slow'er  character,  athetoid-like  jactitations  of  the  former, 
the  ataxia,  the  scoliosis,  the  scanning  speech,  the  nystagmus  and  the 
familial  nature  of  the  disease,  ought  to  make  clear  the  differentiation. 

Choreic  patients  with  marked  maniacal  symptoms  have  often 
been  sent  to  the  asylum  as  cases  of  insanity.  The  age  in  which  insanity 
usually  occurs,  the  garrulity  and  other  mental  symptoms  and  the  rela- 
tive insufficiency  of  the  muscular  spasms  will  aid  in  making  the  diag- 
nosis of  a  primary  psychosis. 

Progxosis. — The  prognosis  of  chorea  varies  with  the  nature  of 
the  underlying  cause.  As  a  rule  it  is  good,  especially  in  those  mild 
forms  of  the  trouble  known  as  acute  minor  chorea.  These  cases  usually 
get  well  in  two  or  three  months.  Occasionally  they  last  only  a  few 
weeks,  and  very  rarely  they  last  six  months  or  a  year,  or  even  become 
incurable.  The  recovery,  as  a  rule,  is  complete,  but  relapses  are  not 
uncommon.  Only  in  the  most  violently  severe  cases,  and  even  rarely 
in  these,  is  the  disease  fatal.  Death  is  the  result  of  malnutrition  caused 
by  the  inability  to  feed  the  patient.  The  dangerous  signs  of  this  seri- 
ous state  of  affairs  are  delirium,  elevated  temperature,  irregular  pulse 
and  rapid  emaciation.  In  most  of  these  cases  there  is  distinct  heart 
trouble. 

About  one-quarter  of  the  choreas  of  pregnancy  die.  though  the 
fatality  is  due  to  such  factors  as  the  severe  psychosis,  the  cachexia,  the 
heart  complication  and  the  abortion  or  unnatural  parturition. 

Choreas  late  in  life  are  more  apt  to  become  chronic  or  permanent 
than  are  those  of  childhood.  Senile  chorea  is  practically  always  per- 
manent. 

Treatment. — In  the  treatment  of  chorea  three  well-defined  ob- 
jects are  to  be  aimed  at — the  removal  of  the  cause,  the  quieting  of  the 
mind  and  nervous  system  and  the  rapid  nutrition  of  the  patient. 

In  most  cases  some  form  of  infection  will  call  for  the  first  atten- 
tion. If  it  is  rheumatism  and  its  congeners,  an  antirheumatic  line  of 
treatment  is  to  be  instituted,  including  the  regitlation  of  the  diet  and 


296  THE   NEURONIC   DISEASES 

the  use  of  such  remedies  as  the  saHc}-lates,  alkahes.  iodides,  cardiac 
remedies,  etc.  This  is  not  the  place  to  discuss  the  treatment  of  rheuma- 
tism, but  it  is  pertinent  to  remark  that  the  same  treatment  is  to  be 
employed  in  the  management  of  rheumatic  chorea. 

Other  infections  should  be  attacked  in  the  same  way.  A  syphilitic 
history  calls  for  the  iodides  and  mercury.  Autointoxications  should 
draw  the  attention  to  the  emunctories.  Cathartics,  diuretics  and  dia- 
phoretics are  all  indicated  in  such  cases.  If  a  thorough  and  honest 
search  is  made  for  the  cause  of  the  chorea,  predisposing  or  exciting, 
organic,  functional  or  reflex,  and  that  cause  removed,  the  disease  will 
get  well  promptly  and  without  further  direct  medication. 

In  chorea,  however,  there  is  always  a  more  or  less  exalted  excita- 
bility of  the  mind  and  nervous  system  that  needs  particular  care.  The 
patient  should  be  removed  from  all  mental  strain.  He  should  be  taken 
out  of  school.  Threatenings  and  scoldings  should  be  avoided.  Even 
his  games  and  playmates  should  be  selected  with  the  purpose  of  lessen- 
ing mental  strain.  In  some  instances  seclusion  for  a  time,  with  a 
well-selected  nurse  and  the  adoption  of  a  modified  Weir  Mitchell 
treatment  used  for  hysteria  and  neurastiienia,  may  prove  most  useful. 
Of  this  nature  is  a  sojourn  on  a  country  farm  or  other  change  of 
residence.  Of  course,  all  stimulants,  such  as  tea,  coftee  and  alcohol^ 
are  to  be  prohibited  absolutely,  and  milk  given  in  place  of  them. 

Hypnotics  and  sedatives,  such  as  the  bromides,  come  into  play  and 
ofttimes  give  the  happiest  results.  In  extreme  cases  chloral  hydrate 
may  have  to  be  administered  continuously  and  even  continuous  inhala- 
tions of  chloroform.  Morphine  hypodermically  and  antipyrine  have 
been  borne  well  and  given  good  results  in  a  few  cases  of  extreme  sever- 
ity. The  zinc  salts,  conium,  cannabis  indica,  hyoscin,  physostigmine, 
exalgin,  salol,  salophen,  etc.,  may  all  be  tried,  but  w^ill  probably  be 
found  more  or  less  unsatisfactory. 

The  exhaustion,  whether  general  or  neural,  whether  a  primary  or 
secondary  factor  of  the  disease,  is  the  condition  that  in  many  cases 
seems  to  demand  the  promptest  attention.  The  best  and  the  most 
.  rapidly  acting  tonics  are  here  loudly  called  for.  Of  this  class  of  reme- 
dies, arsenic  still  carries  the  palm.  So  prompt  and  generally  satisfac- 
tory is  the  effect  of  arsenic  upon  the  diseased  neurones  that  it  has 
come  to  be  regarded  as  almost  a  specific  in  chorea.  Any  form  of 
arsenic  may  be  employed,  though  the  favorite  forms  are  arsenious  acid 
and  liquor  potassii  arsenitis  (Fowler's  solution).  I  prefer  the  latter. 
Beginning  with  a  minimum  dose,  the  remedy  should  be  rapidly  in- 
creased until  the  first  signs  of  intolerance  show  themselves — namely,, 
nausea  and  oedema  under  the  eyelids.  The  medicine  should  be  dis- 
continued for  a  few  days  and  then  renewed,  to  be  gradually  increased 
again.  In  this  way  I  have  administered  as  much  as  twxnty-five  drops 
three  times  a  day.  Arsenical  toxsemia  can  be  largely  avoided  by  ad- 
ministering it  well  diluted  in  water,  and  when  there  is  food  in  the 
stomach.  •  A  few  drops  of  nux  vomica  will  cause  it  to  be  borne  well  in 
some  cases.  And  as  anemia  is  so  generally  present,  some  form  of 
easily  assimilated  iron  may  be  judiciously  given  at  the  same  time.  I 
have  never  had  herpes  develop  and  I  have  never  observed  in  my  own 


THE    NEURONIC   DISEASES 


297 


practice  arsenical  neuritis,  though  both  are  possible  and  have  been 
reported.  In  some  cases  arsenious  acid  seems  to  act  more  powerfully. 
It  is  a  convenient  form  to  use  with  a  chalybeate. 

OTHER  CHOREIC  DISORDERS. 

The  desirability  of  dropping  the  term  chorea  as  the  name  of  a 
disease  and  of  using  it,  like  the  term  paralysis,  merely  to  indicate  a 
symptom,  is  shown  by  the  multiplicity  of  choreas,  spoken  of  in  litera- 
ture and  which,  pathologically,  ofttimes  have  absolutely  nothing  in 
common.  We  are  not  able  to  banish  it  entirely  yet,  because  we  do  not 
know  all  that  we  should  of  these  so-called  choreas.  Of  the  pre-  and 
post-hemiplegic  choreas,  and  one  or  two  others,  we  have  learned  enough 
to  cease  speaking  of  them  as  diseases  and  to  merely  note  the  choreic 
manifestation  as  one  of  the  symptoms  of  certain  well-recognized  patho- 
logical conditions.  In  time  no  doubt  all  the  other  choreas  will  be 
the  same.  Their  division  into  essential  and  symptomatic  choreas  will 
do,  temporarily,  as  a  coarse  classification,  but  it  also  will  do  when  we 
learn  positively  whether  the  lesion  is  purely  neuronic  or  extra-neuronic, 
whether  the  irregular,  incoordinated  jactitations  now  referred  to  as 
choreic  can  be  produced  by  intimate  molecular  changes  in  the  nerve 
cells,  as  well  as  by  the  irritation  of  these  cells  by  minute  hemorrhagic 
inflammatory  lesions. 

The  former  is  what  is  meant  to-day  by  essential,  •  or  idiopathic, 
chorea,  and  undoubtedly  underlies  the  degenerative,  hereditary,  infec- 
tious and  embolic  types  of  the  trouble ;  the  latter  is  referred  to  in  the 
term  symptomatic  chorea. 

CHRONIC  HEREDITARY  CHOREA.     HUNTINGTON'S 

CHOREA. 

Huntington,  of  Long  Island,  first  described  this  affection  in  1872. 
It  was  referred  to,  and  probably  Huntington's  own  cases  described,  by 
Waters  in  a  letter  to  Dunglinson  in  1842.  In  1863  Lyon  referred  to  it 
under  the  head  of  chronic  hereditary  chorea  in  a  paper  in  the  American 
Medical  Times.    It  is,  therefore,  not  justly  called  Huntington's  disease. 

It  is  an  independent  disease,  with  choreic  manifestations  prominent 
in  its  symptomatology  and  has  no  direct  connection  with  Sydenham's 
minor  chorea. 

It  has  been  observed  everywhere,  here  as  well  as  in  Europe,  though 
it  seems  to  be  more  common  in  and  around  New  York.  It  is  vulgarly 
called  in  the  communities  where  it  exists  the  "magrums"  or  "megrims," 
though  it  is  as  remote  from  migraine  as  anything  possibly  can  be. 

The  prime  traits  of  the  disease  are  its  direct  hereditarv  character, 
its  late  onset,  its  progressive,  incurable  nature  and  its  association  with 
pronounced  mental  deterioration. 

It  is  so  distinctly  recognized  as  a  purely  inherited  disease  that 
children  are  interdicted  in  every  possible  way  from  intermarrying  with 
families  in  which  it  occurs.  Where  a  member  of  an  afflicted  family 
escapes  the  disease  and  marries,  his  descendants,  usually,  though  not 
always,  escape  also. 


298  THE    XEUROXIC   DISEASES 

Literature  contains  numerous  reports  now  of  some  remarkable  in- 
stances of  the  disease  and  its  hereditary  origin.  The  reports  of  Zacher, 
Hoffmann,  Lannois,  Sinkler  and  some  others  are  of  special  note. 
D'Ormea  has  described  it  in  eleven  members  of  one  family  of  four 
generations.  I  recently  saw  a  case  whose  father  had  had  the  disease, 
but  could  get  nothing  further  of  the  history.  The  age  of  the  patient, 
the  choreic  symptomatology  and  the  marked  mental  deterioration  were 
all  typical. 

The  disease  appears  so  uniformly  between  the  ages  of  thirty  *nd 
fifty  that  a  member  of  a  family  cannot  be  said  yet  to  have  escaped  it 
who  has  not  arrived  at  that  period  of  life.  This  late  onset  of  the  trou- 
ble is  a  marked  characteristic  and  differentiates  this  from  most  of  the 
other  choreas  of  a  general  nature.  It  has  been  seen  by  Hoffmann, 
however,  as  early  as  ten  years  of  age. 

It  occurs  about  equally  in  both  sexes.  The  families  in  which  it 
occurs  are  strikingly  numerous,  eight  and  ten  children  being  not  un- 
common. In  some  cases  it  has  started  after  a  severe  emotion.  Gen- 
erally, however,  there  is  no  known  exciting  cause  for  it.  When  it  has 
skipped  a  generation,  epilepsy  or  hysteria  has  been  seen  in  that  gen- 
eration replacing  it. 

The  motor  manifestations  are  typically  choreic,  consisting  of  ir- 
regular, sudden,  incoordinate  jactitations  of  all  the  muscles  of  the  body. 
The  arms  and  legs  jerk  and  the  face  grimaces  just  the  same  as  in 
ordinary  minor  chorea. 

The  patient  is  to  a  certain  extent  rendered  helpless  by  the  move- 
ments when  they  are  severe.  His  gait  is  affected,  his  speech  is  imperfect 
or  even  impossible,  his  respirations  are  embarrassed  and  he  cannot  use 
his  hands  in  writing,  hold  knife  and  fork,  etc. 

In  mild  cases  the  will  can  for  a  time  repress  the  movements,  but 
they  are  apt  to  be  more  violent  elsewhere  or  later  on.  The  reflexes 
are  usually  increased. 

The  senses  are  not  affected. 

The  mind  is  always  affected  and  its  condition  is  one  of  the  special 
features  of  the  disease.  There  is  a  steady  and  progressive  dementia, 
ending  in  complete  idiocy  in  many  cases.  In  the  early  stages,  as  in 
most  dementias  of  the  progressive,  degenerative  type,  there  is  depres- 
sion, melancholia,  suicidal  tendencies  and  absolute  apathy.  The  mental 
phenomena  usually  follow,  though  they  may  precede,  the  motor. 

The  anatomical  basis  of  the  disease  is  unknown.  In  a  few  post- 
mortem examinations  there  w'ere  indications  of  a  chronic  meningo- 
encephalitis. Pachymeningitis,  leptomeningitis,  hemorrhagic  foci, 
hvdrocephalus  and  disseminated  miliary  inflammatory  spots  in  the  brain 
tissue  were  seen.  The  findings,  according  to  Binsw^anger,  were  the 
same  as  in  dementia  paralytica. 

Some  authors  base  their  opinion  upon  these  indefinite  findings  that 
hereditary  chorea  is  pathologically  a  chronic  meningo-encephalitis. 

It  is  hard  to  reconcile  primary  inflammatory  changes  wath  such 
pronounced  direct  heredity.  To  inherit  inflammation  and  hemorrhagic 
foci  without  other  cause  for  them  is  a  new  idea  in  pathology. 

In  my  own  opinion  the  disease  is  a  primary  nenronic  degeneration. 


THE    XEUROXIC  DISEASES  299 

an  inherited  developmental  defect.  Tlie  gross  findings  referred  to 
above  are  purely  accidental  and  secondary.  This,  it  seems  to  me,  har- 
monizes both  the  indefinite  character  of  these  findings  and  the  marked 
heredity  in  the  disease. 

The  patient  never  gets  well,  but  steadily  progresses  toward  idiocv 
and  death.    It  may  last  many  years,  however. 

All  treatment  hitherto  tried  has  proved  futile,  a  result  one  would 
almost  expect  from  the  developmental  character  of  the  trouble.  Were 
it  a  primary  inflammatory  trouble,  some  hope  from  treatment  might  be 
entertained,  if  not  towards  producing  a  cure,  at  least  in  checking  the 
onward  progress.     Such  a  hope  has  never  been  realized. 

ELECTRIC  CHOREA. 

Henoch,  Dubini  and  others  have  described  forms  of  choreic  mani- 
festations that  occur  at  various  ages,  sometimes  endemically,  in  various 
parts  of  the  body  and  are  especially  characterized  by  the  quick,  light- 
ning-like character  of  the  movements.  In  Dubini's  disease  there  are 
short,  rapid  spasms,  that  involve  successively  different  parts  of  the 
body,  painful  sensations,  epileptiform  and  even  paralytic  symptoms. 
There  are  often  atrophy  and  electrical  reactions  present.  Heart  failure 
and  coma  usually  terminate  them. 

Recovery  is  exceedingly  rare. 

Bergeron's  electric  chorea  is  hysteria.  Henoch's  electric  chorea 
is  in  all  probability  a  form  of  paramyoclonus  multiplex  observed  in 
children.  It  is  obvious  that  the  sooner  we  get  rid  of  the  term  electric 
chorea  the  better,  for  none  of  the  diseases  described  under  it  are  chorea 
or  have  any  relationship  to  the  genuine,  irregular,  incoordinated,  non- 
sensitive  jactitations  of  the  latter. 

What  is  called  habit  chorea  is  a  coordinated  movement  more  nearly 
related  to  the  tics. 

Chorea  major  is  hysteria ;  so  is  what  is  technically  called  hysterical 
€horea.  Laycock's  procursive  chorea,  wherein  young  girls  exhibit 
rhythmical  rotating  and  procursive  movements  of  the  body,  is  clearly 
hysteria.     It  has  been  called  chorea  festinans  by  some  writers. 

PARALYSIS  AGITAXS.     SHAKING  PALSY.     PARKINSON'S 

DISEASE. 

This  is  a  disease  of  advanced  age  characterized  by  a  peculiar  fine 
■rhythmical  tremor,  muscular  rigidity,  with  a  more  or  less  distinctive 
attitude,  and  a  striking  modification  of  the  gait;  without  a  known 
■constant  pathological  basis ;  and  without  any  encouraging  amenability 
to  treatment.  The  largest  individual  statistical  studies  of  this  disease 
have  been  made  by  Gowers  upon  115  cases  seen  in  private  and  hospital 
practice,  and  by  Hart  upon  219  cases  seen  in  the  clinic  of  M.  Allen 
Starr.  Upon  these  reports,  as  well  as  upon  a  few  personal  observations, 
the  following  description  is  based. 

Etiology. — It  is  true  that  paralysis  agitans  is  a  disease  of  the 
aged,  for  rarelv  is  a  case  seen  under  fortv  and  most  of  them  occur 


300  THE   NEURONIC   DISEASES 

much  later.  The  decade  between  fifty  and  sixty  is  the  favorite  period 
for  its  appearance,  about  forty  per  cent,  of  the  cases  beginning  then. 
Between  sixty  and  seventy  there  were  only  twenty  per  cent,  between 
forty  and  fifty,  twenty-five  per  cent.  Gowers  says  it  is  rare  over 
sixty-five.  It  has  been  seen  to  occur  as  late  as  seventy-eight  and  per- 
haps later. 

That  it  is  not  solely  a  disease  of  advanced  years  is  shown  by  the 
fact  that  Lannois  recorded  it  in  a  child  of  twelve  and  Berger  in  a 
patient  of  seventeen.  The  youngest  case  that  has  been  reported  is  that 
of  Huchard  in  a  child  of  three  years. 

It  is  obviouslv  a  disease  of  the  beginning  degenerative  period  of 
life. 

Heredity  seems  to  exercise  so  slight  a  role  that"  it  may  practically 
be  neglected.  In  about  fifteen  per  cent,  of  cases  a  direct  heredity  has- 
been  traced.  A  neuropathic  tendency  may  underlie  the  disease  and  take 
the  place  of  the  direct  heredity  which  is  seen  in  the  small  number  of 
cases  so  characterized. 

The  influence  of  sex  is  probably  not  direct,  but  indirect,  through 
exposure,  occupation,  etc.  Males  are  afflicted  with  the  disease  about 
twice  as  frequently  as  females. 

The  exciting  causes  that  have  been  mentioned  are  numerous. 
They  include  psychic  shock  and  depression  caused  by  worry,  fright,. 
anxiety,  overzvork,  trauma,  exposure,  infections  diseases,  such  as- 
grippe,  malaria,  typhoid  fever,  pneumonia,  rheumatism,  syphilis,  poisons- 
like  lead  and  carbolic  acid,  intoxications  with  alcohol,  tea  and  cofifee,. 
menopause,  confinement,  sunstroke,  insomnia,  abscess,  piano  playing,, 
etc.  As  forty  per  cent,  of  the  cases  gave  persistent  worry  as  the  prob- 
able cause,  and  as  worry,  dread  and  anxiety  must  have  been  more  or 
less  an  accompaniment  of  the  various  other  alleged  causes,  it  may  be 
assumed  that  psychic  strain  is  the  preeminent  factor  among  the  excit- 
ing causes.  Many  of  the  others  may  have  paved  the  way  for  the  gen- 
eral degeneration  which  seems  to  lurk  beneath  the  disease  process. 
On  the  other  hand,  it  is  always  well  to  be  mindful  of  the  fact  that 
worry  is  often  a  sign  and  result  of,  rather  than  a  mere  cause  of,  these 
degenerative  troubles. 

The  cause  of  paralysis  agitans,  therefore,  it  must  be  admitted,  is 
obscure,  though  along  certain  lines  a  certain  definite  etiological  picture 
can  be  outlined. 

Pathology  and  Pathogenesis.— ^Little  need  be  said  upon  this 
subject,  since  so  little  is  known,  and  what  is  known  does  not  help  very 
much  in  explaining  the  raison  d'etre  of  the  symptomatology.  So  far 
as  any  constant  reliable  findings,  post-mortem,  within  the  nervous 
structures  are  concerned,  our  knowledge  is  absolutely  negative.  The 
hypertrophy  of  the  nerve  cells  of  the  pons  Varolii  described  by  Luys  ; 
the  induration  of  the  pons,  medulla  and  cord  mentioned  by  Parkinson ; 
and  even  the  more  recent  observations  of  Ketcher,  Borgherini,  Koller, 
Dana,  Redlich  and  others  involving  sclerotic  conditions  of  the  blood 
vessels  and  the  glia,  and  other  findings  similar  to  those  noted  in  senile 
processes  generally,  are  only  worthy  of  historical  interest. 

This  total  absence  of  any  distinct  discoverable  lesions  is  remark- 


THE   NEURONIC   DISEASES  3OI 

able,  especially  in  view  of  the  fact  that  the  symptoms  are  sometimes 
unilateral,  monoplegic  and  otherwise  indicative  of  a  definite  focal  lesion. 
Gauthier  seems  to  have  hopelessly  abandoned  the  nervous  system  en- 
tirely, for  he  looks  upon  the  trouble  as  primarily  one  of  the  muscular 
system.  Gauthier's  position  is  not  a  plausible  one,  as  Gowers  has  well 
5hown. 

The  character  of  the  symptoms  being  so  purely  motor,  and  in  a 
remote  way  similar  to  chorea,  the  source  of  the  trouble  must  in  all 
probability  be  looked  for  in  the  cerebral  cortex  and  the  motor  centers. 
As  Gowers  well  says,  this  is  strengthened  by  the  great  similarity  of 
these  patients  to  a  person  under  the  excessive  emotion  of  fear.  There 
is  a  loss  of  inhibitory  control  with  a  regular  explosion  of  abnormal 
nerve  force  from  the  lower  cells,  all  due  probably  to  certain  physio- 
chemical  intracellular  changes  as  the  result  of  a  sort  of  senile-like 
degeneration  and  lowered  nutrition. 

With  Oppenheim,  however,  I  agree  that  paralysis  agitans  should 
not  be  looked  upon  as  a  mere  condition  of  presenility.  It  is  a  distinct 
disease  of  a  more  or  less  definitely  localized  pathogenetic  process,  and 
tiot  a  mere  side  issue  to  a  general  lowering  of  all  the  bodily  forces  and 
functions.  ^  _ 

Symptoms. — There  are  four  special  symptoms  that  characterize 
every  case  of  paralysis  agitans — namely,  the  tremor;  the  steady  muscu- 
lar rigidity  upon  which  the  characteristic  attitude  depends ;  the  slightly 
paretic  or  retarded  movements ;    and  the  gait. 

A  typical  case  of  the  disease  cannot  be  mistaken  for  anything  else, 
•even  at  the  first  glance,  for  the  symptoms  in  their  combination  are 
unique.  With  the  head  slightly  bent  forward  and  every -joint  in  the 
arms,  legs  and  body  slightly  flexed,  the  hands  and  arms  trembling 
with  a  fine,  rhythmical  oscillation,  the  patient  trips  forward  with  a 
sort  of  mincing  step,  as  if  he  were  on  the  point  of  breaking  into  a  run. 
The  tremor  and  rigidity  are  usually  seen  in  the  same  set  of  muscles. 
They  may  involve  the  entire  body  or  only  parts  of  the  body.  The  move- 
ments of  a  voluntary  sort  in  the  arms  and  legs  are  distinctly  sluggish 
and  delayed. 

I  will  now  discuss  the  symptoms  a  little  more  in  detail. 

The  tremor  is  the  special,  obtrusive  sign  of  the  disease.  It  usually 
precedes,  though  it  may  follow,  the  appearance  of  the  muscular  rigidity. 
It  may  be  limited  to  the  fingers,  which,  being  flexed,  look  as  if  they 
were  rolling  a  pea  between  them.  It  extends  to  the  muscles  of  the 
arm  or  it  may  involve  the  arm  and  leg,  usually  on  the  same  side.  When 
all  four  extremities  are  involved,  one  side  seems  to  be  generally  a 
little  worse  than  the  other.  This  characteristic  one-sided  distribution 
of  the  tremor,  and  its  tendency  to  progress  from  the  ends  of  the  ex- 
tremities upward,  indicates  its  hemiplegic  nature  and  cerebral  origin. 
The  body  sometimes  oscillates,  though  for  obvious  reasons  its  tremoi 
is  not  so  noticeable  as  that  in  the  extremities.  Some  writers  have  de- 
clared that  the  head  never  shakes.  That  is  certainly  an  error.  I  have 
seen  it  exhibit  the  same-  sort  of  tremor  in  both  a  to  and  fro  and  a  rota- 
tory manner,  as  the  hands  show.  It  is  rare,  however,  in  the  head.  Only 
in  four  instances  amonsf  Hart  and  Starr's  cases  was  the  tremon  absent. 


302 


THE   NEURONIC    DISEASES 


That  the  parts  of  the  body  in  which  the  vokintary  movements  are  the 
most  delicate  and  comphcated  are  the  preferential  parts  for  the  mani- 
festation of  the  tremor  is  shown  by  the  greater  number  of  cases  that 
begin  on  the  right  side  and  in  the  fingers  of  the  right  hand.  The 
upper  extremities  were  involved  seven  times  more  frequently  than  the 
lower,  and  the  right  side  a  third  oftener  than  the  left.  Sometimes  the 
tremor  advances  very  rapidly  from  one  part  of  the  extremity  or  body 
to  another,  at  other  times  it  will  continue  for  years  to  be  limited  to 

FIGURE  41. 


Paralysis  agitans.     (After  Charcot.) 

one  part.  Gerhardt  and  Hart  both  cite  cases  in  which  the  tremor  was 
intentional. 

In  addition  to  the  head,  trunk  and  extremities,  the  tongue,  the 
lips,  the  angle  of  the  mouth,  one  side  of  the  face,  the  eyeballs  and  the 
orbicularis  palpebrarum  have  all  been  seen  to  be  affected  with  the 
tremor. 

The  tremor  is  a  stereotyped  one,  fine,  rapid  and  rhythmical.  The 
oscillations  are  four  or  five  to  the  second  and  the  extent  of  the  excur- 
sions is  small.     Sometimes  the  tremor  is  so  fine  that  it  is  onlv  observa- 


THE  NEURONIC   DISEASES  303 

ble  in  the  patient's  penmanship ;  at  other  times  it  is  very  large  and 
coarse.  Voluntary  active  movements  usually  put  a  stop  to  the  tremor 
for  a  few  seconds.  The  same  may  be  said  of  passive  exercise  and 
the  fixing  of  the  patient's  attention.  Mental  excitement  always  in- 
creases the  shaking.  In  sleep  it  usually  ceases,  but  not  in  all  cases. 
Neither  the  attitude  of  the  patient  nor  the  position  of  the  limbs  at  all 
modifies  it.     At  times  it  shows  a  tendency  to  remit. 

Next  to  the  tremor  the  muscular  rigidity  is  the  important  symptom 
of  paralysis  agitans.  It  usually  coexists  with  the  shaking  and  reveals 
itself  about  the  same  time.  In  some  cases  it  comes  on  later  than  the 
tremor,  in  a  still  smaller  number  it  even  precedes  the  latter.  Schlapp 
and  Hart  both  report  cases  with  rigidity,  but  without  tremor.  It  is  the 
muscles  of  the  neck  and  back  that  reveal  the  rigidity,  especially  in  the 
patient's  stooping  attitude.  The  slight  flexion  of  the  joints  in  the 
members  affected  with  the  disease  is  due  to  the  muscular  rigidity. 
When  the  face  is  involved  the  appearance  is  statuesque  and  wax-like 
indeed. 

The  rigidity  is  noticeable  also  in  the  resistance  offered  by  the 
muscles  when  passive  motion  is  attempted.  The  same  cause  explains 
the  delayed  active  movements.  It  seems  as  though  the  muscles  could 
not  respond  as  promptly  as  usual  to  the  will. 

The  modification  of  the  gait  is  a  striking  feature  of  the  disease. 
The  patient  takes  short,  mincing  steps  on  the  tips  of  his  feet  and  seems 
as  if  he  were  about  to  start  into  a  run  or  to  stride  forward  as  though 
he  were  on  the  point  of  falling  at  every  step.  This  is  termed  propulsion. 
Sometimes  he  exhibits  a  curious  tendency  to  walk  backward,  retropul- 
sion.  Lateropulsion  has  been  noted,  but  it  is  not  common.  Contrac- 
tures sometimes  occur  and  incomplete  paralysis  in  the  later  stages. 

The  deep  reflexes  may  be  diminished  or  increased.  They  are  often 
normal,  never  absent.  There  is  neither  atrophy  nor  electrical  altera- 
tions in  connection  with  the  musculature.  In  two  of  Hart's  cases, 
typical  in  every  respect,  the  pupils  were  of  the  Argyll-Robertson  type. 

The  speech  is  often  altered  and  there  are  changes  in  the  voice. 
Slowness  and  irregularity,  but  not  true  dysarthria,  scanning  or  stutter- 
ing characterizes  the  former ;  while  the  latter  is  monotonous  and 
whining. 

Oppenheim  says  that  hyperidrosis  is  rather  a  frequent  occurrence. 
It  does  not  bear  any  special  relation  to  the  parts  affected  with  the 
tremor,  though  it  may  not  be  a  generalized  sweating. 

General  restlessness  is  a  characteristic  in  a  goodly  number  of 
cases.  This,  however,  may  be  due  to  the  fact  that  active  'movement 
puts  a  certain  amount  of  quiescence  upon  the  tremor  and  so  makes  the 
patient  feel  more  comfortable. 

Among  the  sensory  symptoms  occasionally  spoken  of  by  these 
patients  may  be  mentioned  slight  darting  pains,  aching,  pricking,  numb- 
ness, tingling  and  heat  and  cold,  all  very  changeable,  evanescent  and 
subjective. 

The  mind  remains  unaffected,  or  if  it  is  aft'ected  it  is  a  complication 
and  not  a  part  of  this  disease.  Slightly  depressive  emotional  states 
may  occur,  but  as  a  rule  the  patients  are  cheerful  and  satisfied. 


304 


THE   NEURONIC  DISEASES 


FIGURE  42. 


,  '^^^^ 


.\' 


Paralysis  agitans.      (From  photograph  in  the   Pathological  Museum  of  the 
Med.  Depart,  of  the  University  of  Illinois.) 


THE   NEURONIC   DISEASES  305 

A  slight  elevation  of  temperature  and  an  nicrease  of  the  pulse  rate 
have  been  observed  in  some  cases. 

Diagnosis. — A  typical  case  of  paralysis  agitans  with  its  tremor, 
attitude,  muscular  rigidity,  sluggish  movements  and  peculiar  gait  can 
offer  no  difficulty  in  diagnosis.  Other  diseases  may  have  a  ion.i  of 
tremor  that  may  be  suggestive  of  shaking  palsy.  Multiple  sclerosis  has 
caused  doubt  in  some  instances.  The  earlier  development  of  the  dis- 
ease, the  nystagmus,  the  intentional  character  of  the  tremor,  the  optic 
nerve  involvement  and  the  bladder  disturbances  wfll  readily  indicate 
the  trouble  as  one  of  multiple  sclerosis. 

Senile  tremor  is  sometimes  very  much  like  paralysis  agitans.  The 
head  is  involved  here  more  frequently  and  the  shaking  is  always  in- 
creased upon  voluntary  movement.  Moreover,  the  other  symptoms  of 
paralysis  agitans,  the  rigidity,  the  attitude,  the  gait  are  wanting. 

Oppenheim  calls  attention  to  senile  paraplegia,  a  spastic  paralysis 
of  old  age  in  which  there  is  arteriosclerosis  of  the  brain  and  cord, 
which  presents  a  clinical  picture  not  wholly  unlike  paralysis  agitans. 
In  the  senile  paraplegia,  however,  there  are  true  paralytic  symptoms, 
such  as  dysphagia,  dysarthria,  bladder  disturbances,  etc. 

Sometimes  a  form  of  traumatic  neiirosis  occurs  that  is  almost 
the  counterpart  of  Parkinson's  disease.  These  cases  are  difficult  to 
differentiate  at  times,  because  it  is  a  recognized  fact  that  paralysis 
agitans  sometimes  follows  trauma.  However,  in  the  traumatic  neuro- 
sis hysterical  or  neurasthenic  symptoms  predominate  and  the  charac- 
teristic symptoms  of  true  paralysis  agitans  are  not  all  present. 

Prognosis. — The  prognosis  of  shaking  palsy  is  good  in  regard  to 
life,  bad  in  regard  to  recovery.  The  disease  usually  involves  the  whole 
body  in  the  course  of  a  couple  of  years,  then  it  may  remain  stationary 
for  a  great  many  years.  Death  often  occurs  from  exhaustion.  Apo- 
plexy sometimes  closes  the  scene.  A  worse  prognosis  than  death  is 
that  of  the  late  paralysis,  contracture  and  general  bedridden,  helpless 
state  that  sometimes  obtains.  Fortunately  this  is  not  a  frequent  condi- 
tion, in  spite  of  the  fact  that  the  disease  is  most  emphatically  a  pro- 
longed one.  A  mild  delirium,  a  slight  fever  and  a  complete  physical 
breakdown  are  the  usual  accompaniments  of  the  end. 

Treatment. — The  treatment  of  paralysis  agitans  is,  if  carried 
•out  on  proper  and  conservative  lines,  attended  with  a  fair  degree  of 
success,  considering  the  chronicity  and  fundamental  nature  of  the 
disease. 

Mental  and  physical  rest,  quiet  and  nutrition  are  the  main  indica- 
tions of  treatment.  All  sources  of  mental  shock,  disturbance  and  de- 
pression should  be  removed.  Hence  it  is  well  to  get  these  patients 
away  into  the  country.  Popular  and  fashionable  resorts,  sanataria  and 
all  places  where  there  is  likely  to  be  a  crowd  of  people,  with  the  at- 
tendant excitement,  had  better  be  avoided.  Cheerful  company,  pleasant 
occupation,  light  exercise,  reading,  simple  games  should  all  be  urged. 
Good  ventilation  and  a  comfortable  bed  at  night  are  important  items. 
It  is  strange  that  because  movement,  such  as  carriage  and  railroad 
riding,  makes  these  patients  often  feel  better,  as  Charcot  long  ago 


3o6  THE   NEURONIC   DISEASES 

pointed  out,  that  any  one  should  thnik  of  introducuig;  vibratory  chairs 
and  other  apparatus  for  their  treatment ! 

The  nutrition  should  be  plain  and  abundant.  Alcohol,  tobacco, 
tea  and  coffee  should  all  be  discontinued. 

In  the  words  of  Oppenheim,  all  forced  therapeutic  measures  should 
be  avoided,  such  as  cold  water  cures,  massage,  electricity,  nerve- 
stretching,  suspension. 

Purgatives,  diaphoretics  and  antip}retics  are  of  little  benefit  and 
may  be  dangerous. 

The  following  drugs  have  been  recommended  in  this  disease: 
Salicylates,  Dover's  powder,  arsenic.  Indian  hemp,  nitrate  of  silver, 
curare,  bromides,  atropine,  phosphorus,  cod-liver  oil,  picrotoxin.  They 
are  practically  useless.  The  most  advantageous  medications  are  those 
that  have  a  sedative  and  hypnotic  influence.  The  hydrobromate  of 
hvoscine,  the  sulphate  of  duboisine,  morphine,  codeine  are  the  best 
of  the  palliative  remedies.  Podack  recommends  sparteine.  Veratrum 
viride,  gelsemium  and  nux  vomica  in  the  form  of  tinctures  have  quieted 
the  tremor  in  some  cases.  Erb  speaks  highly  of  arsenic.  My  own 
experience  inclines  me  to  favor  the  hyoscine  or  duboisine. 

B.       THE    SYMPATHETIC    NEUROSES.       ANGIONEUROSES    AND    TROPHONEU- 
ROSES. 

AXATOMY   AND    PHYSIOLOGY    OF   THE    SYMPATHETIC 
XERVOUS  SYSTEM. 

The  division  of  the  nervous  system  into  the  cerebro-spinal  and 
svmpathetic  is  an  artificial  one.  Both  parts  are  intimately  united 
anatomically  and  functionally  and  we  cannot  draw  any  sharp  line  of 
division  between  the  diseases  of  the  one  or  of  the  other.  And  it  is 
probable  that  we  never  will,  because  it  would  seem,  from  both  experi- 
mental and  pathological  observation,  that  the  sympathetic  merely  regu- 
lates and  controls  in  some  way  impulses  that  pass  between  the  cerebro- 
spinal centers  and  the  organs  of  vegetative  life.  In  this  fact,  however, 
we  can  detect  a  slight  specialization  in  the  functions  of  the  sympathetic. 
Symptoms  of  disturbance  in  the  vegetative  and  nutritive  organs  indi- 
cate more  or  less  involvement  of  the  sympathetic,  though  doubtless 
conjointly  with  the  cerebro-spinal  apparatus.  As  the  latter,  however, 
cannot,  it  seems,  produce  certain  manifestations  without  the  conjoined 
activity  of  the  former,  we  are  justified  in  part  in  making  a  division  .be- 
tween cerebro-spinal  and  sympathetic  diseases.  The  latter  probabl\ 
never  occur  without  the  fonner;  the  former  very  often  occur  without 
the  latter.  To  illustrate,  angioneurotic  oedema  is  said  to  be  a  disease 
of  the  sympathetic  nerve,  but  it  always  has  associated  with  it  cerebro- 
spinal symptoms.  A  localized  myospasm  is  a  cerebro-spinal  nerve 
trouble,  but  it  rarely  has  accompanying  symptoms  that  point  to  the 
sympathetic. 

Much  of  our  present  knowledge  of  the  Anatomy  and  Physiology 
of  the  Sympathetic  Nervous  System  we  owe  to  the  researches  of  Gas- 
kell,  and  in  the  following  brief  account  I  will  follow  his  teachings. 


VIIID 


THE   NEURONJC   DISEASES  307 

FIGURE  43- 

SWFRIOR   CERVICAL  GaNGUON   OF  THE   SYMPATHETIC  J    It.    CONNECTIONS   AND    BRANCHES. 

(Reduced  from  Flower.)  i 

IC  to  IVC,  Branches  of  commu- 
nication  to  lour  upper  cervical 
nerves. 

PS,  Branches  of  communication 
to  petrosal  ganglion 

Vr,  Branches  of  communication 
to  ganglion  of  root  of  pneumogas- 
tric 

V,  Branches  of  communication  to 
ganglion  of  trunk  of  pneum  igastric. 

H,  Branches  of  communication  to 
hyp  'glossal  nerve. 

C  -",  Carotid  plexus. 

C'P,  Cavernoui  plexus. 

CA,  Branches  accompanying  in- 
ternal carotid  artery. 

00,  Branches  to  ophthalmic 
ganglion 

tA,  To  tympanic  branch  ot  glosso- 
pharyngeal. 

3,  to  third  nerve    4,  to  fourth  nerve. 
5',  to  fifth  nerve,     6,  to  sixth  nerve 

V,  Vidian  nerve  to  spheno-pala- 
tine  ganglion. 

S/»,  Large  superficial  petrosal 
from  facial  nerve. 

EAC,  Accompanying  branches 
of  exiernal  carotid  artery. 

PP,  Pharyngeal  plexus,  formed  by 
union  with  branches  of  vagus  and 
glosso-pharyngeal  nerves. 

SG,  Superior  cardiac  nerve. 
TAe  Middle  Ctrvical,  or  Thyroid 
Gang  lion, 

IVC  to  VIC,  Branches  of  com- 
munication with  fourth,  fifth,  and 
sixth  cervical  nerve. 

IT,  Inferior  thyroid  branches. 

MC,  Middle  cardiac  nerve. 

Rl ,  To  recurrent  laryngeal. 
Tkt  Inferior   Cervical   Ganglion. 

VIIC  to  Vine,  Branches  of 
communicaiion  with  seventh  and 
eight  cervical  nerves. 

IC,  Inferioi  cardiac  nerve. 

C*^,  Cardiac  plexus. 

GW,  Ganglion  of  Wrisberg, 

TCP,  Posterior,  or  left  coronary 
plexus. 

RCP,  Anterior,  or  right  coronary 
plexus. 

CRL,  Cardiac  branches  from 
pneuniogastiic  or  recurrent  laryn- 
geal nerves. 

aPP,  To  right  anteiior  pulmonary 
plexus. 

LPP,  To  left  anterior  pulmonary 
plexus. 

ID  to  IID,  Branches  of  commu- 
nication from  the  first  to  the  twelfth 
dorsal  nerve. 

a,  a.  To  a-rta,  vertebrse,  .  ceso- 
pha'gus,  and  posterior  pulmonary 
plexus. 

GSN,  Great  splanchnic  nerve. 

SSN.  Small  splanchnic   nerve.  SSN',  Smallest  splanchnic   nerve  D,  Diaphragm 

PN    Phrenic  nerve  SP,  Epigastii   ,  or  solar  plexus.  CLP,  Cceliac  plexus.      ^^'p^^^S^ 

ner^e  GSD    Gastro-du'odenll  plexus.         C.P,  Gastric,  pr  coronary  plexus  P/^„^J^l°n= 

pfexus  S/>P,  Splenic  plcxu..  '  G.E.  Left  g   stro-ep.ploic  plexus.      ^P^p'^'j)ja"hragm- 

^kxus!         HV.H.patic  plexus.      /^  Branches  f^ompneumogastrc.      ^^ «^ P   D.^aphragm 

ly^  tpTrmatlct?ex'ur"  SMpfrufeH°o;  mes'ent'en'c'pTexr.^^KMiddle  colic.  R.^  Right 
S/P,  Spermatic  plexus       ="'f>  .    'jj      i^^us        IMP,  Inferior  mesmteiic  plexus.      LCI,  left 

^^!lc  plexli^.-  '''^i^'^i^rr-^^t:  ^="isto°*^s'  tr^n^ches  o'M'j:^^- 
Branches  of  communicat.  n  with  the  ^ve  lumbar  nerves  .^_^^^^'°  J^j '„  ^.^jh  the  coccygeal 
„.cation  ^uh  th^  five^s^acr.^^  nerves.         C.  ^Bra^n^che^s  of  c-mun.at.on^        ^,^^^^^   ^^^^^^ 

branches  to  all  the  pelvic  viscera. 


308  THE   NEURONIC   DISEASES 

The  sympathetic  apparatus  consists  of  a  double  chain  of  inter- 
connected gangha,  lying  on  either  side  of  the  vertebral  column  and 
extending  from  the  head  to  the  pelvis;  of  a  number  of  more  or  less 
isolated  ganglia,  including  the  ophthalmic,  the  otic,  the  spheno-palatine 
and  submaxillary  in  the  head,  various  ganglia  and  plexuses  in  the 
thorax  and  abdomen,  called  cardiac,  solar,  hypogastric,  aortic,  sper- 
matic and  renal ;  and  finally  of  various  ganglia  and  plexuses  in  many 
of  the  viscera,  such  as  the  stomach,  intestines  and  urinary  bladder. 
.  Some  physiologists  regard  the  ganglia  on  the  posterior  spinal  roots,  the 
glosso-pharyngeal,  vagus  and  sensory  root  of  the  fifth  nerve  as  largely 
sympathetic  in  function. 

Rami  communicanteSj,  so-called,  the  visceral  branches  of  the 
cerebro-spinal  nerves,  pass  out  from  the  latter  into  the  lateral  chain  of 
the  sympathetic,  from  which  rami  eiferentes  again  emerge  to  enter  the 
collateral  ganglia,  from  whence  pass  still  other  branches  to  the  various 
terminal  ganglia  in  the  organs  of  the  body.  Some  fibres  which  can 
be  traced  back  into  both  the  anterior  and  posterior  spinal  roots  are  seen 
to  enter  partly  into  the  sympathetic  chain  and  partly  into  the  great 
splanchnic  nerves. 

The  zvhite  rami  from  the  second  to  the  hflli  proceed  upwards  and 
join  the  superior  cervical  ganglion.  Other  white  rami  enter  the  lumbar 
and  sacral  plexuses. 

The  gray  rami  do  not  represent,  apparently,  visceral  branches 
below  the  second  thoracic  nerve-root  and  above  the  second  lumbar. 

The  white  rami  are,  it  would  seem,  the  proper  visceral  branches. 
The  white  rami  of  the  second  and  third  sacral  roots,  however,  com- 
mingle with  the  non-medullated  fibres  that  pass  from  the  ganglia  to  be 
distributed  chiefly  to  the  spinal  column,  the  spinal  membrane  and  the 
spinal  nerve-roots  themselves. 

All  unstriated  muscles  receive  branches  from  the  sympathetic 
nerve ;  hence  all  the  viscera  are  innervated  by  it.  The  dilator  of  the 
pupil,  the  unstriated  muscle  of  the  lid,  the  erectores  pilorum  and  the 
.sweat  and  the  salivary  glands  are  all  under  its  control. 

The  cells  are  generally  small  and  multipolar  and  possess  an  axis- 
cylinder  process  and  numerous  dendrites.  The  rami  communicantes 
from  the  cord  usually  terminate  in  arborizations  around  the  cell  bodies 
in  the  sympathetic  ganglia,  making  up  thus  the  sympathetic  neurones 
of  the  first  order.  The  cell  bodies  lying  in  the  sympathetic  ganglia, 
with  their  neuraxones  extending  out  to  the  unstriated  muscles,  con- 
stitute the  sympathetic  neurones  of  the  second  order. 

The  following  facts  in  regard  to  the  distribution  of  the  inedullated 
insccral  nerves  emerging^  from  the  cord  and  entering  the  sym.- 
pathetic  and  other  nerves  are  of  some  clinical  importance:  They 
iDelong  chiefly  to  the  thoracic  spinal  nerve-roots.  In  the  second  and 
third  sacral  nerves  they  constitute  the  nervi  erigentes,  which  pass 
directly  to  the  hypogastric  plexus  and  not  into  the  lateral  chain.  From 
this  plexus  other  fibres  proceed  to  the  inferior,  mesenteric  ganglia,  to 
the  bladder,  the  rectum  and  the  generative  organs.  The  white  visceral 
rami  of  the  upper  cervical  and  cervico-cranial  regions  do  not  associate 
with  the  corresponding  gray  rami,  but  form  the  internal  branch  of  the 


THE   NEURONIC   DISEASES 


309 


spinal  accessory  nerve.  This  branch  passes  into  the  gangHon  of  the 
trunk  of  the  vagus.  Visceral  fibres  are  found  also  in  the  roots  of  the 
vagus,  of  the  glosso-pharyngeal  and  in  the  chorda  tympani,  small 
petrosal  and  other  cranial  nerves. 

The  origin  of  these  visceral  rami  is  presumed  for  many  reasons 
to  be  in  the  cells  of  the  posterior  vesicular  column  of  Clarke  in  the  cord. 
They  are  also  probably  connected  with  the  cells  of  the  lateral  horn  of 
the  spinal  gray  matter  and  its  representative  in  the  medulla,  the  antero- 
lateral nucleus  of  Clarke. 

The  efferent  nerve  fibres  of  the  sympathetic  supply  the  muscles 
of  the  vascular  system  with  vasoconstrictor,  vasodilator,  cardiac  ac- 
celerator and  cardiac  inhibitory  branches ;  the  visceral  muscles  with 
viscero-motor  and  viscero-inhibitory  branches ;  and  the  secretory  gland 
cells  with"  their  special  branches.  Their  names  indicate  sufficiently 
their  functions. 

Not  much  is  known  of  the  functions  of  the  sympathetic  ganglia 
themselves  beyond  that  of  modifying  the  histological  structure  and 
maintaining  the  nutrition  of  the  fibres  that  pass  through  and  out  of 
them.  They  are  probably  not  reflex  centers  such  as  are  those  in  the 
spinal  cord.  How  much  of  the  metabolism  of  the  body  is  directly  pre- 
sided over  by  the  sympathetic  nerve  is  not  known.  Gaskell  believes 
that  in  it  are  anabolic  and  katabolic,  constructive  and  destructive  fibres 
respectively,  which  go  to  every  tissue  and  gland  in  the  organism.  The 
functions  of  the  system  may  be  said  ni  general  to  be  motor,  vasomotor 
and  secretory.  The  last  may  also  be  trophic,  though  that  is  still  an 
open  question. 

Symptoms  of  Lesions  in  the  Sympathetic  Nervous  Apparatus. — ■ 
Some  of  these  have  been  long  known  from  early  physiological  experi- 
mentation. Bernard  many  years  ago  severed  the  cervical  sympathetic 
and  observed  dilatation  of  the  blood  vessels  on  the  same  side  of  the 
head,  with  increase  of  cutaneous  temperature,  contraction  of  the  pupil, 
and  occasionally  retraction  of  the  eyeball.  Stimulation  of  the  nerve 
produced  contraction  of  the  bloodvessels,  decrease  of  the  temperature, 
dilatation  of  the  pupils,  dilatation  of  the  palpebral  fissure,  protrusion 
of  the  eyeball  and  sweating,  all  on  the  same  side  of  the  head  as  the 
nerve  stimulated. 

Lesions  and  diseases  of  the  nerve  in  which  disturbance  of  the 
physiological  phenomena  belonging  to  it  have  been  noted  are  numer- 
ous. Traumata,  compression  from  neighboring  neoplasms,  apical  in- 
flammatory alterations  of  the  lungs  and  pleurse  and  abscesses  are  among 
them.  The  symptoms  are  both  irritative  and  paralytic.  In  such  dis- 
eases as  glaucoma  and  exophthalmic  goitre  we  cannot,  as  Weeks 
points  out,  say  there  is  any  constant  peculiar  change  in  the  cervical 
sympathetic.  In  the  aged,  the  diabetic  and  the  syphilitic,  in  leukgemia, 
pellagra,  tuberculosis  and  infectious  diseases,  changes  have  been  ob- 
served of  the  nature  either  of  atrophy,  hypersemia,  sclerosis,  pigmentary 
and  fatty  infiltration,  amyloid  degeneration,  accumulation  of  colorless 
blood  cells  and  microccocci  in  the  ganglionic  blood  vessels.  We  know 
scarcely  anything  of  the  diseases  of  the  thoracic  or  abdominal  sympa- 
thetic, either  pathologically  or  symptomatically. 


3IO  THE   NEURONIC   DISEASES 

In  associating-  tlie  physiological  disturbances  sometimes  observed 
in  the  vasomotor,  cardiac  and  secretory  spheres  with  disease  of  the 
sympathetic,  one  must  remember  that  the  same  symptoms  may  be  pro- 
duced by  lesions  in  the  cerebro-spinal  system.  Thus  it  is  always  an 
open  question  as  to  the  exact  location  of  the  trouble  in  even  fairly  well 
defined  sympathetic  manifestations.  Exophthalfhic  goitre,  for  instance, 
shows  in  many  of  its  symptoms  a  possible  relationship  to  sympathetic 
disease ;  but  those  same  symptoms  might  be  well  produced  by  a  lesion 
in  the  cerebro-spinal  apparatus,  revealing  themselves  only  secondarily 
through  the  sympathetic. 

The  angioneitrotic  and  trophoneurotic  exhibitions  generally  are 
thus  often  only  secondary  sympathetic  disturbances,  the  primai-y  trou- 
ble being  back  in  the  cerebro-spinal  apparatus.  Tn  universal  inherited 
and  acquired  degenerative  states,  in  general  cachexia  and  infection,  it 
would  seem  singular  for  the  cerebro-spinal  system,  to  suft'er  and  the 
sympathetic  to  escape.  Hence  we  conclude  that  in  these  general  neu- 
roses both  parts  of  the  nervous  apparatus  are  implicated.  We  insist 
therefore  that  the  nervous  organism  of  the  entire  body  is  a  unit  and 
cannot  be  artificially  divided  physiologically  as  it  is  done  anatomically. 
Among  these  sympathetic  neurotic  exhibitions  we  note  flushing  and 
pallor  of  the  face,  sensations  of  heat,  rapid  pulsations  and  excessive 
sweating.  The  heart  palpitates,  the  head  seems  to  suddenly  fill  up 
with  blood,  the  ears  ring,  the  eyes  grow  misty.  It  may  be  a  sign  of  the 
sympathetic  origin  of  these  manifestations  that  through  them  all  the 
conscious  state  is  not  disturbed  nor  are  there  any  somatic  muscular 
disorders  or  objective  sensory  phenomena.  In  hysteria,  neurasthenia, 
profound  nervous  shocks,  marked  physiological  strains  such  as  puberty 
and  the  climacteric  period  involve,  masturbation,  sexual  excesses  and 
high  mental  excitement,  the  angioneurotic  symptoms  are  not  infre- 
quently observed. 

SYMMETRICAL  GANGRENE.     RAYNAUD'S  DISEASE. 

This  is  a  rare  affection  of  the  peripheral  vascular  system,  charac- 
terized by  a  local  asphyxia  and  gangrene,  and  dependent  upon  some 
disturbance  of  the  vasomotor  nervous  apparatus.  It  occurs  independ- 
ently or  in  the  course  of  other  nervous  affections,  such  as  hysteria, 
tabes  dorsalis,  syringomyelia,  spinal  tumor,  epilepsy,  exophthalmic 
goitre,  scleroderma,  etc. 

Etiology. — Heredity  does  not  enter  into  its  etiology,  but  a  neu- 
ropathic constitution  is  probably  a  factor  in  every  case.  The  young 
and  middle-aged  are  most  liable  to  it.  Women  are  more  frequently 
its  victims  than  men.  It  has  been  observed  in  the  nursing  babe.  A 
child  three  years  of  age  completely  recovered  after  losing,  from  this 
disease  and  spontaneous  amputation,  both  arms  above  the  elbow  and 
the  left  leg  below  the  knee.  In  children  the  disease  occurs  largely 
through  the  influence  of  the  ner\^ous  system.  In  old  people  through 
the  influence  of  the  heart  and  circulation. 

Ancemia,  chlorosis,  exhaustion  and  physical  defects,  such  as  a 
congenitally  small  aorta,  serve  as  predisposing  causes.     Exposure  to 


THE   XEUROXIC   DISEASES  3II 

cold,  emotional  stress,  suppression  of  menstruation  and  traumata  of 
various  sorts  have  been  invoked  as  causes  of  the  disease.  It  has 
followed  various  infectious  and  cachectic  and  debilitated  states,  such 
as  malarial  fever,  rheumatism,  neurasthenia.  It  has  occurred  in  asso- 
ciation with  tuberculosis  and  nephritis  and  in  morphine  and  chloral 
intoxication.     Diabetes  and  syphilis  have  been  blamed  for  i- 

Pathology. — Of  the  pathology  of  Raynaud's  disease  we  know 
very  little.  Raynaud  himself  suggested  that  there  was  a  local  spasm  or 
contraction  of  the  finer  blood  vessels.  The  smaller  arteries  are  com- 
paratively abundantly  furnished  with  muscular  tissue  and  so  are  capable 
of  active  changes  in  their  calibre.  Their  nerve-supply  from  the  sympa- 
thetic is  under  the  control  of  the  spinal  cord  and  is  subject  to  influences 
in  the  way  of  cold,  heat  and  dampness  from  the  periphery,  or  from 
central  disturbances  caused  by  a  toxic  and  vitiated  state  of  the  blood, 
or  from  an  abnormal  and  unwonted  impression  sent  down  from  the 
brain  and  the  higher  psychical  centers.  These  provoke  a  spasin  of  the 
arteries  and  veins.  An  endarteritis  and  an  eiidophlebitis  have  both 
been  seen  by  Dehio,  while  Pitres  and  X'aiilard  have  found  neuritic 
changes  in  the  nerves  of  the  fingers.  These  were  all  probably  secondary 
effects  and  have  no  bearing  upon  the  pathogenesis  of  the  disease. 

Symptoms. — The  chief  symptom  of  Raynaud's  disease  is  a  pecu- 
liar vascular  spasm,  appearing  suddenly,  paroxysmally  and  symmetri- 
cally at  the  ends  of  the  limbs.  Usually  two  or  three  fingers  of  both 
hands  or  several  toes  on  both  feet  experience  a  paraisthetic  sensation  of 
some  sort,  crawling,  numbness,  deadness  (digiti  mortui).  They  as- 
sume a  waxy  paleness,  are  cold  and  look  shrunken.  Some  anaesthesia 
is  present  and  often  severe  pain  precedes  and  continues  during  the 
onset.    Blood  does  not  flow  if  the  fingers  are  pricked  with  a  needle. 

This  is  the  stage  of  local  syncope  or  regional  ischcBmia.  As  a  rule 
it  lasts  about  an  hour  or  so,  and  is  then  followed  by  a  reaction  in 
w^hich  burning  sensation,  redness  and  heat  are  observed.  This  may 
disappear  in  the  course  of  a  few  hours  more  and  the  limb  remain 
perfectly  normal.  ]More  frequently,  however,  the  syncope  returns  and 
becomes  more  of  a  permanent  condition. 

In  a  few  minutes  or  hours  cyan.osis  or  local  asphyxia  takes  the 
place  of  the  initial  pallor.  The  skin  becomes  dusky,  mottled,  blue-black 
and  finally  black.  The  paijis  become  intense  and  unbearable  in  the 
hands  and  arms.  Anaesthesia  is  not  usually  present,  though  it  may  be. 
The  fingers  are  swollen  and  subject  to  slight  hemorrhages  and  bullae. 
On  account  of  the  tension  of  the  muscles  and  skin  the  fingers  are  stifif 
and  awkward.  The  gait  may  be  affected  or  the  patient  may  not  at- 
tempt to  walk  at  all. 

Any  part  of  the  body  may  be  the  seat  of  these  manifestations. 
Usually,  however,  they  appear  in  the  fingers  and  toes  first,  one  finger  or 
toe  being  affected  sooner  and  more  extensively  than  its  neighbor. 
After  the  extremities  the  ears,  the  nose  and  areas  of  skin  upon  the 
arms  and  legs  are  involved. 

Such  attacks  may  occur  paroxysmally  for  years,  being  provoked 
by  exposure  to  cold,  as  in  winter,  or  by  gastric,  miental  and  other  forms 
of  disturbance.     Duringr  all  this  time  the  general  health  remains  good. 


312  THE   NEURONIC   DISEASES 

More  commonly  this  second  stage  of  local  asphyxia  is  followed  by 
local  gangrene.  In  the  painful  and  mottled  areas  necrosis  bey^ins  and 
may  go  on  to  the  formation  of  complete  sloughs,  or  it  may  retrograde 
and  leave  only  a  scar.  Black  spots  first  appear  in  the  gangrenous  areas, 
with  vesicles  and  blisters  which  fill  with  bloody  serum,  burst  and  leave 
an  exfoliating  dark  crust,  or  a  slow-healing  ulcer.  The  ulceration  is 
superficial  and  when  healed  leaves  a  permanent  scar.  The  repetition 
of  this  process  leaves  the  tips  of  the  fingers  shrunken,  irregular  and 
unshapely  from  cicatricial  formation.  In  severe  cases,  which,  however, 
are  rare,  the  necrotic  process  extends,  mummif}'ing  the  w'hole  end  of 
the  finger  or  toe  and  establishing  a  line  of  demarkation  at  which 
spontaneous  amputation  may  take  place.  Suppuration  is  slight  and  in 
the  course  of  a  little  time  the  stump  gradually  heals.  In  this  way.  a 
part  of  the  foot  or  hand,  the  lobe  of  the  ear,  the  tip  of  the  nose  or 
tongue  may  be  lost.  Symmetrical  areas  upon  the  trunk  ma}-  be  aflfect- 
ed  and  a  condition  even  of  multiple  gangrene  be  set  up.  Such  cases 
occur  chiefly  among  young  children,  and  on  account  of  the  intense 
suffering,  the  restriction  of  movement  and  the  exhaustion,  terminate 
in  death  in  a  few  days. 

The  relationship  of  hcenioglobinnria  to  Raynaud's  disease  is  re- 
markable and  mysterious.  It  usually  occurs  in  connection  with  the 
gangrenous  stage.  It  may  be  present  in  the  attack  or  it  may  take  the 
place  of  an  outbreak.  The  similarity  of  symmetrical  gangrene  and 
hsemoglobinuria  is  shown  in  the  fact  that  both  may  be  brought  on  by 
exposure  to  cold,  the  paroxysms  often  being  preceded  bv  a  chill.  In 
the  one  case  the  nerves  and  blood  vessels  are  chiefly  affected  ;  in  the 
other  the  blood  and  blood-making  organs.  Albumin,  haemoglobin,  and 
red  corpuscles  are  all  found  in  the  urine.  Epilepsy  has  been  seen  in 
these  haematuric  cases. 

As  a  rule  there  is  no  fever,  but  the  general  strength  and  constitu- 
tional vigor  are  lowered  by  the  continuous,  unbearable  pain,  insomnia 
and  loss  of  appetite. 

Mental  dullness,  temporary  attacks  of  unconsciousness  and  other 
psychic  and  cerebral  manifestations  are  not  uncommonly  observed. 
^^'ith  depression  they  may  even  appear  among  the  prodromes  of  the 
disease.  Aphasia  has  been  noted  wdth  transient  right-sided  hemiplegia. 
Delirium,  delusions  and  mania  must  be  added  to  the  occasional  cerebral 
manifestations. 

Sensibility  is  usually  disturbed  and  conduction  noticeably  dimin- 
ished. Analgesia  is  probably  the  most  common  of  the  sensorv  modi- 
fications. Tactile  sense  is  usually  blunted,  though  the  thermic  sense 
remams  intact. 

Trophic  disturbances  are  exhibited  in  the  joint  chansres,  including 
acute  synovitis,  sw^elling.  thickening  of  the  phalangeal  articulations  and 
anchylosis.  These  are  multiple  and  attack  several  joints  at  the  same 
time.  Scleroderma  may  be  associated  with  Raynaud's  disease,  and 
paronychia  may  develop  between  the  attacks.  The  nails  may  be  altered, 
the  skin  hypertrophied  and  the  smaller  muscles  of  the  hand  somewhat 
atrophied. 

Ocular  disturbances,  loss  of  hearino-,  tinnitus  aurium  and  modifica- 


THE   NEURONIC   DISEASES 


313 


tions  of  taste  and  smell  are  not  unknown,  and  sympathetic  paralysis 
has  been  evidenced  in  certain  oculo-pupillary  phenomena. 

Thus  the  symptoms  and  complications  of  Raynaud's  disease  point 
to  an  implication  of  the  entire  nervous  system.  The  immediate  cause 
of  the  symmetrical  gangrene,  however,  is  obscure,  though  the  indica- 
tions point  to  a  functional  instability  of  the  vasomotor  apparatus. 

The  remote  cause  of  this  instability  is  in  all  probability  a  constitu- 
tional and  neuropathic  one ;  the  immediate  cause  may  reside  in  some 
form  of  disease  in  the  peripheral  nerves,  the  cord,  the  brain  or  the 
sympathetic  system. 

Diagnosis. — The  diagnosis  of  Raynaud's  disease  must  take  into 
account  the  early  age  of  the  patient,  the  bilateral  and  symmetrical 
character  of  the  symptoms,  the  successive  order  of  local  syncope, 
asphyxia  and  gangrene,  the  implication  of  sensory,  motor  and  trophic 

FIGURE  44. 


Raynaud's  disease.     (After  Affleck.) 

functions  and  the  absence  of  primary  disease  of  the  heart  and  blood 
vessels.    It  is  not  difficult  in  typical  cases. 

Erythromelalgia  is  closely  related  to  Raynaud's  disease,  but  it 
never  produces  gangrene  and  the  pains  are  usually  relieved  by  cold 
instead  of  being  made  worse  by  it,  as  in  the  latter  affection. 

Endarteritis  obliterans  does  not- present  in  successive  paroxysms 
the  syncope,  asphyxia  and  gangrene  observed  in  Raynaud's  symptom- 
complex. 

In  lepra  mutilans  several  fingers  are  simultaneously  and  equally 
affected  with  gangrene  and  fall  off,  without  the  presence  of  any  pain. 

Neuritis  is  not  paroxysmal  nor  gangrenous,  though  it  may  give 
rise  to  confusing  trophic  symptoms  in  the  skin.  Moreover,  the  etiolog}- 
and  symptoms  of  neuritis  are  so  characteristically  different  from  those 
of  this  disease  that  a  differential  diagnosis  can  usually  be  easily  made. 

In  senile  gangrene  the  age  of  the  patient,  the  presence  of  cardiac 
and  vascular  disease  and  the  non-paroxysmal  course  of  the  trouble  is 
to  be  remembered. 

Ergot  poisoning  resembles  symmetrical  gangrene  in  some  respects, 
and  Ehlers  has  argued  that  this  and  the  allied  tropho-neuroses  were 


314  J^'HE    XEUROXIC   DISEASES 

all  due  to  ergot  intoxication.  Tingling  in  the  fingers  and  feet,  cramps 
in  the  legs,  arms  and  chest,  dizzmess  and  weakness,  cold  feeling  all 
over  the  body,  dilatation  of  the  pupils  and  feebleness  of  the  pulse,  with 
retching,  vomiting,  diarrhoea  and  increased  salivary  secretion  are  the 
usual  symptoms  of  ergot  poisoning.  Epidemics  of  gangrene  have 
occurred  from  eating  bread  made  from  ergotized  rye. 

Prognosis. — The  prognosis  is  favorable  in  regard  to  life,  except 
in  the  severe  and  multiple  types  of  the  disease.  And  yet  patients  even 
recover  from  these  though  mutilated  and  deformed.  Death  has  very 
rarely  occurred  directly  from  this  disease  ;  some  complication  has  usu- 
ally been  the  cause  of  the  fatal  issue. 

No  cure  is  known  for  it.  Usually,  therefore,  it  continues  for  years, 
appearing  in  periodical  attacks. 

Tre.\tmext. — There  is  no  known  specific  remedy.  General  hy- 
gienic measures  must  be  instituted  and  the  nervous  system  especially 
must  be  kept  quiet  and  in  a  high  state  of  health.  The  nutrition  especial- 
iy  must  be  maintained  by  gentle  stimulation  and  abundance  of  easily- 
digested  food.  The  bowels  must  not  be  allowed  to  become  costive,  the 
kidneys  sluggish  or  the  skin  inactive.  A  regular  and  systematic  out- 
door life  and  exercise  must  be  adopted.  The  patient  must  be  guarded 
from  cold  by  suitable  clothing  and  the  removal  to  a  warmer  climate 
in  winter. 

The  administration  of  the  iodides,  chloral  and  nitroglycerin  may 
be  tentatively  tried.  Benefit  from  the  nitrites  is  very  doubtful.  Hutch- 
inson advises  the  tincture  of  opium  in  three  or  four  drop  doses,  three 
or  four  times  a  day,  in  combination  with  general  tonics.  Galvanism 
to  the  spine  and  sympathetic  has  been  recommended. 

The  pains  are  best  combatted  by  local  warmth,  very  gentle  mas- 
sage and  lukewarm  hand  and  foot  baths.  Anodynes  may  be  resorted 
to,  but  the  hypodermic  use  of  morphine  may  excite  local  gangrene. 
Gushing  obtained  relief  from  the  intense  burning  pains,  and  improve- 
ment of  the  circulatory  condition,  by  the  gentle  application  of  the 
tourniquet  daily  to  one  or  the  other  limb,  according  as  the  symptoms 
indicated. 

ERYTHROMELALGL\. 

This  interesting  symptom-complex  was  described  by  Weir  Mitchell 
in  1872  and  named  thus  by  him  in  1878.  Our  knowledge  of  it  is 
almost  entirely  clinical,  in  spite  of  the  fact  that  there  are  now  about 
fifty  cases  on  record.  It  has  been  studied  by  Mitchell,  Lannois,  Collier, 
Hamilton,  Sachs,  Eisner,  Rost,  Dehio,  Auerbach,  Shaw  and  others. 
Mitchell  regarded  the  trouble  as  morbus  siii  generis,  but  the  opinion  is 
growing  that  it  is  nothing  more  than  a  symptom  of  disease  of  the 
central  nervous  system,  or  peripheral  arterial  apparatus. 

Males  are  more  frequently  stricken  with  the  trouble  than  females. 
The  only  known  causes  for  it  are  cold,  a  neuropathic  diathesis  and 
syphilis. 

The  pathology  of  the  trouble  is  but  very  little  known  and  the 
pathogenesis  not  at  all.  The  only  cases  that  have  been  examined 
satisfactorily    post-mortem    were    those    of   Auerbach,    Hamilton    and 


THE   NEURONIC   DISEASES  315 

Shaw.  Edingef's  findings  ni  Aiierbach's  case  consisted  chiefly  of  ^ 
thickening  of  the  intima  and  media  of  some  of  the  distal  blood  vessels  ; 
.some  degeneration  in  the  nerve  bundles  of  the  cauda  equina ;  degen- 
eration of  the  lower  part  of  the  posterior  columns  of  the  cord  ;  and 
.some  degeneration  in  the  median  part  of  Coil's  column  in  the  thoracic 
and  cervical  cord.  The  peripheral  nerves  were  normal.  In  Sach's  case 
the  nervous  tissues  were  normal,  but  the  arteries  were  all  diseased  in  the 
limb  that  was  amputated  on  account  of  gangrene.  In  Hamilton's  case 
there  was  some  neuritic  degeneration,  but  it  was  insignificant  in  coi) 
parison  with  the  arterial  disease.  He  concludes  that  the  disease  is  miore 
-nearly  related  to  Freidlander's  obliterative  arteritis  than  to  a  degenera- 
tion of  the  spinal  cord.     Shaw's  more  recent  findings  lend  support  to 

FIGURE  45. 


1  I  *    i.T    Cf^i 

So".'  •??£■<  -f'.-r^' 


Section  of  an  artery   of  the  great  toe   in   Erythromelalgia.      (After   Mitchell 
-and  Spiller.) 

this  view.  Nevertheless  it  is  believed  by  many  that  erythromelalgia 
-is  a  symptom-complex  indicative  of  organic  or  functional  disease  of 
the  central  or  peripheral  nervous  apparatus.  By  some  it  is  considered 
to  be  an  angioneurosis ;  by  others  a  disease  of  the  posterior  and  lateral 
.spinal  gray  matter.  Plantar  neuritis  and  acroneurosis  are  two  other 
explanatory  hypotheses.  In  view  of  its  uncertain  pathology  and 
liypothetical  pathogenesis,  we  must  still  look  upon  it  as  simply  a  re- 
markable symptom-complex. 

Burning  pain  and  reddening  of  the  skin  in  the  feet,  and  more 
rarely  in  the  hands,  are  its  chief  clinical  manifestations.  The  pains 
usually  appear  suddenly,  with  or  without  fever,  especially  in  the  soles 
of  the  feet  and  in  the  hands  and  fingers.  They  may  extend  into  the 
legs  and  arms.  The  parts  soon  become  intensely  red,  hot  and  swollen. 
The  blood  vessels  pulsate  and  there  is  local  sweating.  The  pain  is 
■of  a  burning  character,  usually  severe  and  even  excruciating.  It  is 
more  or  less  constant,  though  sometimes  it  remits.  It  is  relieved  by 
•cold ;  aggravated  by  heat.  Recumbency  affords  relief,  whereas  walk- 
ing markedly  increases  it.  Standing  increases  the  pain,  the  pulsation 
of  the  arteries,  the  enlargement  of  the  veins  and  the  mottling  of  the 


3l6  THE   NEURONIC   DISEASES 

skin.  (Edema  is  nol  uncommon.  The  objective  sensi-bility  is  not  very 
much  altered,  though  both  hypenesthesia  and  shght  hypsesthesia 
sometimes  obtain.    In  this  there  is  a  suggestion  of  a  peripheral  neuritis.. 

Other  symptoms  besides  these  have  been  observed  in  conjunction 
with  erythromelalgia,  but  they  are  not  considered  as  part  of  the  latter 
symptom-complex.  There  may  be  headache,  vertigo,  palpitation  and 
attacks  of  syncope.  Widespread  arteriosclerosis  and  cardiac  lesions 
have  been  found  in  some  of  the  cases.  Angina  pectoris  and  functional 
disturbances  of  the  heart  have  been  reported  in  other  cases.  Unilateral 
sweating,  thickening  of  the  veins,  enlargement  of  the  bones,  an  atrophic 
condition  of  the  muscles  of  the  limbs,  hemiplegia,  muscular  dystrophy 
with  cerebral  tumor  and  other  indications  of  disease  of  the  central- 
nervous  system  and  of  the  peripheral  nerves  have  all  been  noted  in 
various  cases. 

From  the  standpoint  of  symptomatology  the  conclusion  of  Lewin 
and  Benda  seems  justifiable — namely,  that  there  are  among  the  re- 
corded cases  three  distinct  classes :  i^  i )  Those  with  true  organic  dis- 
ease of  the  central  nervous  system;  (2)  Those  with  functional  disease- 
of  the  central  nervous  system ;  (3)  Those  with  peripheral  disease  of  the 
nervous  system,  either  functional  or  organic. 

Until  more  data  of  a  pathological  character  are  forthcoming  to 
uphold  the  view  that  this  symptom-complex  is  dependent  upon  a 
primary  disease  of  the  arteries  and  theu"  obstruction,  we  must  accept 
the  symptomatic  evidence  that  it  is  a  manifestation  of  some  primary 
trouble  in  the  nervous  system. 

Obstinate  and  chronic,  the  trouble  may  last  for  years  with  remis- 
sions and  exacerbations.  The  heat  of  summer  aggravates  it.  During 
its  course  temporary  convulsions  and  spells  of  unconsciousness  have 
been  witnessed.  It  is  not  dangerous  to  life  in  the  absence  of  serious. 
complications,  but  exhaustion,  gangrene  and  complicating  diseases  add 
to  the  gravity  of  its  prognosis. 

It  is  very  resistant  to  all  forms  of  treatment.  Faradism,  cold  and 
the  antipyretics  of  the  coal-tar  group  have  been  tried  for  the  pains. 
In  exceptional  instances  warmth  has  seemed  to  give  the  most  relief- 
In  one  case  it  disappeared  after  extirpation  of  the  ulnar  nerve. 

ACROP.\  R  7ESTHESI A . 

This  is  a  vasomotor  neurosis  of  the  extremities  which  sometimes 
may  be  regarded  as  a  disease,  though  in  the  vast  majority  of  cases  it 
is  a  mere  symptomatic  trouble.  Without  objective  signs  of  any  sort, 
it  leveals  itself  in  paroxysmal  attacks  of  numbness,  tingling  and  other 
forms  of  parsesthesia  in  the  hands  and  feet. 

The  condition  was  described  by  Putnam,  of  Boston,  in  1880  and" 
by  Dana,  of  New  York,  in  1885.  It  remained,  however,  for  Schultze,. 
of  Bonn,  to  name  it  acropar?esthesia  in  1893  and  to  awaken  the  pro- 
fessional interest  in  it.  Many  writers  have  since  extensively  treated  of 
it,  notably  Laquer,  Ormerod,  Bernhardt,  Berger,  Friedman,  Sinkler, 
Gallois,  Charbo.  Collins  and  others. 

Etiology. — Females  are  almost  twice  as  often  affected  as  males> 


THE  NEURONIC   DISEASES 


317 


Most  of  them  are  about  thirty  or  forty  years  of  age.  The  cHmacteric 
-seems  to  favor  it.  Nationahty  or  occupation  does  not  seem  to  have  any 
special  influence.  The  heredity,  if  any,  is  only  that  of  a  mild,  general 
neuropathy.  Convalescence  from  disease,  a  general  cachexia  and  a 
state  of  debility  have  underlain  it.  Syphilis  is  not  a  cause.  The  things 
■to  which  it  has  been  attributed  are  so  numerous  that  one  is  forced  to 
the  conclusion  that  none  of  them  are  causative  except  as  mere  excitants 
■or  as  factors  in  producing  a  general  nervous  debility.  In  most  cases 
no  cause  can  even  be  suspected.  Exposure  to  cold,  sudden  changes  of 
temperature,  as  in  laundry  work  with  the  hands,  sewing,  darning,  long 
-bathing,  miscarriage,  free  use  of  alcohol  and  tea,  fright,  pregnancy  and 
-SO  on,  ad  infimtum,  have  been  the  antecedents  of  the  trouble  even  as  in 
all  other  neuroses. 

Pathology  and  Pathogenesis. — Of  the  pathology  we  know 
nothing,  and  of  the  pathogenesis  we  merely  guess  from  the  symp- 
-tomatology  that  there  must  be  a  condition  of  irritation  in  the  vasomotor 
■centers  which  affects  the  nutrition  of  the  peripheral  sensory  apparatus. 
Neuritis  may  be  excluded,  for  it  reveals  none  of  the  symptoms.  All 
that  we  can  say  is  that  it  is  a  vasomotor  neurosis.  Where  the  primary 
trouble  is  would  hardly  be  worth  guessing. 

Symptoms. — These  are  entirely  subjective  and  sensory.  They 
come  on  suddenly,  often  at  night,  even  awakening  the  patient  out  of 
her  sleep.  The  sensations  are  as  varied  in  number  as  the  patients 
themselves.  The  term  parccsthesia  covers  them  all.  Most  prominent 
among  them  are  numbness,  tingling,  formication, '  a  feeling  as  if  the 
iimb,  or  rather  more  often,  the  finger-tips,  were  asleep.  In  rare  cases 
the  toes  are  affected.  Sometimes  the  condition  is  actually  painful ;  at 
•other  times  it  is  a  distressing,  itching,  cold,  wooden,  swollen,  stiff'  sen- 
-sation.  The  movements  of  the  extremity  are  usually  restricted  on 
account  of  the  feeling.  The  trouble  is  more  or  less  continuous,  with 
exacerbations.  It  has  been  known  to  endure  from  a  week  to  somewhat 
more  than  a  year.  The  trouble  may  be  confined  to  certain  parts  of  the 
hand  and  foot,  or  to  one  hand.  The  rubbing  and  warming  attitude 
and  performances  of  the  patient  are  characteristic.  There  are  no  uni- 
form objective  signs;  usually  none  at  all.  Sensation  may  be  some- 
what decreased  in  the  fingers  or  there  may  be  a  pallor.  There  are  no 
motor  disturbances.  Other  angioneurotic  manifestations  have  been 
witnessed,  such  as  the  complaint  of  the  patient  of  blood  rushing 
to  the  head,  of  palpitation  of  the  heart,  etc.  The  disease  is  chronic, 
and,  like  all  the  primary  neuroses,  has  an  unsatisfactory  prognosis. 

The  diagnosis  involves  its  differentiation  from  symptomatic 
parsesthesia,  from  vascular  disease  and  from  other  central  organic  and 
functional  troubles.  Care  in  the  examination  will  make  the  differen- 
tiation easy,  however.  Raynaud's  disease  may  simulate  it,  but  there 
is  local  asphyxia  and  gangrene  in  this  serious  affection.  Tetany,  hys- 
teria, acromegaly  may  all  at  times  exhibit  a  resemblance  to  acropar^es- 
thesia,  but  the  appearance  of  other  symptoms  will  soon  distinguish 
them. 

Treatment. — Remove,  of  course,  any  discoverable  cause.  Gen- 
eral tonics,  such  as  arsenic,  phosphorus,  strychnine,  quinine  and  iron 


3l8  J'HI';    Nia.'KONIC   DISEASES 

are  all  useful  on  general  principles  in  couibating  a  neurosis.  ErgotiiT 
was  recommended  by  Sinkler.  Electricity  in  the  form  of  central 
galvanization,  medulla,  cervical  cord  and  sympathetic  being  brought 
within  the  current,  and  local  faradization  may  be  tried. 

ANGIONEUROTIC  CEDEMA. 

Angioneurotic  oedema,  first  definitely  described  by  Quincke  and 
his  pupil  Dinkelacker,  is  chiefly  remarkable  for  the  circuniscribed 
szvellings  that  appear  on  the  face,  neck  and  extremities,  without  ap- 
parent cause  or  previous  warning.  For  this  reason  it  has  sometimes 
been  called  periodic  szvelling,  urticaria  tuherosa,  giant  sivelling.  There 
is  almost  always  present  gastro-intestinal  disturbance,  which  is  prob- 
ably of  an  oedematous  nature,  like  that  of  the  exterior  of  the  body.. 
The  mucous  membrane  of  the  larynx  may  be  the  seat  of  the  sudden 
oedema  and  so  cause  an  alarming  dyspnoea  or  even  death  by  suffocation. 

Etiology. — The  etiology  of  the  disease  takes  cognizance  of  the 
early  adult  age  of  the  patient,  its  more  common  occurrence  in  the  male 
sex,  the  occupations  which  tend  to  excessive  fatigue  of  mind  and 
body,  and  a  certain  natural  or  acquired  neurotic  state  of  the  constitu- 
tion. Heredity  seems  to  play  an  important  role,  as  shown  by  the 
surprising  series  of  cases,  all  in  one  family,  reported  by  Osier  and 
Milroy.  In  six  generations  of  this  family  twenty-two  individuals  were 
the  victims.  Krieger's  case  was  a  young  man  twenty-five  years  of  age, 
whose  mother  was  similarly  afifected. 

Cold  and  traumiatism  are  frequent  exciting  causes  oi  the  attacks. 
The  former  in  conjunction  with  lowered  vitality  may  explain  to  a 
certain  extent  why,  as  in  one  of  my  own  cases,  the  trouble  was  so  prone 
to  appear  toward  the  early  morning  before  the  patient  awakened- 
Unusual  muscular  exercise  will  sometimes  precipitate  an  attack.  1 
have  seen  a  hard  day's  shopping,  the  patient  passing  from  one  store 
to  another  through  the  cold  wintry  air  and  climbing  flights  of  stairs, 
do  it. 

Alcoholism  predisposes  to  this  disease,  likewise  in  some  cases  a 
sojourn  near  the  sea.  Nervous  individuals  are  more  frequently  the 
victims.  It  has  been  observed  in  association  with  neurasthenia,  exoph- 
thalmic goitre,  hysteria  and  urticaria. 

Pathology  and  Pathogenesis. — The  disease  being  so  rarely 
fatal,  very  little  opportunity  has  been  afforded  for  making  a  thorough 
pathological  examination.  Its  occurrence  in  markedly  neurotic  in- 
dividuals, and  'its  many  resemblances  to  a  general  neurosis,  suggest 
that  it  probably  has  no  discoverable  lesion  in  the  nervous  system.  It 
is  probably  related  to  hysteria,  though  the  absence  of  the  usual,  well- 
known  stigmata  of  the  latter  disease  and  other  symptoms  tend  to  prove 
that  it  is  not  pure  hysteria.  It  is  most  likely  a  functional  trouble  of 
the  sympathetic  and  central  nervous  apparatuses,  but  the  cause  and 
character  of  this  trouble  are,  at  the  present  time,  entirely  unknown.  In 
this  connection  it  is  suggestive  to  note  that  Schlesinger  reported  a 
case  in  which  this  acute  oedema  was  seen  in  combination  with  ery- 
thromelalgia  and  Raynaud's   disease.      Quincke  himself   regarded  the 


THE   NEURONIC   DISEASES  319 

basis  of  the  trouble  as  a  vasomotor  neurosis,  the  vessels  being  suddenly- 
dilated. 

Symptoms. — The  patient  may  be  apparently  perfectly  well  and 
remain  indoors  all  day.  Then  upon  going  out  into  the  open  air  toward 
evening,  or  upon  taking  a  longer  walk  than  usual,  there  may  come 
on  suddenly  and  without  the  slightest  premonition  an  attack  of 
dyspnoea,  completely  frightening  and  unnerving  him.  The  extremities 
become  cold,  perspiration  ceases,  a  slight  cough  arises  and  a  feeling  as 
if  the  stomach  were  suddenly  distended.  Then  quickly  follows  the 
characteristic  oedematous  enlargements  upon  the  arms  and  face  and 
elsewhere.  These  swellings  are  circiiinscribed  and  resemble  giant 
hives,  except  that  they  neither  itch  nor  give  any  pain.  They  measure 
from  two  to  ten  centimeters  in  diameter,  are  pale  in  color  or  of  a 
deeper  red  than  the  surrounding  skin.  They  do  not  pit  upon  pressure, 
like  ordinary  dropsical  effusions,  but  if  firmly  pressed  with  the  tip  of 
the  finger  they  quickly  rise  to  their  former  level.  Some  patients  com- 
l)lain  of  a  local  sense  of  burning  or  scalding,  otherwise  these  tumefac- 
lions  do  not  produce  any  distress. 

This  circumscribed  oedema,  which  may  attack  the  mucous  mem- 
branes as  well  as  the  skin  and  subcutaneous  tissues,  is  to  be  differen- 
tiated in  this  disease  by  the  abruptness  of  its  onset,  its  brief  duration 
and  its  rapid  disappearance.  Any  part  of  the  body  may  become  its 
site,  especially  the  face  and  extremities.  In  a  migratory  sort  of  a 
way  it  may  vanish  from  one  part,  to  quickly  reappear  in  another.  It 
rarely  lasts  over  a  few  hours.     It  is  strictly  non-inflammatory. 

It  is  probably  true  that  the  alarming  dyspnoea  and  associated 
^^astro-intestinal  trouble  are  the  result  of  the  same  cedematous  process 
going  on  within  the  mucous  membrane.  Krieger's  case,  a  typical  one, 
was  found  dead  in  bed  one  morning  and  an  autopsy  showed  that  death 
was  caused  by  sudden  oedema  of  the  glottis.  Collins  finds  that  out  of 
seventy-two  cases  three  showed  their  initial  symptoms  to  be  located  in 
the  stomach  and  in  thirty-four  per  cent,  of  them  all,  gastro-intestinal 
manifestations  were  of  sufficient  importance  to  attract  notice.  The 
throat  was  involved  in  about  twenty-one  per  cent,  of  all  cases,  a  fact 
which  should  be  carefully  remarked,  as  death  has  more  than  once 
resulted  from  oedema  of  the  larynx.  The  stomach  symptoms  are,  gen- 
erally, a  sense  of  uneasiness  and  extreme  tension,  loss  of  appetite, 
enlargement  of  the  epigastrium,  colic  and  sometimes  profuse  vomiting 
and  intolerable  thirst.  Osier  says  the  pains  may  become  so  severe  at 
times  as  to  require  the  administration  of  morphia. 

In  one  of  my  cases  there  was  at  no  time  any  marked  pain,  but 
an  intolerable  sense  of  fullness  and  of  retained  undigested  matter,  with 
a  bloated  appearance  of  the  epigastrium. 

Nausea  and  periodical  vomiting  may  occur  and  are  thought  to  be 
due  to  the  internal  urticaria.  The  patients  are  usually  constipated, 
though  a  colliquative  diarrhoea  sometimes  follows  the  subsidence  of  an 
attack. 

Often  the  urine  is  voided  in  large  amounts.  Albuminuria  oc- 
casionally occurs  and  in  one  instance  led  to  the  erroneous  diagnosis  of 
renal  disease.     Oppenheim  saw  a  case  where  the  suddenly  appearing 


320  THE   NEURONIC  DISEASES 

articular  swelling  simulated  an  attack  of  gout.  Higier  reported  a 
case  in  which  the  oedema  of  the  velum  palati  led  to  attacks  that  resem- 
bled pseudocroup.  Hemorrhages  have  occurred  from  the  mucous 
membranes  and  in  one  case  Joseph  saw  a  paroxysmal  hemoglobinuria 
complicated  with  this  disease. 

The  frequent  association  of  angioneurotic  oedema  with  hysterical 
or  hysteroid  inanifestations  is  striking.  For  a  long  time  I  regarded 
one  of  my  cases  as  pure  hysteria.  In  some  cases,  as  in  one  reported  by 
Collins,  hysteric  attacks  preceded  for  some  years  the  outbreaks  of  the 
oedematous  trouble. 

Irregularities  of  the  menstrual  function  seem  to  perform  as  much 
a  part  in  the  disease  under  consideration  as  they  do  in  true  hysteria. 
Collins,  Lewin  and  Quincke  cite  instances  in  which  the  onset  and  dis- 
appearance of  the  migrator}'  oedematous  swellings  bore  a  certain  rela- 
tionship to  menstruation.  Amenorrhoea  was  sometimes  accompanied 
by  a  monthly  swelling  of  the  ankles,  lips  or  eyelids. 

Complete  exhaustion  and  nervous  anxiety  often  terminate  an 
attack  of  the  oedema.  It  was  with  great  difficulty  that  one  of  my 
patients  could  be  persuaded  that  her  heart  action  was  normal,  so  weak 
and  prostrated  did  she  feel  when  about  to  recover.  Between  the  at- 
tacks the  general  health  is  good. 

Diagnosis. — The  diagnosis  of  angioneurotic  oedema  is  not  dif- 
ficult if  the  characteristic  symptoms  are  present.  These  symptoms 
are  especially  the  local  szvelling  of  the  skin,  the  gastro-intestinal  dis- 
turbance and  the  nervous  depression. 

Giant  urticaria  is  a  disease  so  closely  related  to  angioneurotic 
oedema  that  some  have  thought  they  were  the  same. 

The  oedematous  manifestations  of  hysteria  are  usually  associated 
with  the  well-known  motor,  sensory  and  psychic  symptoms  of  this 
latter  disease. 

Prognosis  and  Course. — Angioneurotic  oedema  is  rarely  fatal, 
in  spite  of  the  severity  of  the  attacks  and  the  nervous  depression  often 
associated  with  them.  The  fatal  cases  that  have  been  reported  were 
probably  due  to  asphyxia  caused  by  the  closure  of  the  glottis  from  the 
oedematous  swelling.  This  oedema  of  the  glottis  is  to  be  dreaded  as 
a  possibility  in  all  cases.  One  of  my  own,  a  woman,  had  been  seized 
one  night  with  one  of  her  usual  attacks  and  died  of  suffocation  before 
the  physician  in  the  neighborhood  summoned  in  the  emergency  was 
able  to  do  anything. 

The  disease  is  essentially  a  chronic  one,  lasting  sometimes  a  whole 
lifetime.     The  general  health  is  not  greatly  disturbed. 

While  much  can  sometimes  be  done  to  lessen  the  frequency  and 
severity  of  the  attacks,  the  underlying  constitutional  trouble,  the  dis- 
ease itself,  so  far  has  proved  intractable  to  all  forms  of  treatment. 

Treatment. — No  remedy  has  yet  been  suggested  for  its  relief. 
Neither  the  disease  itself  nor  the  attacks  are  amenable  to  any  known 
treatment.  The  salicylates,  especially  the  salicylate  of  soda,  have  given 
the  best  results  in  the  hands  of  others,  as  well  as  in  my  own.  By  them 
the  intervals  between  the  attacks  appeared  to  be  lengthened,  but  as 
for  lessening  the  severity  of  the  attacks,  or  in  any  way  actually  pro- 


THE   NEURONIC   DISEASP:S  32I 

ducing  anything  like  a  permanent  cure,  I  could  not  see  that  this  or 
any  other  of  the  long  list  of  remedies  which  I  have  experimented  with 
were  of  the  least  avail. 

Special  measures  to  regulate  the  digestion  and  bowels  are,  of 
course,  always  indicated.  Baths,  exercise,  an  even  mode  of  life,  the 
avoiding  of  all  forms  of  mental  and  nervous  strain  go  far  towards 
ameliorating  the  trouble. 

Atropine  and  quinine  have  been  lauded,  though  they  were  in- 
effective in  my  cases.  Quinine  is  said  to  have  produced  a  complete 
recovery  in  one  instance,  and  in  one  of  Oppenheim's  it  caused  a  rapid 
disappearance  of  the  symptoms ;  an  assumption,  however,  hard  to 
establish  where  the  symptoms  often  disappear  rapidly  without  any 
medication.  Psychotherapy  suggests  itself  in  some  cases  on  account 
of  the  close  relationship  of  hysterical  manifestations. 

CHRONIC  HEREDITARY  TROPHCEDEMA. 

Aleige  recently  described  a  remarkable  series  of  cases,  all  in  one 
family,  to  which  he  has  given,  for  the  disease,  the  above  name.  Plis 
first  cases,  reported  in  1898,  were  tv>fO  sisters,  seventeen  and  twenty-one 
years  of  age.  In  both,  at  about  the  age  of  thirteen,  a  swelling  began  in 
the  feet  and  gradually  extended  as  far  as  the  trunk.  It  was  not 
oedematous  in  the  true  sense  of  the  word,  for  it  was  hard,  did  not 
vary  with  the  elevation  of  the  limb,  and  pitted  only  slightly  after  pro- 
longed heavy  pressure.  None  of  the  ordinary  causes  of  oedema  were 
present.  There  were  no  signs  of  inflammation,  no  varicose  veins,  no 
pain.  No  other  sensory  symptoms,  or  motor  either,  for  that  matter, 
were  present.  A  slight  stiffness  in  the  walk  was  caused  by  the  tension 
of  the  parts.  When  Meige  first  saw  the  cases  the  mother  of  the  girls 
was  found  to  have  the  same  condition  well  developed  in  both  legs 
as  far  as  the  knees,  and  a  brother  beginning  to  reveal  it  in  one  lower 
extremity.  The  mother  had  had  the  trouble  for  twenty-seven  years, 
without  it  causing  her  any  special  inconvenience.  The  grandmother, 
living  at  the  age  of  sixty,  showed  the  disease  well  developed  in  both 
legs,  and  the  great-grandfather  had  suffered  from  it.  Two  maternal 
luicles  of  the  two  sisters  first  seen,  dying  at  the  ages  respectively  of 
twenty-five  and  twenty-seven,  had  been  victims  of  the  disease  also. 
In  Lartat-Jacob's  cases  of  two  children,  aged  respectively  five  and  ten 
months,  a  similar  condition  was  seen.  Not  only  was  the  oedema  con- 
genital, but  also  hereditary,  as  shown  by  the  fact  that  the  maternal 
grandmother,  her  sister,  her  brother  and  a  first  cousin  of  the  little 
patient's  mother  all  had  the  disease.  Similar  cases  have  been  reported 
i3y  De  Bove  and  Moyer. 

INTERMITTENT    ARTICULAR    HYDROPS. 

This  is  a  condition  referred  to  by  Moore,  who  first  described  it, 
hy  Oppenheim,  by  Fere  and  others.  Usually  the  knee,  sometimes  the 
other  joints  of  the  extremities,  the  spinal  column  or  the  maxillary 
articulations  are  effused  with  fluid  regularly  every  few  davs  or  weeks. 


322 


THE    XEUROXIC   DISEASES 


A  mild  fever  has  occurred  in  some  cases.  There  are  absolutely,  how- 
ever, no  other  local  or  general  symptoms.  It  is  said  to  be  an  inde- 
pendent disorder  or  an  accompaniment  of  one  of  the  general  neuroses, 
like  exophthalmic  goitre.  Fere  has  described  a  permanent  hydrops. 
The  disease  has  been  associated  with  trauma,  malaria  and  other  causes* 
without  good  reason.  It  has  no  relationship  to  rheumatism,  but  is  a 
pure  neurosis.  It  is  obstinate,  but  sometimes  goes  away  of  itself  or 
alternates  with  polyuria,  hyperidrosis  or  the  symptoms  of  exophthalmic 
goitre. 

Treatment  is  not  satisfactory,  though  it  includes  the  salicylates, 
arsenic,  quinine,  ergotine,  laxatives,  electricity  and  hypnotism. 

EXOPHTHAL^IIC  GOITRE. 

Thi-s  is  often  called  Graves'  disease  because  this  English  practi- 
tioner wrote  a  clinical  account  of  it  in  1835,  which  attracted  the  atten- 
tion of  the  medical  world.  On  the  Continent  the  name  of  Basedow, 
of  Germany,  is  usually  employed,  because  he  described  it  independently 
in  1840.  If  any  physician's  name  is  to  be  attached  to  it,  that  of  Parry 
has  the  strongest  claim,  since  he  has  left  in  his  posthumous  writings 
a  very  fair  clinical  portrayal  of  his  first  case,  seen  in  1786,  and  others 
observed  later.  The  contention  of  the  Italians  that  Flajani  fully  de- 
scribed it  in  1800  is  not  well  substantiated. 

Our  present  knowledge  of  the  affection  does  not  permit  of  its 
exact  classification.  Clinically  it  is  a  neurosis.  Pathologically  and 
pathogenetically  there  is  some  ground  for  suspecting  that  it  is  a 
thyroid  disease.  A  strict  definition,  therefore,  can  only  include  a 
few  meager  facts  in  regard  to  its  etiology  and  the  symptom-complex 
tachycardia,  enlarged  thyroid,  protrusion  of  the  eyeballs  and  certain 
neurasthenic  and  vasomotor  manifestations. 

Etiology. — Heredity  enters  as  an  important  factor  in  the  etiology 
of  Graves'  disease.  In  a  few  instances  it  is  direct.  A  mother  and  two 
sons  under  my  care  have  had  it,  the  latter  recovering  completely.  In 
another  instance  an  aunt  of  the  patient  suffered  from  it.  Similar 
examples  have  been  observed  and  reported  by  others.  In  the  majority 
of  cases,  however,  the  heredity  is  only  indirect.  Various  other  neu- 
roses, such  as  neurasthenia,  chorea,  epilepsy,  hysteria,  psychoses  and 
nervous  strains  from  excessive  indulgence  in  alcohol  and  tobacco,  can 
be  recorded  in  the  family  history.  A  neuropathic  condition  is  trans- 
mitted to  the  offspring  and  through  the  female  line.  The  affection  is 
sometimes  called  a  ''woman's  disease,"  as  it  has  been  observed  to 
occur  ten  times  more  frequently  in  women  than  in  men. 

It  appears  at  all  periods  of  life,  but  most  commonly  in  the  second 
decade  of  women,  and  the  third  of  men.  Worry,  fright,  anxiety  and 
extreme  emotional  depression  have  often  been  observed  to  precede  it, 
but  whether  they  were  causative  or  symptomatic  has  not  always  been 
clear.  All  exhausting  iniinences,  general  debility  and  anaemia  predis- 
pose toward  it.  I  have  seen  cases  that  followed  pregnancy,  abortion, 
the  puerperium  and  prolonged  spells  of  illness.  Abnormal  menstrua- 
tion, cardiac  disease,  infection  (scgirlet  fever,  rheumatism,  pneumonia. 


THE   NEURONIC   DISEASES  323 

syphilis,  etc.),  diarrhoea,  excessive  use  of  alcohol,  over-exertion,  like 
mountain-climbing,  and  injuries  to  the  head,  have  at  various  times 
been  assigned  as  causes. 

If  exophthalmic  goitre  is  primarily  due  to  disease  of  the  thyroid 
gland,  some  of  the  above-named  factors  cannot  reasonably  be  looked 
upon  as  causes,  much  less  as  symptoms.  And  yet  they  are  too  fre- 
quently and  too  intimately  associated  with  it  to  be  regarded  in  the 
mere  light  of  accidents  or  coincidences.  As  etiological  factors  they 
can  fit  in  with  the  conception  of  the  disease  as  a  primary  neurosis — a 
conception  which  is  further  supported  by  such  elements  in  the  etiology 
as  the  sex,  age  and  heredity. 

Pathology  and  Pathogenesis.- — The  post-mortem  findings  are 
so  indefinite  that  even  at  the  present  day  nothing  but  hypotheses  can 
be  offered  in  explanation  of  the  nature  of  the  disease.  Among  the 
various  theories  only  two  are  worthy  of  special  consideration — namely, 
the  one  that  regards  the  trouble  as  a  primary  neurosis,  and  the  other 
that  looks  upon  it  as  an  intoxication  from  primary  disease  in  the  thyroid 
gland. 

In  the  former  theory  it  is  assumed  that  there  is  a  functional  dis- 
turbance, toxic  or  quasi-physiological,  within  the  cellular  elements  of 
the  central  nervous  apparatus,  and  that  all  of  the  symptoms  of  the 
disease,  cardiac,  glandular  and  ophthalmic,  are  the  direct  result  of  the 
neurosis  and  are  in  no  way  dependent  upon  one  another.  Attempts 
have  been  made  to  localize  the  neurotic  process  in  the  medulla  ob- 
longata (Filehne,  Durdufi,  Bienfait,  Sattler,  Fitzgerald),  the  cerebral 
cortex  (Newman)  or  the  peripheral  apparatus,  including  especially 
the  vasomotor  sympathetic  system  (Abadie).  None  of  these  efforts 
have  proved  successful.  The  immediate  cause  of  the  neurosis  is  wholly 
unexplained. 

The  other  theory  of  the  disease  is  the  so-called  "hyperthyroida- 
tion"  or  "dysthyroidation"  theory.  It  was  first  promulgated  by 
Mobius,  of  Berlin,  in  1886,  and  has  been  ably  supported  by  Wette, 
Muller,  Joffroy,  Brissaud,  Segnault,  Boinet,  Bramwell,  Murray,  Adam 
and  Greenfield.  As  a  result  of  disease  in  the  thyroid  gland,  an  exces- 
sive or  altered  secretion  is  poured  out  into  the  circulation  and  this, 
either  by  its  direct  toxic  effect  or  by  its  disturbance  of  the  general 
metabolism,  causes  all  of  the  nervous  manifestations  and  their  sec- 
ondary results. 

Chronic  iodism  or  tJiyroidisni,  depending  upon  the  thyroiodin  or 
iodothyrin,  a  normal  substance  found  in  the  gland,  both  free  and  in 
combination  with  a  proteid  and  containing  9.3  per  cent,  of  iodine  and 
0.56  per  cent,  of  phosphorus,  is  believed  to  be  the  essential  trouble. 

The  origin  of  this  glandular  disease  is  not  explained,  though  a  few 
authors  fall  back  upon  some  form  of  nervous  trouble,  possibly  a  neu- 
rosis, in  accounting  for  it.  This  thyroidation  theory  is  popular  just 
at  present ;  is  supported  by  various  more  or  less  logical  arguments ; 
and  affords  a  basis  for  the  surgical  treatment  of  the  disease. 

Hypertrophy  and  persistence  of  the  thymus  gland  has  often  been 
seen.  The  other  pathological  findings,  such  as  the  degenerative  changes 
in  the  sympathetic,  the  inflammatory  and  other  foci  of  disease  in  the 


324  THE   .\EURU.\IC    DISEASES 

restiforin  bodies  and  elsewhere,  and  even  the  cirrhosis,  hyperplasia  and 
vascular  alterations  in  the  thyroid  gland  itself,  are  scarcely  constant 
and  decisive  enough  to  be  regarded  as  the  histopathological  foundation 
for  the  disease. 

Cntil  more  constant  post-mortem  evidence  to  the  contrary  ■  is 
forthcoming  we  must  still  regard  exophthalmic  goitre  as  a  mere  symp- 
tom-complex and  largely  of  the  nature  of  a  neurosis.  The  numerous 
hypotheses  put  forth  to  explain  its  pathogenesis,  while  interesting  and 
suggestive,  are  none  of  them  established  as  positive  facts. 

Symptoms. — The  onset  of  the  disease  varies.  After  some  un- 
wonted exertion,  hemorrhage  or  mental  shock  the  symptoms  may 
promptly  appear  and  rapidly  increase.  After  some  prolonged  physical 
strain,  worry  or  infectious  disease  they  usually  come  on  gradually  and 
develop  slowly.  Once  developed  they  are  more  or  less  permanent, 
though  the}'  ma\"  be  subject  to  occasional  remission.  In  some  mild 
cases  they  quickly  appear  and  disappear.  In  the  acute  severe  cases 
they  usually  subside  somewhat  and  the  disease  becomes  stationary  and 
chronic. 

The  clinical  presentation  of  Graves"  disease  includes  the  tripod  of 
symptoms  tachycardia,  struma  and  exophthalmos.  Xot  all  of  these 
are-  present  in  every  case,  nor  are  they  all  equally  prominent  when 
present.  There  are  other  symptoms  that  are  almost  of  like  importance, 
as,  for  example,  trembling,  hyperidrosis  and  mental  depression.  After 
these  are  a  long  list  of  neurasthenic  and  hystero-neurasthenic  mani- 
festations in  regard  to  which  it  is  not  always  easy  to  say  whether  they 
are  symptoms  or  complications. 

The  tachycardia,  or  irregular  rapid  action  of  the  heart,  is  the 
earliest,  the  most  constant  and  subjectively  the  most  obtrusive  of  all 
the  svmptoms.  So  pathognomonic  is  it  that  when  it  cannot  be  account- 
ed for  on  the  basis  of  any  other  organic  or  functional  heart  disease,  a 
diagnosis  of  incipient  exophthalmic  goitre  is  allowable.  It  may  come 
on  abruptlv  or  gradually.  Often  it  is  the  only  symptom  that  sends  the 
patient  to  his  physician ;  at  other  times  it  is  only  discovered  as  the 
result  of  a  most  painstaking  examination.  The  phenomenon  is  like 
that  which  occurs  when  a  person  is  unduly  excited.  Subjectively  the 
heart  seems  to  throb  Anolently  and  spasmodically  without  rhyme  or 
reason.  Xervous  excitement  may  induce  an  exacerbation  or  increase 
it.  Objectively  it  is  observed  to  beat  irregularly  and  with  an  exalted 
degree  of  force.  In  bad  cases  it  flutters  and  pounds  and  seems  like 
a  caged  animal  struggling  to  set  itself  free.  The  impulse  is  sharp  and 
noticeable  over  a  wnder  area  than  normally.  In  mild  cases  the  beats 
number  about  100  to  the  minute:  in  the  majority  of  the  cases  it  rises 
to  120  or  140  •.  in  the  more  severe  cases  it  may  even  o^o  to  200.  Rarely 
does  it  ever  subside  to  the  normal,  except  in  the  mild  cases.  Some- 
times the  pulse  is  regular  and  small,  while  the  arteries  beat  vigorously. 

With  all  this  energy  the  circulation  Is  not  actvially  hastened.  The 
condition  is  merely  a  sort  of  delirium  cordis,  representing  not  strength, 
but  rather  lack  of  Inhibition. 

Usuallv  there  is  no  indic?itlon  of  an  organic  lesion  upon  physical 
examination.     Slight  enlargement  of  the  heart  mav  be  detected  later 


THE   NEURONIC   DISEASES  325 

on,  this  being  due  to  dilatation  rather  than  to  hypertrophy.  Occasion- 
ally a  systolic  murmtrr  is  heard  near  the  base  of  the  heart.  Graves 
stated  that  in  one  case  this  was  audible  at  a  distance  of  four  feet  from 
the  patient.  As  the  result  of  the  dilatation  a  sound  suggestive  of 
mitral  regurgitation  may  be  heard  at  the  apex.  All  of  these  are  sec- 
ondary manifestations  and  when  dependent  upon  actual  organic  lesions 
are  to  be  looked  upon  as  complications.  \'alvular  defects  from  slight 
endocarditis  have  been  occasionally  fotuid  post-mortem. 

Severe  paroxysms  of  palpitation,  extreme  violence  of  action,  accom- 
panied by  dyspnoea  and  signs  of  dilatation,  without  hypertrophy,  are 
among  the  later  cardiac  manifestations.  The  arterial  system  becomes 
dilated  from  the  lowered  tone  of  the  vascular  walls  and  the  increased 
pulsations  of  the  heart.  The  carotid  arteries  especially,  the  thyroids 
and  even  the  abdominal  aorta,  exhibit  an  exalted  pulsation.  A  loud 
systolic  murmur  may  be  heard  in  the  neck  and  is  rarely  ever  entirely 
absent.  A  curious  fact  is  that  the  smaller  arteries  beat  comparatively 
less  forcibly  than  the  larger-sized  vessels.  The  entire  arterial  system, 
however,  is  subject  to  the  peculiar  throb.  In  a  few  instances,  which 
are  exceedingly  rare  and  in  which  the  thyroid  was  markedly  enlarged 
and  variable,  the  exophthalmos  slightly  observable,  and  the  tremor, 
sweating  and  neurasthenic  symptoms  were  present,  I  could  not  detect 
the  slightest  alteration  in  the  heart  action.  T'hese  cases  sought  medical 
advice  solely  on  account  of  the  increased  size  of  the  neck. 

Xext  to  the  heart  phenomena  the  enlargement  of  the  thyroid  gland 
is  the  most  frequent  and  important  symptom.  Occasionally,  as  I  have 
seen,  the  first  and  only  thing  to  attract  the  patient's  attention  is  the 
increasing  tightness  of  her  collar.  In  one  or  two  instances  the  friends 
detected  the  enlargement  before  the  patient  did.  Objectivelv  it  is  the 
most  noticeable  symptom,  and  as  it  appears  sooner  or  later  in  almost 
every  case,  it  is  to  be  regarded  as  a  cardinal  symptom. 

Those  who  believe  that  the  thyroid  is  the  primary  seat  of  the 
entire  disease  find  some  difficidty  in  explaining  the  cases  m  which  it 
fails  to  enlarge,  and  in  the  exceedingly  uncommon  cases  in  which  it 
actually  diminishes.  They  are  driven  to  assume  that  the  gland  is 
just  sufficiently  diseased  to  produce  an  abnormal  secretion  without  be- 
ing itself  altered  in  size. 

The  enlargement  of  the  gland  is  gradual  and  slow.  It  begins 
usually  after  the  tachycardia  has  existed  for  some  time.  It  is  not  a 
uniform  enlargement.  ^lost  frequently  the  right  side  is  bigger  than 
the  left.  It  may  be  equal  on  both  sides.  The  isthmus  is  rarely  in- 
creased. Sometimes  there  are  remissions,  or  rather  the  gland  alter- 
nately enlarges  and  recedes.  Later  on  it  becomes  permanent.  The 
patient  realizes  the  change  in  the  gland  by  the  tightness  in  her  dress 
and  occasionally  by  a  distressing  sensation  as  though  something  were 
about  to  choke  her.  The  degree  of  enlargement  is  usually  not  ex- 
cessive and  very  rarely  as  much  as  it  is  in  ordinary  goitre.  The  super- 
ficial veins  over  the  gland  are  dilated.  Palpation  sometimics  reveals 
a  slight  thrill  and  auscultation  enables  one  to  detect  a  soft,  blowing 
murmur  synchronous  with  the  cardiac  systole.  Guttmann  declares 
that  a  double  murmur  is  pathognomonic. 


326 


THE    NEURONIC    DISEASES 


The  protrusion  of  Ihc  eyeball  is  a  variable  symptom,  though  highly 
characteristic  of  the  disease  when  present.  It  is  the  least  frequent  of 
the  three  cardinal  symptoms  and  it  is  often  entirely  absent.  It  usually 
appears  with  the  enlargement  of  the  thyroid.  It  rarely  occurs  alone. 
It  may  be  unilateral,  more  commonly  it  is  bilateral.  The  right  eye 
is  apt  to  be  a  little  more  prominent  than  the  left.  Generally  the 
condition  is  slight  and  sometimes  it  is  barely  noticeable.  It  may  be  so 
marked,   however,   that   the   insertions    of   the   recti   muscles   may   be 

FIGURE  46 


Exophthalmic   goitre.      (Eisendrath.) 

exposed.  The  lids  are  drawn  back,  the  white  sclerotic  coat  is  widely 
visible  and  the  patient  exhibits  a  highly  exaggerated  surprise-look  or 
stare.  The  movements  of  the  eyeball  are  limited,  the  lids  cannot  close 
and  the  conjunctiva  is  slightly  irritated.  The  eyeball  is  actually  in- 
creased in  size  somewhat  and  may  be  painful  as  well  as  prominent 
Vision  is  not  generally  disturbed,  though  myopia  has  occurred,  prob- 
ably on  account  of  the  increase  in  the  size  of  the  globe.  The  fundus 
appears  normal,  though  the  retinal  arteries  may  pulsate  abnormally. 
Secondary  effects,  like  ulceration,  sloughing  and  opacity  of  the  cornea, 


THE   NEURONIC   DISEASES 


327 


have  followed  the  insufficient  protection  of  the  eye.     (Edema  of  the 
lids  and  even  optic  atrophy  have  been  observed. 

A  remarkable  symptom,  which,  however,  is  only  present  when 
there  is  exophthalmos,  is  that  known  as  Voii  Graefe's.  If  the  patient 
holds  her  head  still  and  is  asked  to  follow  with  her  gaze  the  finger  of 
the  examiner,  carried  slowly  downward  about  twelve     or     fourteen 

FIGURE  47. 


Exophthalmic   goitre.      (Colburn.) 


inches  in  front  of  her  eyes,  it  will  be  noticed  that  as  the  ball  of  the 
eye  rolls  downward  the  upper  lid  fails  to  follow  it  as  it  does  in  health. 
'This  is  not  due  merely  to  the  physical  obstruction,  for  the  symptom 
does  not  occur  when  the  eyes  are  protruded  from  any  other  cause. 
The  upper  lid  is  in  a  state  of  spasmodic  elevation  from  implication  of 
the  fibers  of  the  muscle  of  Miiller.     The  presence  of  this  symptom  is 


328  THE   NEURONIC   DISEASES 

therefore  dependent  in  no  way  upon  the  exophthahnos  and  consequent- 
ly may  be  observed  when  the  latter  is  very  slight.  It  is  usually  bilat- 
eral and  may  vary  in  degree  of  severity. 

Winking  does  not  take  place  ais  often  as  it  does  in  normal  indi- 
viduals (Stellicag's  symptonij,  and  there  is  some  retraction  of  the  lids 
so  that  even  in  the  mildest  cases  of  exophthalmos  the  palpebral  fissure 
is  wider  than  would  be  expected. 

The  internal  rectus  of  one  eye  may  be  weakened,  as  shown  by 
asking  the  patient  to  look  at  the  tip  of  his  nose.  External  ophthal- 
moplegia has  been  observed,  though  as  a  rule  there  is  no  paralysis  of 
the  ocular  muscles  in  this  disease.  There  may  be  a  vibratory  tremor 
of  the  eyeball,  as  is  sometimes  seen  in  other  parts  of  the  body.  Lacry- 
mation  may  be  a  symptom. 

So  constant  is  tremor  that  some  authors  add  it  to  the  three  cardinal 
symptoms  of  the  disease.  I  have  not  found  it  so  frequently  as  this, 
though  I  have  seen  it  many  times.  Basedow  first  described  it.  The  ex- 
tremities and  the  head  oscillate  with  a  fine,  regular  movement,  eight  to 
ten  oscillations  to  the  second.  As  the  symptom  usually  occurs  early 
in  the  disease,  and  does  not  always  continue  throughout  its  course,  it 
is  important  always  in  the  diagnosis.  It  is  suggestive  of  the  tremor 
of  paralysis  agitans.  Mental  excitement  and  exertion  increase  it,  but  it 
is  never  abseat  even  during  rest.  Choreiform  jactitations  have  been 
occasionally  noticed  in  conjunction  with  this  tremor. 

In  addition  to  the  four  important  symptoms  of  exophthalmic 
goitre  just  described  there  are  many  others,  less  constant,  but  often  of 
much  assistance  in  arriving  at  a  diagnosis.  x\mong  these  hyperidrosis 
has  seemed  to  me  to  be  rather  frequent.  iMearly  all  of  the  patients 
complain  of  sweating  more  than  they  have  been  accustomed  to  doing, 
especialW  under  the  arms.  Sometimes  it  is  unilateral  and  even  local, 
as  in  the  palms  of  the  hands,  about  the  head,  etc.  On  account  of  this 
dampness  of  the  skin  the  local  resistance  to  the  electric  current  is 
markedly  diminished. 

A  psychosis  of  some  sort  is  nearly  always  noticeable  in  exoph- 
thalmic goitre.  It  may  amount  only  to  a  slight  degree  of  irritability, 
anxiety,  restlessness  and  melancholy — a  mild  phrenasthenia.  The 
memory,  the  power  of  attention  and  the  will  may  be  somewhat  weak- 
ened. Sleep  may  be  disturbed  so  as  to  be  either  very  light  or  very 
profound.  Unpleasant  dreams  are  not  uncommon.  In  rare  cases 
actual  delirium,  mania,  melancholia,  with  distinct  hallucinations  and 
illusions,  may  break  out.  An  elTort  must  always  be  carefully  made  to 
determine  whether  the  psychosis  is  primary  or  secondary.  Exoph- 
thalmic goitre  occasionally  occurs  among  the  insane.  The  psychosis 
that  is  a  symptom  of  Graves'  disease  usually  assumes  an  atypical  form 
and  its  course  is  variable.  Acute  mania  may  appear  and  terminate  in 
death  in  a  few  days. 

The  general  health  of  these  patients  is  usually  deteriorated.  They 
are  ansemic,  weak,  emotional  and  emaciated.  In  spite  of  a  good  appe- 
tite and  the  ingestion  of  abundance  of  food,  they  even  go  on  to  a 
condition  of  complete  marasmus.  The  bowels  become  loose,  attacks 
of  vomiting  take  place,  the  temperature  rises  a  little  and  there  are  hot 


THE   XEUROXIC   DISEASES 


329 


flashes  that  sweep  over  the  entire  bod}'.  ^Inscular  weakness,  vertigo, 
headache,  various  parsesthesise,  sHght  alteration  of  the  reflexes,  spinal 
tenderness,  want  of  energy  and  staying  qualities  all  indicate  a  pro- 
nounced condition  of  neurasthenia.  A  true  motor  paresis  .does  not 
occur,  though  persistent  paraparesis  in  the  legs,  and  even  a  monoplegic 
and  hemiplegic  condition  have  been  recorded. 

Among  the  trophic  manifestations  a  muscular  atrophy  is  exceed- 
ingly rare.  The  skin,  however,  may  be  pigmented  somewhat,  as  it  is 
in  Addison's  disease.  The  hair  occasionally  turns  gray  and  falls  out. 
Leucoderma,  urticaria,  local  oedema,  myxoedematous  swellings  and 
pruritus  are  some  of  the  occasional  and  distressing  associated  phe- 
nomena. 

Polyuria  is  frequent  enough  to  be  regarded  as  an  important  symp- 
tom. In  rare  instances  it  may  be  associated  with  albuminuria  or 
glycosuria.  As  in  hysteria,  epilepsy  and  other  neuroses,  the  micturition 
may  be  excessive  at  times.  AMth  the  polyuria  and  hyperidrosis,  a  cer- 
tain degree  of  polydipsia  is  apt  to  be  present.  Amenorrhcea  has  not 
been  so  rare  in  my  observations  as  the  authorities  state.  Delayed 
menstruation  has  been  associated  with  the  disease  in  some  of  the  young 
girls  that  I  have  seen.  The  relationship  between  the  two  I  am  unpre- 
pared to  explain.  It  has  been  thought  that  there  is  some  connection 
between  the  sexual  apparatus  and  the  thyroid  gland.  The  latter  is  said 
to  undergo  changes  at  puberty  and  often  to  vary  in  size  with  each 
menstrual  period.  The  role  played  by  sex  in  exophthalmic  goitre  is 
due,  in  my  opinion,  not  so  much  to  the  sexual  organs  as  to  the  differ- 
ences in  the  nervous  constitution. 

The  respiratory  function  exhibits  some  anomalies  in  Graves"  dis- 
ease. Paroxysmal  cough  and  dyspnoea  are  not  to  be  made  light  of. 
Bryson  has  shown  that  there  is  a. lessened  expansion  of  the  chest  in 
inspiration,  though  Patrick  has  found  this  to  run  pari  passu  with  the 
weakness  of  the  muscular  apparatus.  It  is  not  therefore  a  characteristic 
symptom  in  itself. 

CoMPLiCATioxs. — The  complications  of  exophthalmic  goitre  are 
numerous  and  must  not  be  confused  with  the  symptoms  of  the  disease. 
Among  the  nervous  troubles  with  which  it  is  sometimes  associated  are 
the  psychoses  already  referred  to,  hysteria,  epilepsy,  tabes,  tetany,  dia- 
betes, rheumatoid  arthritis,  Raynaud's  disease  and  migraine.  The 
osseous  system  has  been  affected,  as  in  osteomalacia,  and  has  combined 
with  or  passed  into  myxoedema.  Optic  neuritis  and  optic  atrophy  are 
complications  rarely  seen.  Enlargement  of  the  lymphatic  glands, 
vertigo  and  bronzing  of  the  skin  have  been  noted  by  several  observers. 
\'alvular  defects  of  the  heart  are  complicating  rather  than  symptomatic. 
Organic  lesions  of  all  sorts,  both  in  and  out  of  the  nervous  system, 
except  that  of  the  thyroid  gland,  are  so  exceedingly  rare  that  they  may 
all  be  put  down  as  complications  or  mere  secondary  results. 

Diagnosis. — A  typical  case  of  Graves'  disease  is  easily  recognized. 
Typical  cases,  however,  are  not  often  seen  and,  moreover,  the  physician 
is  usually  called  upon  for  a  diagnosis  early  in  the  disease  when  the 
symptoms  are  few  and  not  well  marked.  It  is  most  desirable  to  make 
the  diasrnosis  earlv,  as  then  the  disease  is  most  amenable  to  treatment. 


330  THE  NEURONIC  DISEASES 

The  tachycardia  may  be  the  only  symptom  present  when  the  pa- 
tient first  comes  under  observation.  If  it  has  come  on  rather  suddenly, 
after  a  severe  strain  or  shock  in  a  neuropathic  individual,  especially  a 
woman  with  hysteroid  tendencies  and  a  neurotic  ancestry,  and  espe- 
cially if  it  cannot  be  accounted  for  on  any  other  organic  or  functional 
basis,  a  diagnosis  of  incipient  exophthalmic  goitre  may  be  made  with 
reasonable  justness.  The  changeability,  excited  character  and  appar- 
ently causeless  origin  of  the  tachycardia  are  strongly  suggestive  of 
Graves'  disease.  It  is  less  paroxysmal  in  its  exacerbations  in  the  latter 
than  in  any  other  neurosis.  If  neurasthenic  symptoms  of  a  marked 
character  occur  with  a  tachycardia  that  does  not  change  after  the 
patient  has  maintained  quiet  for  some  time,  a  strong  suspicion  of 
exophthalmic  goitre  should  be  formed.  If  any  of  the  minor  symptoms, 
such  as  a  mild  psychosis,  local  hyperidrosis,  vertigo,  vasomotor  dis- 
turbances, trembling  and  muscular  weakness,  reveal  themselves  with 
this  form  of  tachycardia,  the  diagnosis  is  all  the  more  strengthened. 
A  careful  examination  for,  or  at  least  an  expectant  anticipation  of, 
enlargement  of  the  thyroid  and  prominence  of  the  eyeballs  may  re- 
ward the  examiner  with  grounds  for  making  an  absolutely  positive 
diagnosis. 

If  only  struma  is  present  with  the  tachycardia  it  is  to  be  remem- 
bered that  ordinary  goitre  sometimes  provokes  cardiac  overaction  by 
pressure  upon  the  sympathetic  and  vagus  nerves.  Ordinary  goitre,, 
however,  occurs  mostly  endemically,  has  not  a  neurotic  heredity  be- 
hind it,  is  not  associated  with  marked  neurotic  symptoms,  appears 
gradually,  grows  larger  and  maintains  its  size  more  uniformly  than 
does  the  goitre  of  Graves'  disease.  In  ordinary  goitre  the  exophthalmos 
is  more  apt  to  be  unilateral,  and  the  direct  irritation  of  the  sympathetic 
is  shown  in  the  marked  unilateral  mydriasis. 

It  must  be  admitted  that  the  differential  diagnosis  between  exoph- 
thalmic goitre  and  ordinary  goitre  with  pressure  symptoms  is  some- 
times extremely  difficult.  In  the  exophthalmic  goitre  I  iiave  made 
the  differentiation  by  placing  the  fingers  well  to  the  side,  and  behind, 
the  tumor  and  experiencing  a  lateral  pulsation  or  thrill.  If  the  tumor 
is  an  ordinary  bronchocele,  throbbing  from  mere  promixity  to  the 
great  underlying  blood  vessels,  there  will  be  no  lateral  thrill,  but  the 
whole  mass  will  pulsate  forward. 

Acute  iodism  (Oppenheim)  and  cocaine  intoxication  (Durdufi) 
have  produced  a  clinical  picture  resembling  that  of  exophthalmic 
goitre. 

Some  of  the  complications  may  lead  to  confusion  in  the  diagnosis, 
but  if  the  cardinal  symptoms  of  Graves'  neurosis  be  sought  for,  and 
if  it  be  remembered  that  most  of  these  complications  have  other  symp- 
toms that  belong  only  to  them  and  not  to  the  exophthalmic  symptom- 
complex,  the  differential  diagnosis  will  not  be  a  matter  of  such  extreme 
difficulty. 

Prognosis.- — In  its  ordinary  form  the  disease  is  essentially  a 
chronic  one.  It  lasts  for  years,  with  remissions  and  exacerbations. 
Though  complete  recovery  takes  place  in  only  about  one-quarter  of  the 
cases,  and  these  the  milder  ones,  death,  on  the  other  hand,  need  not 


THE   NEURONIC   DISEASES 


33  i 


be  feared,  except  in  the  more  rapid  and  severe  cases.    Intermissions  oc- 
cur in  some  cases,  so  that  the  patient  suffers  from  a  series  of  attacks. 

The  Ught  cardiac  cases  are  the  most  hopeful.  These  sometimes 
return  to  health  in  three  or  four  weeks.  They  may  become  chronic, 
develop  other  symptoms  and  last  for  years.  Gowers  finds  that  the 
prognosis  in  these  cases  is  a  trifle  better  in  women  than  in  men  and 
where  the  disease  seems  to  run  through  the  family. 

With  the  appearance  of  struma  and  exophthalmos  the  prognosis 
becomes  more  grave.  Very  serious  is  it  if  the  apparent  cause  is 
irremediable,  if  there  is  marked  emaciation,  if  the  thyroid  is  unusually 
enlarged  and  if  the  muscular  weakness  is  extreme.  Organic  heart 
disease  renders  the  outlook  unfavorable. 

No  case,  however  severe  and  prostrated  it  may  be,  is  absolutely 
beyond  all  hope  of  restoration  to  health.  Some  very  remarkable  and 
unlooked-for  recoveries  have  taken  place.  In  those  that  do  recover 
the  heart  disturbance  is  apt  to  linger  or  be  the  last  symptom  to  go. 
Death  is  dependent  usually  upon  the  cardiac  weakness.  Gowers  .c- 
marks  that  the  average  prognosis  is  worse  among  hospitpJ.  patients 
than  in  those  of  better  position  in  private  practice.  My  own  observa- 
tion confirms  this. 

Treatment. — The  treatment  of  exophthalmic  goitre  is  still  un- 
satisfactory, whatever  the  means  employed.  Every  line  of  treatment 
has  been  followed  by  some  cures ;  no  line  of  treatment  has  been  tried 
without  a  certain  percentage  of  failures.  In  view  of  this  fact,  one  is 
inclined  at  times  to  believe  in  the  self-limitation  of  some  of  the  cases, 
especially  when  we  recall  how  remittent  and  even  intermittent  the 
disease  often  is  in  its  course.  Credit  must  not  be  too  hastily  gTven, 
therefore,  to  any  particular  mode  of  treatment  that  happens  to  be  fol- 
lowed by  improvement. 

The  treatment  of  this  disease  may  be  profitably  discussed  under 
the  five  heads,  specific,  hygienic,  medicinal,  electrical  and  surgical. 

There  is  no  known  specific  remedy  that  will  cut  the  disease  short. 
Recently,  however,  some  favorable  results  from  the  exclusive  adminis- 
tration of  milk  drawn  from  thyroidectomized  goats  have  been  reported 
by  Ballet,  Enriques,  Mobius,  Lanz  and  others.  The  theory  is  that 
animals  from  which  the  thyroid  gland  has  been  removed  develop 
in  their  bodies  a  substance  that  would  fix  or  neutralize  the  poisons 
of  Graves'  disease.  Goebel  argues  that  in  Graves'  disease,  depending 
upon  a  hypersecretion  of  thyroidin,  iodin  is  advantageously  excluded 
from  the  dietary  and  this  is  accomplished  by  the  giving  of  milk  only 
from  an  animal  deprived  of  its  power  of  secreting  any  iodin  through 
the  removal  of  its  thyroid  gland. 

The  duration  of  this  treatment  varies  from  several  weeks  to  six 
months,  and  has  been  followed  by  very  encouraging  results. 

The  serum  from  thyroidectomized  goats  and  sheep  has  been  used 
by  Mobius,  Burghardt  and  Blumenthal  with  some  degree  of  success. 
It  is  administered  per  os  and  subcutaneously.  By  the  latter  method 
I  ccm.  has  been  injected  daily,  while  at  the  same  time  rodagen,  a 
powder  prepared  from  the  milk  of  thyroidectomized  sheep,  was  given 
three  times  a  day  in  doses  of  3  to  6  grams.    Cases  with  organic  cardiac 


;^2i~  THE   XEUKU-XIC   DISEASES 

affections  generally  got  worse  and  in  some  instances  the  serum  pro- 
duced erythema,  rheumatoid  troubles  and  general  depression. 

All  forms  of  serum  treatment  have  as  yet  been  tried  in  too  small 
a  number  of  cases  to  be  positively  recommended  or  condemned. 

There  are  no  prophylactic  measures  to  be  noted,  as  the  disease 
usually  makes  its  appearance  more  or  less  abruptly.  General  hygienic 
measures  are  of  immense  value  when  the  trouble  has  once  announced 
itself.  First  among  these  is  rest  and  absolute  quietude  of  mind  and 
body.  Removal  of  all  sources  of  worry,  a  change  of  environment  and 
a  certain  amount  of  rest  daily  in  bed  will  cause  an  amelioration  in  the 
symptoms  of  nearly  every  case,  and  their  disappearance  completely  in 
not  a  few  of  them.  A  sojourn,  therefore,  in  the  country  where  plenty 
of  fresh  air  and  good  food,  with  quiet,  can  always  be  obtained,  is. 
judicious. 

The  food  should  be  plain,  non-stimulating  and  largelv  vegetable. 
Alcohol,  tea  and  coft'ee  should  be  prohibited  absolutely  and  meats- 
largely  restricted. 

Most  patients  do  better  at  the  seashore  than  in  the  mountains,, 
though  some  have  improved  in  high,  dry  altitudes.  Sea-bathing  and 
mountain-climbing  are  decidedly  dangerous,  as  is  also  a  sea-voyage,, 
unless  the  patietit  is  proof  against  inal  de  mer.  Gentle  outdoor  exer- 
cise and  moderation  in  bathing  are  to  be  recommended.  Sexual  ex- 
citement, smoking  and  all  forms  of  dissipation  and  unwonted  mental 
and  physical  stimulation  must  be  interdicted.  The  patient  must  adopt 
a  most  regular  mode  of  life  in  regard  to  his  sleeping,  rising,  eating, 
etc.  Some  cases  do  better  when  they  keep  their  bed  absolutely  for  a 
few  weeks,  though  in  the  majority  of  cases  this  is  not  required. 

As  advanced  cases,  in  which  operative  measures  have  been  sug- 
gested as  a  dernier  ressort,  have  recovered  when  the  above  line  oi 
treatment  has  been  rigidly  and  persistently  carried  out,  too  much  stress 
cannot  be  laid  upon  the  hygienic  treatment  of  the  disease. 

In  addition  to  the  sedative  and  tonic  effect  of  these  hygienic  meas- 
ures, the  effect  of  the  physician's  personality,  the  hopefulness  of  mind 
that  can  be  inspired  by  the  companions  of  the  patient,  and  the  remarka- 
ble influence  of  psychic  suggestibility  are  important  and  rather  favor  the 
neurotic  theory  of  the  disease.  It  is  a  curious  fact  that  ]\Iobius,  who 
first  propounded  the  glandular  theory  of  the  disease,  has  reported  some 
good  results  from  the  use  of  hypnotism.  Oppenheim,  who  questions 
the  thyroidation  theory  and  favors  the  neurotic,  has  never  seen  hypno- 
tism do  a  particle  of  good.  I  am  convinced,  nevertheless,  that  a  certain 
amount  of  psychic  suggestibility  play5  a  useful  part  in  the  management 
of  the  disease,  and  I  am  not  sure  that  some  of  the  vaunted  cures  from 
surgical  as  well  as  from  other  measures  may  not  be  due  to  profound 
mental  impression. 

The  medicinal  agoits  that  have  been  employed  to  combat  the  dis- 
ease are  many.  Most  of  them  are  used  to  combat  the  symptoms.  Suc- 
cesses and  failures  have  followed  all  of  them.  None  of  them  can 
be  recommended  wath  certainty,  though  all  of  them  should  be  given  a 
trial  before  the  case  is  declared  hopeless  or  subjected  to  the  risk  of  a 
severe  operation.     Like  all  experimenters,    I   have  my   owni   favorite 


THE   NEURONIC   DISEASES  333 

xemedy,  though  at  times  I  have  found  it  to  fail  me.  I  have  seen  codeia, 
in  gradually  increasing  dosage,  continued  for  a  considerable  time, 
produce  prompt  and  happy  amelioration  of  both  subjective  and  ob- 
jective symptoms.  I  give  this  alkaloid  a  trial  in  every  case  before  re- 
sorting to  other  measures.  Sometimes  I  have  had  better  results  from 
the  administration  of  asafoetida  m  full  doses  at  the  same  time.  The 
heart  action  has  quieted  down,  the  struma  has  seemed  to  lessen  in  size, 
and  above  all,  the  patient's  general  nervous  condition  has  disappeared. 
The  bromides  have  been  less  effective  in  my  hands,  though  beneficial  in 
some  cases.  I  have  seen  no  results  from  belladonna  or  its  alkaloid, 
atropia,  such  as  others  have  reported.  I  have  given  it  until  the  physio- 
logical effects  were  decided.  The  administration  of  iodine  and  the 
iodides  is  full  of  uncertainties.  Tlie  symptoms  are  less  liable  to  be 
increased  under  the  use  of  h^'driodic  acid.  In  a  few  instances  good 
has  followed  all  of  them  and  they  are  open  to  trial  if  watched  and 
given  cautiously.  Painting  the  skin  over  the  gland  with  iodine,  or 
rubbing  into  it  daily  the  ointment  of  the  red  iodide  of  mercury,  is 
urged  by  some  authorities.  Iron,  quinine,  arsenic  and  the  mineral  acids 
serve  as  useful  general  tonics.  Oppenheim  urges  the  avoidance  of 
opium  for  the  diarrhoea  and  says  that  he  has  had  better  success  with 
Colombo.  For  their  symptomatic  effect  tincture  of  aconite,  aconitia, 
strophanthus,  digitalis,  cactus  grandifllorus,  veratrmu  viride  and  picrate 
of  ammonium  have  received  various  indorsement.  Phosphate  of 
sodium  daily  in  doses  of  two  to  ten  grains  has  been  praised  by  Kocher 
and  others. 

The  very  multiplicity  and  diversity  of  these  remedies  suggest  their 
own  criticism.  They  are  probablv  useful  in  combating  certain  condi- 
tions in  individual  cases,  but  as  distinct  therapeutic  agents  for  the 
cure  of  exophthalmic  goitre  they  are  practically  worthless.  They  are 
merely  adjuvants  in  fostering  the  nervous  quietude  and  bodily  nutri- 
tion upon  which  the  real  cure  of  the  disease  depends. 

Before  leaving  the  discussion  of  medicinal  agents,  a  word  should 
be  said  in  regard  to  the  administration  of  thyroid  extract,  so  much 
lauded  a  few  years  ago  and  noAv  so  extensively  condemned.  It  is 
true  that  the  symptoms  of  the  disease  are  usually  increased  by  it,  and 
for  that  reason  it  must  be  given,  if  given  at  all.  with  great  caution. 
It  is  curious  logic  to  base  the  thyroidation  origin  of  the  disease  upon 
this  fact,  as  many  do ;  for  as  the  administration  of  thyroid  extract  in 
all  neuropathic  individuals  will  provoke  more  or  less  nervous  dis- 
turbance (a  quarter  of  a  grain  produced  a  disturbing  degree  of  excite- 
ment in  a  case  of  myxoedema,  and  in  another  of  sporadic  cretinism 
tmder  my  observation),  the  increase  of  symptoms  produced  by  its 
administration  in  Graves'  disease  merely  indicates  the  neurotic  origin 
of  them  in  this  affection.  I  have  seen  a  case  in  a  young  man  whose 
mother  had  the  disease  in  an  advanved  stage,  and  whose  brother 
showed  it  in  its  incipiency,  completely  cured  and  without  any  distress- 
ing phenomena,  during  its  intermittent  administration  in  five-grain 
doses  during  a  period  of  almost  eighteen  months.  I  do  not  think, 
therefore,  that  it  is  open  to  absolute  condemnation,  though  I  would 
tirge  caution,  and  some  hesitancv.  in  its  administration. 


334  '^'HE   NEURONIC   DISEASES 

Electrical  treatment  should  always  be  given  a  trial,  as  some  very- 
favorable  results  have  followed  it.  Galvanization  of  the  cervical  sym- 
pathetic is  the  method  of  choice.  Two  or  three  times  a  day,  in  ten- 
minute  seances,  and  in  doses  of  three  or  four  milliamperes,  the  stable 
current  should  be  transmitted  along  the  anterior  edge  of  the  sterno- 
mastoid  muscle.  It  is  a  ciuestion  whether  the  effect  is  upon  the  sym- 
pathetic or  the  vagus  nerve.  The  same  mode  of  application  in  health 
does  not  cause  any  pupillary  changes,  which  seems  to  indicate  that 
the  sympathetic  is  not  very  much  involved.  Strong  currents  must  not 
be  used,  and  it  is  better  to  err  on  the  side  of  too  small  and  too  brief 
an  application  than  vice  versa.  The  patient  should  lie  down  during  the 
treatment.  Dana  recommends  placing  the  positiye  pole  beneath  the  ear 
and  the  negative  over  the  thyroid  gland  for  two  minutes,  then  over  the 
cardiac  region  one  minute,  positive  pole  over  the  eyes,  and  finally  the 
negative  over  the  thyroid  one  minute.  Vigouroux  and  Charcot  long 
ago  recommended  the  direct  galvanization  of  the  cardiac  region.  The 
static  breeze  in  the  same  area  is  said  to  have  done  good.  General 
faradism  and  central  galvanization  are  useful  for  their  general  tonic 
effect.  Electrical  treatment  often  fails,  and  I  am  prone  to  think  that 
some  of  the  good  accomplished  by  it  is  due  to  psychic  suggestion,  ex- 
pectancy, hopefulness  and  the  systematization  of  the  patient's  general 
regimen  inculcated  by  it.     It  therefore  has  its  use. 

One  enters  a  battlefield  in  discussing  the  surgical  treatment  of 
exophthalmic  goitre.  Here,  as  elsewhere,  good  reports  are  forthcom- 
ing. All  of  the  operations  are  dangerous,  and  the  danger  increases 
with  the  stage  of  the  disease  and  the  inexperience  of  the  operator. 
Whereas  so  great  an  operator  as  Kocher  may  report  a  hopeful  per- 
centage of  cures  in  carefully  selected  cases,  physicians  will  be  loath 
to  regard  exophthalmic  goitre  as  purely  a  surgical  affection  vmtil  no 
cases  are  cured  by  other  measures,  and  until  the  statistics  and  tech- 
nique of  the  average  surgeon  make  a  better  showing. 

This  is  not  the  place  to  discuss  the  relative  merits  of  medical  and 
surgical  treatment.  Many  analyses  will  have  to  be  scrutinized  and  all 
the  bearings  taken  fully  into  account  before  the  question  receives  any- 
thing like  a  definite  answer. 

Five  operative  procedures  are  to-day  before  the  medical  world  for 
consideration.  In  the  order  of  their  popularity  and  usefulness  they 
may  be  enumerated  about  as  follows :  Sympathectomy,  or  exsection 
of  the  cervical  sympathetic  nerve ;  thyroidectomy,  with  a  mortality 
ranging  about  fifteen  per  cent ;  ligation  of  the  thyroid  arteries : 
Jaboulay's  exothyropexie  (exposure  of  the  gland  to  the  air)  ;  and 
operations  upon  distant  organs,  as,  for  example,  the  uterus. 

By  operative  procedures  good  results  are  claimed  in  from  sixty 
to  eighty-five  per  cent,  of  cases.  The  mortality  is  so  varied  in  the  hands 
of  different  operators  that  at  present  nothing  definite  can  be  affirmed. 

MYXOiDEMA  AND  CRETINISM.     ATHYREA. 

Myxocdcma,  cretinism  and  cachexia  struniipriva  are  three  condi- 
tions dependent  upon  disease  of  the  thyroid  gland  and  characterized 


THE   XEUROXIC  DISEASES  335 

by  a  peculiar  condition  of  the  skin  and  mucous  membranes,  by  weak- 
ness and  certain  nervous  manifestations,  and  by  a  psyciwsis  of  a  more 
or  less  uniform  and  typical  sort.  Absence  of  the  thyroid  gland  is  the 
basis  of  the  trouble,  as  shown  both  by  post-mortem  examination  and 
by  the  brilliant  results  obtained  from  the  administration  of  thyroids. 
The  three  diseases  may  therefore  be  well  considered  together,  and  on 
account  of  the  prominence  of  their  nervous  symptoms  be  included  in  a 
work  on  nervous  diseases. 

It  was  Sir  William  Gull,  and  later  on  Ord,  who  in  the  seventies 
first  described  a  cretinoid  condition  in  which  mental  failure  and  a 
myxoedematous  condition  of  the  subcutaneous  tissues  were  associated 
with  atrophy  of  the  thyroid  gland.  There  were  no  pathological  find- 
ings of  any  moment,  though  the  pathogenesis  of  the  disease  was 
attributed  to  the  loss  of  the  thyroid  gland.  The  suspicion  was  trans- 
formed into  a  certainty  when  a  similar  condition  was  produced  by 
extirpation  of  the  gland  by  several  investigators.  Horsley  established 
the  condition  by  a  complete  removal  of  the  gland  in  monkeys,  and 
Kocher  and  Reverdin  showed  that  it  followed  complete  extirpation  in 
the  human.  This  operative  myxoedema,  or  cachexia  strumipriva,  is 
characterized  by  a  tired  feeling,  pains  and  heaviness  in  the  limbs, 
tetanoid  contractures,  sensations  of  cold,  temporary  swelling  of  the 
face,  hands  and  feet,  mental  apathy  and  coma.  A  chronic  state  gen- 
erally follows  this  in  which  the  mentality  becomes  sluggish,  the  skin 
cold,  dry  and  scaly,  and  the  strength  decidedly  diminished.  The  hair 
may  fall  out,  the  bones  cease  to  grow  and  the  patient  die  if  not  treated. 

This  cachexia  appears  more  promptly  in  the  young  than  in  the 
old  and  is  believed  to  occur  only  when  the  gland  is  entirely  and  com- 
pletely removed.  The  identity  of  these  symptoms  with  those  of 
myxoedema  in  the  adult  and  cretinism  in  the  child  has  confirmed 
pathologists  in  the  view  that  the  same  pathogenesis  is  applicable  to  all 
these  conditions. 

^lYXCEDE^IA. 

This  is  sometimes  called  Gull's  disease.  Charcot  named  it  cachexie 
pachyderuiique.  It  has  been  referred  to  as  cretinism  in  the  adult. 
The  disease  comes  on  insidiously  and  progresses  slowly.  Women  are 
more  affected  than  men  in  the  proportion  of  six  to  one.  It  occurs 
mostly  between  the  ages  of  thirty  and  fift}-.  It  has  been  seen  in  in- 
fants, but  not  earlier  than  at  six  months  of  age.  There  is  a  slight 
hereditary  influence  on  the  maternal  side,  and  several  cases  have  ap- 
peared at  times  in  the  same  family.  Other  neuroses  have  preceded  it 
and  exophthalmic  goitre  has  been  replaced  by  it.  Alcoholism  and 
syphilis  do  not  predispose  to  it.  Though  it  occurs  so  largely  in  women, 
the  sexual  accidents  of  women  do  not  seem  to  have  any  bearing. 

Various  exciting  causes  have  been  assigned,  such  as  exposure  to 
cold,  emotional  excitement,  traumata,  etc. 

Symptoms. — Trophic  changes  constitute  the  main  symptoms  in 
the  clinical  picture.  There  is  a  slow  and  gradual  increase  in  the 
general  bulk  of  the  body.  The  head  and  extremities  enlarge,  assume 
a  new  contour  and  take  on  a  new  shape.     The  countenance  especiallv 


336  THE   NEURONIC    DISEASES 

appears  swollen  and  puffy.  The  lines  of  expression  are  obliterated,  the 
lips  thickened,  the  nostrils  broadened,  the  mouth  enlarged  and  the 
entire  features  rendered  coarse  and  brutal.  Apathy  and  stupidity  are 
suggested  b}-  the  physiognomy.  The  tongue  is  thickened  and  hard- 
ened. Local  swellings  occur  in  the  neck  and  on  the  extremities.  The 
tumefaction,  especially  in  the  supra-clavicular  region,  nicludes  the  skin 
and  subcutaneous  tissues.  The  hands  and  feet  are  stubby,  the  fingers 
and  toes  broad  and  separated.  The  skin  is  dry,  hard  and  scaly,  is 
rough  and  does  not  pit  upon  pressure  as  in  ordinary  cedema.  It  feels 
cold  and  dead,  looks  pale,  seems  elastic  to  the  touch  and  does  not 
perspire.  The  mucous  membrane  of  the  mouth  is  also  infiltrated. 
Imperfect  nutrition  is  shown  in  the  falling  out  of  the  hair,  nails  and 
teeth.  Muscular  weakness  and  mental  deterioration  added  to  the 
physical  deformity  render  these  individuals  awkward,  imgainly  and 
clumsy  in  all  their  movements. 

The  psychic  condition  is  the  second  important  characteris.tic  of 
this  disease.  There  is  a  gradual  impairment  of  the  mental  faculties. 
The  thoughts  and  perceptions  are  slow,  the  speech  is  delayed  and  the 
general  intelligence  greatly  lowered.  At  first  the  memory  is  weakened. 
The  disposition  becomes  irritable  and  suspicious.  Hallucinations  and 
delusions  that  are  inconstant  and  systematized,  and  suicidal  impulses 
may  all  be  observed.  Sometimes  there  is  merely  inability  to  fix  the 
attention  and  lack  of  mental  energ}'.  At  other  times  there  is  a  total 
lack  of  interest  and  a  settled  state  of  stupor.  Finally  a  condition  of 
complete  dementia  obtains,  in  which  there  seems  to  be  an  obstruction 
in  all  the  avenues  of  both  afiferent  and  efl'erent  impulses.  The  five 
senses  are  all  more  or  less  impaired.  At  times  there  is  great  depression 
and  despair,  which,  however,  is  not  identical  with  true  melancholia. 
Mania,  melancholia  and  hallucinatory  paranoia  have  been  observed. 
This  group  of  mental  symptoms  dift'ers  in  its  course  from  those  of  the 
ordinary  psychoses  and  is  as  typical  in  its  general  characteristics  of 
myxoedema  as  are  the  physical  signs. 

Headache,  Tertigo  and  coldness  are  often  complained  of  b}-  these 
patients.  The  bodily  temperature  is  not  unfrequently  found  to  be  sub- 
normal to  the  extent  of  one  or  tw"0  degrees  Fahrenheit.  The  muscles 
are  w^eak  and  sometimes  atrophied.  Incoordination  and  contractures 
are  observed  in  rare  instances.  The  electrical  resistance  of  the  skin 
is  increased  and  it  is  often  hypgesthetic  or  even  anaesthetic.  The  voice 
is  unnatural,  hoarse  and  monotonous.  The  reflexes,  the  electrical  re- 
action of  the  nerves  and  muscles,  the  functions  of  the  abdominal  and 
thoracic  viscera  are  all  normal.  Hemorrhages  are  not  infrequent. 
Albuminuria  is  observed  in  about  tAventy  per  cent,  of  the  cases ;  gly- 
cosuria rarely.  Synovitis  of  the  knee-joint,  optic  neuritis  and  optic 
atrophy  are  among  the  rarest  symptoms  that  have  been  noted. 

The  physical  deformity,  the  peculiar  iniiltration  of  the  skin  and 
subcutaneous  tissues,  the  mentalisation,  the  hoarse  voice,  the  weakness 
and  awkwardness  are  so  characteristic  a  group  of  symptoms  that  the 
diagnosis  of  myxoedema  is  never  a  very  difficult  matter.  Were  any 
doubt  present,  the  therapeutic  test  w-ith  thyroid  extract  would  soon 
remove  it. 


THE   NEURONIC   DISEASES  337 

The  course  of  the  disease  is  chronic  and  progressive,  often  ex- 
tending over  five,  ten  and  fifteen  years. 

The  prognosis  without  treatment  is  unfavorable ;  with  treatment 
it  is  extremely  bright,  so  far  as  complete  or  partial  restoration  to  a 
normal  condition  is  concerned.  The  treatment,  however,  has  to  be 
continuous,  as  its  cessation  is  usually  followed  by  a  prompt  relapse. 
When  death  occurs  it  is  usually  the  result  of  some  cardiac  trouble  or 
some  intercurrent  malady,  such  as  tuberculosis. 

In  view  of  the  accepted  pathogenesis  of  myxoedema,  it  is  hard  to 
explain  those  cases  in  which  exophthalmic  goitre  is  associated  with  it, 
as  well  as  those  in  which  an  enlargement  of  the  thyroid  in  young  per- 
sons gives  rise  to  an  acute  and  temporary  manifestation  of  it.  I  have 
seen  it  follow  exophthalmic  goitre,  but  this  is  not  so  difficult  to  ac- 
count for. 

Probably  in  all  these  conditions  there  is  an  enlargement  of  the 
thyroid  generally  with  complete  atrophy  of  its  parenchymatous,  secret- 
ing structures. 

CRETIXISM. 

This  is  a  form  of  myxoedema  occurring  endemically  and  sporadi- 
cally, appearing  congenitally  or  during  infancy,  having  the  same  gen- 
eral symptoms  as  the  adult  form,  and  depending  upon  disease  or  ab- 
sence of  the  thyroid  gland.  Endemic  cretinismi  occurs  chiefly  in 
Switzerland,  Italy  and  France  and  is  associated  with  goitre.  It  is 
"believed  to  be  due  to  the  loss  of  function  in  the  thyroid  gland. 

Sporadic  cretijiisin  is  rare,  especiall}'  in  this  country,  and  is  in  all 
respects  identical  with  infantile  myxoedema.  Cases  of  so-called 
■infaiitiUsm  are  probably  mild  grades  of  the  same  condition. 

Rarelv  before  the  age  of  six  or  seven  months  is  the  disease  rec- 
ognized. Then  the  same  general  trophic  and  mental  deterioration  is 
noted.  The  growth  and  mentality  of  the  child  are  seen  to  be  retarded. 
The  face  assumes  a  bloated,  coarse,  stupid  appearance.  The  tongue 
is  large,  the  lips  protuberant,  the  mouth  increased  in  size,  the  eyelids 
thick  and  drooping  and  the  facial  lines  obliterated.  The  body  is 
dwarfed  and  thick,  the  abdomen  pendulous,  the  extremities  short,  club- 
shaped  and  bowed.  The  hands  and  feet  resemble  paws.  Hair  is  scarce, 
the  teeth  are  undeveloped  or  decayed,  the  nails  are  deformed  or  absent. 
The  skin  is  pale,  sallow  and  waxy :  it  is  dry  and  leathery  to  the  touch. 
Fatty  tumors  abound  in  and  about  the  neck.  The  disproportion  be- 
tween the  various  parts  of  the  body  is  very  remarkable.  The  mind  fails 
of  development  and  a  condition  of  idiocy  thus  obtains.  The  muscula- 
ture is  weak  so  that  the  child  has  to  be  supported  when  walking.  Usu- 
ally walking,  like  speaking,  is  quite  impossible.  The  fontanelles  com- 
mionly  remain  unclosed. 

There  are  mild  degrees  of  the  trouble  in  which  the  physical  symp- 
toms are  only  slightly  indicative  of  delayed  development  and  the 
mental  state  is  that  of  medium  grade  imbecility.  Such  a  case  I  have 
seen  restored  almost  to  a  normal  condition  by  the  administration  of 
thyroid  extract.  The  thyroid  gland  is  supposed  to  be  affected  by  a 
transient  functional  disturbance. 


338 


THE   XEURO.XIC    DISEASES 


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o 


THE   NEURONIC   DISEASES  339 

Death  occurs  early  in  most  cretins,  though  some  have  Hved  to 
middle  adult  life.  If  treatment  is  mstituted  early  and  before  puberty ^ 
or  the  age  at  which  puberty  should  occur,  most  brilliant  results  in 
some  cases  may  be  obtained. 

Treatment. — There  is  only  one  remedy  that  is  effective  in  all 
these  forms  of  athyrea  or  atJiyreosis,  and  that  is  the  thyroid  gland  or 
thyroid  extract.  We  are  originally  indebted  to  Murray  for  this  remark- 
ably brilliant  therapy,  though  much  has  been  done  in  the  way  of  es- 
tablishing it  by  Schiff,  Bercher,  Horsley,  MacKenzie,  Horwitz  and 
others. 

Beginning  with  one  grain  three  times  a  day,  the  dose  may  be 
continuously  increased  until  fifteen  or  twenty  grains  three  times  a  day 
are  taken.  Forty  grains  or  more  is  about  the  maximum  average  daily 
dose. 

Unpleasant  symptoms  that  are  to  be  guarded  against  are  those  of 
general  thyroidism — namely,  parsesthesia,  restlessness,  tachycardia, 
dyspnoea,  anorexia,  emaciation,  delirium,  etc.  These  occur,  however, 
in  only  a  small  number  of  cases.  On  the  other  hand,  the  results  of 
thyroid  treatment  are  so  positive  and  happy  that  nothing  in  the  way  of 
therapeutical  success  can  compare  with  it. 

Relapses  occur  if  the  remedy  is  discontinued ;  hence,  as  Murray 
himself  suggested,  full  doses  should  be  given  at  first  to  efifect  the  cure 
and  moderate  doses  should  be  continuously  administered  thereafter 
to  maintain  the  normal  or  acquired  metabolism. 

Thyroidin,  thyroiodin,  idiothyrin  have  all  been  prepared  from  the 
thyroid  glands  of  sheep  and  tried  in  place  of  the  thyroid  extract. 
While  some  advantages  are  claimed  for  them,  especially  the  iodothyrin, 
none  of  them  equal  in  efficiency  the  whole  gland  or  its  extract. 

ACROMEGALY. 

As  Marie  first  described  this  disease  in  1886,  it  is  sometimes  named 
after  him.  It  has  also  been  called  Pachyakria.  As  its  more  common 
name  indicates,  it  is  chiefly  characterized  by  an  enlargement  of  the  ex- 
tremities and  face. 

Etiology. — -Heredity  seems  to  exercise  no  influence  in  its  etiology. 
All  ages  are  liable  to  it,  though  the  great  majority  of  cases  occur 
between  twenty  and  forty.  Most  authors  declare  that  it  attacks  both 
sexes  about  equally,  though  I  am  inclined  to  think  that  women  are  a 
little  more  prone  to  it  than  men.  Race  and  nationality  exert  no  deter- 
mining force.  It  has  followed  syphilis,  rheumatism,  the  infectious 
fevers  and  alcoholism,  though  it  is  doubtful  if  these  are  in  any  way- 
causative.  Such  recorded  exciting  causes  as  exposure  to  cold,  fright, 
worry,  emotional  shocks  and  traumata  are  too  indefinite  to  be  given 
much  consideration. 

Pathology  and  Pathogenesis. — The  most  constant  post-mortem 
finding  is  enlargement  of  the  pituitary  gland  (cerebral  hypophysis).. 
In  practically  every  case  this  is  found  to  be  altered.  The  other  findings 
in  the  disease  are  comparatively  so  inconstant  the  opinion  has  become 
quite  universal  that  the  primary  seat  of  the  trouble  resides  in  this  gland. 


340  THE   NEURONIC   DISEASES 

Those  who  question  this  hypothesis  base  their  opposition  upon  the  fact 
that  often  the  hypophysis  is  diseased  without  the  appearance  of  the 
acromegahc  symptoms.  \'arious  neoplastic  growths,  such  as  sarcoma, 
ghoma,  adenoma,  have  been  found  as  the  reason  of  the  pituitary  en- 
largement, especially  of  the  anterior  part  of  the  gland.  The  function 
of  the  gland  is  disturbed  and  a  general  nutritive  disorder  is  thus  estab- 
lished. The  exact  function  is  not  positively  known,  though  embryol- 
ogy, evolution  and  pathology  all  seem  to  indicate  that  it  bears  a  close. 
resemblance  to  that  of  the  thymus  and  thyroid  glands. 

Many  symptoms  of  acromegaly  are  comparable  to  those  of 
myxoedema,  especially  in  their  tropho-neurotic  characteristics.  Evolu- 
tion, embryology  and  histology  all  teach  that  before  the  closure  of  the 
post-pharyngeal  vault  there  was  a  direct  connection  between  the  mouth 
and  ventricles  of  the  brain  by  way  of  the  infundibulum.  The  anterior 
part  of  the  pituitary  gland,  having  been  caught  in  the  intracranial 
cavity  when  the  latter  finally  separated  from  the  buccal  cavity,  its 
structures  retained  their  thyroid-like  metabolic  functions,  the  whole 
gland  became  ductless  and  entered  upon  the  role  of  an  organ  of  internal 
secretion,  and  so  in  some  way  assisted  in  regulating  the  general  nutri- 
tion of  the  body. 

In  many  cases  of  acromegaly,  besides  disease  of  the  hypophysis, 
the  thyroids  are  found  to  be  atrophied  and  the  thymus  gland  persistent 
and  hyperplastic. 

The  trophic  changes  found  in  other  parts  of  the  body  include  thick- 
ening and  deformity  of  the  bones,  especially  the  lower  jaw  and  distal 
bones  of  the  extremities;  arthritic  conditions  in  and  about  the  joints; 
hypertrophy  of  the  skin,  connective  tissues,  arteries  and  nerve-sheaths, 
spinal  ganglia  and  sympathetic ;  increase  in  the  size  of  the  brain,  eye- 
balls and  abdominal  organs ;  and  asymmetrical  degeneration  of  the 
posterior  columns  of  the  cord.  From  the  pathological  findings  the  dis- 
ease is  well  classified  as  a  tropho-neurosis,  whatever  may  be  the  seat 
of  the  primary  trouble. 

Symptoms. — The  disease  approaches  insidiously  so  that  often  the 
enlargement  is  first  noticed  by  the  patient's  tailor  or  bootmaker.  There 
may  be  at  the  commencement  various  panesthesiae,  slight  drawing 
pains,  general  debility  and  peculiar  visual  phenomena.  In  women 
the  menstruation  sometimes  ceases.  A  persistent  headache,  vertigo, 
gradual  failure  of  vision  and  other  signs  suggestive  of  intracranial 
tumor  may  awaken  suspicion.  Ere  long,  however,  the  characteristic 
symptom  of  the  disease  makes  its  appearance.  This  consists  of  a 
uniform,  progresswe  enlargement  of  the  hands  and  feet  and  certain 
parts  of  the  head  and  spinal  column.  In  the  hands  and  feet  the  soft 
tissues,  as  well  as  the  bones,  are  increased  in  size.  The  fingers  and 
toes  are  not  deformed,  though  they  are  big,  uncouth  and  easily  mov- 
able. Thev  look  like  links  of  sausage.  The  skin  is  thick,  but.  unlike 
that  of  mvxoedema,  it  is  soft,  moist  and  pliable.  This  enlargement 
rarely  extends  above  the  wrist  or  ankle. 

The  same  excessive  development  attacks  the  lower  jaw  so  that  a 
condition  of  marked  prognathism  is  presented.  The  maxilla  may  pro- 
ject so  far  forward  as  to  almost  seem  to  encompass  the  upper  jaw. 


THE   NEURONIC   DISEASES 


341 


The  nose.  lips  and  ears  are  enlarged.  The  whole  face,  especially 
the  lower  part  of  it.  is  both  lengthened  and  widened.  The  cheek-bones 
are  prominent.  The  eyelids  are  thickened  and  in  some  cases  the  tongue 
is  excessive  in  size. 

While  the  long  bones  of  the  arms  and  legs,  the  metacarpal  and 

FIGURE  51. 


Acromegaly.      (After  ]\Iarie.) 

metatarsal  bones  usuallv  escape,  the  clavicles,  sternum,  ribs,  patella  and 
vertebral  column  are  implicated.  Kyphosis  of  the  upper  dorsal  region 
is  a  very  frequent  symptom.  The  ensiform  process  of  the  sternum  is 
particularly  prominent  and  the  manubrium  is  so  thickened  that  a  per- 
cussion note  sounds  dull  (Erb).  The  abdomen  is  enlarged.  The  skin 
under  all  these  circumstances  may  continue  to  appear  perfectly  normal. 
As  a  patient  of  mine  once  expressed  it,  except  for  his  failing  eyesight 
and  general  change  of  shape,  he  couldn't  sec  that  he  was  in  any  way 


342  THE   NEURONIC   DISEASES 

abnormal.     In  rare  cases  the  heart  is  enlarged ;    the  penis  increased  in 
size  ;   the  testicles  atrophied. 

Eye  symptoms  are  not  infrequent  and  on  account  of  their  early 
appearance  are  often  of  extreme  importance.  Progressive  loss  of  vision 
from  optic  atrophy  is  the  more  common  trouble.  All  signs  of  irrita- 
tion, compression  and  destruction  of  the  optic  nerves  and  chiasma  may 
be  expected.  Optic  neuritis  is  much  rarer  than  optic  atrophy.  Hemi- 
anopsia of  various  types,  hemiachromatopsia,  unilateral  blindness  with 
hemianopsia  in  the  other  eye,  are  some  of  the  more  common  visual 
disturbances. 

Fig.  52  portrays  the  visual  fields  of  a  patient  of  mine  before  he 
went  totally  blind.  For  a  time  he  had  horizontal  hemianopsia,  so 
that  everything  below  the  level  of  his  eyes  was  invisible.  This  lasted 
about  six  months  and  gradually  passed  into  the  bitemporal  type  shown 
in  the  chart. 

The  ocular  muscles  are  sometimes  paralyzed  with  transrent  or 
permanent  attacks  of  diplopia.  Hemianopic  pupillary  rigidity  may  be 
present.  Exophthalmos  has  been  observed,  but  is  exceedingly  rare. 
Pressure  by  the  enlarging  hypophysis  explains  easily  these  various 
transient  and  permanent  ocular  manifestations. 

The  mental  state  of-  these  patients  is  always  somewhat  affected, 
though  not  so  characteristically  as  it  is  in  myxoedema.  They  are 
apathetic,  sluggish  and  devoid  of  energy.  A  sort  of  a  drowsy  air  and 
heaviness  belongs  to  them.  Their  movements  are  slow  and  awkward. 
There  is  a  weakness  of  their  muscles,  though  their  electrical  reactions 
are  unaltered.  The  condition  of  the  reflexes  varies,  but  is  of  no  special 
import. 

There  are  many  other  symptoms  that  may  appear,  but  are  not 
constant  enough  to  be  considered  typical  of  the  disease.  Some  of 
them  are  merely  indicative  of  an  intracranial  new  growth ;  others  are 
partly  due  to  the  disease  itself  and  partly  due  to  associated  derange- 
ments. The  thyroid  may  be  enlarged,  more  commonly  it  is  diminished 
in  size.  The  skin  may  be  thickened,  but  it  is  never  myxoedematous. 
The  muscles  are  sometimes  wasted.  The  larynx  may  be  altered  in 
shape  and  the  voice  rendered  deep  and  rough.  Its  mucous  membrane, 
like  that  of  the  mouth,  is  thickened.  All  of  the  five  senses  may  be 
blunted.  With  the  enlargement  of  the  heart  the  pulse  rate  may  be 
accelerated.  Impotence  is  usually  present.  Sweats  sometimes  occur, 
along  with  polyuria  and  polydipsia.  Bulimia  or  polyphagia  is  rather 
frequent.  Pigmentation,  moles,  warts,  keloids,  fibromata  and  neu- 
romata are  often  observed.  Dyspnoea,  palpitation,  vasomotor  neurosis, 
general  weakness  and  mental  depression  are  not  to  be  unexpected. 
Epileptic  attacks  have  been  recorded  in  rare  instances. 

Diagnosis. — The  diagnosis  depends  upon  the  onset  of  the  disease, 
the  peculiar  enlargement  of  the  lower  part  of  the  face  and  extremities, 
the  kyphosis,  the  ocular  symptoins  and  the  mentality. 

My.rcedema  and  cretinism  are  to  be  dift'erentiated  by  the  limitation 
of  the  enlargement  to  the  soft  tissues,  the  infiltration  of  the  subcutane- 
ous structures  of  the  entire  face,  hands  and  feet,  the  cold,  harsh,  dry 
state  of  the  skin,  the  alopecia  and  the  dementia.     The  bones  are  not 


THE   XEUROXIC   DISEASES 


343 


hypertrophied  as  they  are  in  acromegaly,  ncr  are  the  kyphosis  and 
prognathism  present. 

Gigantism  is  closely  related  to  acromegaly,  if  it  is  not  identified 
with  it.  Many  giants  become  acromegalics.  ]\Iassalongo,  Klebs,  Aleige 
and  others  beHeve  that  the  primary  disease  in  both  conditions  resides  in 
the  hypophysis  cerebri. 

Partial  gigantism  or  hypertrophy  of  special  parts  of  the  bodv 
{ hemihypertrophy,  macropodia,  macrocheiria.  etc.)  is  a  congenital 
trouble  and  is  distinguished  from  acromegaly  by  its  limitation  to  a 
particular  part  of  the  body  and  the  great  deformity  of  that  part. 

Syringomyelia,  adoposis  dolorosa,  elephantiasis,  leontiasis  ossea, 
diffuse  hyperostosis,  osteitis  deformans  have  all  their  own  characteristic 

FIGURE  ^2. 


Bitemporal  hemianopsia  in  a  case  of  acromegaly  in  which  complete  blind- 
ness ultimately  occurred.  Implication  of  the  optic  chiasm  is  clearly  shown  in  the 
perimetric  fields  taken  by  Dodd.  An  autopsy  being  denied,  I  assumed  from  the 
history  and  other  features  of  the  case  that  the  hypophysis  was  the  seat  of  a 
sarcoma. 


symptoms  and  can  be  distinguished  from  acromegaly  by  a  close  study 
of  the  total  clinical  picture  of  the  latter. 

In  osteitis  dcfoiiuans,  Paget"s  disease,  the  shafts  of  the  long  bones 
and  the  bones  of  the  cranium,  not  those  of  the  face,  are  enlarged  and 
softened.  The  long  bones  are  curved  from  the  weight  upon  them. 
Pains  are  present  in  them  almost  constanth".  There  seems  to  be  a 
close  relationship  between  this  affection  and  malignant  tumors.  Noth- 
ing is  known  of  its  etiology  and  its  treatment  is  without  results. 

Leontiasis  ossca  is  characterized  by  a  hyperostosis  of  the  cranial 
bones,  sometimes  also  of  the  face.  The  head,  face  and  neck,  with  both 
the  hard  and  soft  tissues,  increase  slowly  and  progressively.  Starr 
has  named  the  condition  megaloceplialy. 

Microniegalx  is  curious  as  the  antithesis  of  acromegaly.  It  was 
described  bv  Hutchinson  and  Gilford  in   1896.     There  is  a  defect  01 


344 


THE    XEUROXIC    DISEASES 


FIGURE  53- 


Pulmonary  osteo-arthropathj'  of  IMarie. 
(From  a  photograph  in  the  Pathological  :Museum  of  the  Med.  Dept.   of  the 
University  of  Illinois.) 


THE   NEURONIC   DISEASES 


345 


nutrition,  due  to  some  form  of  nervous  trouble,  which  is  seen  in  the 
smallness  and  immaturity  in  some  parts  and  consequently  a  relative 
largeness  and  apparent  prematurity  in  others. 

Marie's  hypertrophic  osteo-arthropathy,  which  occurs  in  associa- 
tion with  cardiac  and  pulmonary  disorders,  deserves  special  attention 
in  the  differential  diagnosis  of  acromegaly.  In  this  disease  the  bones 
are  more  involved  even  than  they  are  in  acromegaly.  Arnold  refers 
to  the  disease  as  a  secondary  hypertrophic  osteitis.  In  this  disease 
prognathism  is  not  present  and  kyphosis,  if  at  all  present,  is  lower  down 
in  the  spinal  column.  The  end  phalanges  are  peculiarly  deformed,  the 
wrist  and  ankle-bones  are  enlarged  and  the  finger  tips  are  club-shaped. 
There  is  no  uniformity  in  the  enlargements.  Moreover,  the  tongue  is 
not  affected  as  it  is  in  acromegaly,  and  the  mind  is  clearer. 

Prognosis. — Sternberg  notes  three  varieties  of  the  disease  in 
regard  to  its  course.  The  first  is  benign  and  may  last  fifty  yeais; 
the  second  is  the  usual  chronic  form  and  may  continue  from  eight  to 
thirty  years ;  the  third  is  the  acute,  malignant  form  that  terminates 
in  about  three  or  four  years.  The  disease  is  incurable,  but  at  times  it 
ceases  to  progress.  Relapses  occur.  Death  is  usualty  the  result  of 
marasmus,  diabetes,  heart  disease  or  some  intercurrent  trouble,  such  as 
cerebral  tumor,  bedsores,  secondary  disease  of  the  genito-urinary  tract. 

Treatment. — Treatment  is  unsatisfactory.  Organotherapy  has 
so  far  proved  to  be  entirely  ineffective.  Thyroid  and  pituitary  extracts 
have  been  administered  without  results.  It  has  been  reported  that  the 
iodides,  mercury  and  arsenic  have  seemed  to  have  arrested  the  disease 
— an  open  question  always  where  the  disease  is  prone  to  cease 
progressing  of  itself  at  times.  The  attempts  of  Caton  and  Paul  to 
bring  about  a  cure  by  extirpating  the  pituitary  gland  are  not  very  en- 
couraging. Symptomatic  treatment  is  about  all  that  we  can  offer  the 
victims  of  this  disease  at  the  present  time. 

ADIPOSIS  DOLOROSA. 

This  is  sometimes  called  Dercum's  disease,  because  it  was  first  de- 
scribed by  Dercum  in  1888.  A  considerable  number  of  cases  have 
been  described  since  and  even  examined  post-mortem. 

The  appearance  of  painful,  fatty  tumors  just  beneath  the  skin  in 
various  parts  of  the  body  is  its  cardinal  clinical  manifestation.  Changes 
in  the  thyroid  and  pituitary  bodies,  and  a  neuritic  condition  in  the 
peripheral  nerves,  are  its  chief  pathological  findings. 

The  disease  usually  appears  in  persons  of  a  nervous  temperament 
in  the  middle  period  of  life.  The  majority  of  the  cases  have  been 
over  forty  years  of  age.  The  women  are  often  hysterical,  and  both 
men  and  women  are  highly  susceptible  to  suggestion.  A  general 
asthenic  and  neuropathic  condition  usually  characterizes  them. 

The  pathology  and  pathogenesis  of  the  disea,se  are  not  clear.  The 
three  prominent  findings  are  the  fatty  tumors,  the  neuritis  and  the 
changes  in  the  thyroid  gland. 

The  fatty  tumors  occur  anywhere  on  the  body  just  beneath  the 
skin,  are  variable  in  size  and  in  no  way  difl'er  from  all  lipomata.     In 


346  THE   XEUROXIC   DISEASES 

the  tumors  the  nerves  seem  to  be  increased  m  number  and  are  in  a 
condition  of  interstitial  inflammation. 

The  thyroid  gland  exhibits  a  state  of  cystic  degeneration  with 
partial  atrophy  and  the  acini  filled  with  colloid  material. 

Adiposis  dolorosa  is  clearly  a  tropho-neurosis,  but  where  the  pri- 
mary source  of  the  trouble  is  to  be  looked  for  we  can  no  more  deter- 
mine here  than  we  can  in  any  other  tropho-neurosis.  As  Billings  has 
said,  it  is  as  yet  only  an  interesting  clinical  entity.  Its  classification 
must  await  further  knowledge  in  regard  to  the  pathogenesis  of  this 
disease  as  well  as  other  tropho-neuroses,  like  acromegaly. 

No  treatment  of  the  trouble  has  been  of  any  avail  in  checking  the 
formation  of  the  tumors.  A  few  cases  have  been  reduced  in  weight, 
the  asthenia  and  mental  depression  removed,  and  the  internal  meta- 
bolism apparently  placed  on  a  somewhat  better  basis  by  the  adminis- 
tration of  thyroid  extract. 

SCLERODERMA. 

This  remarkable  disease  is  believed  by  most  authorities  to-day  to 
be  a  tropho-neurosis. 

The  chief  feature  of  it  is  a  localized  or  diffuse  induration  of  the 
skin. 

Etiology. — iFemales  are  attacked  by  it  far  more  frequently  than 
males.  Kaposi  affirms  that  seventy-five  per  cent,  of  all  cases  are  women. 
The  middle  period  of  life  is  the  time  of  its  appearance  generally.  Osier 
believes  that  it  is  more  frequent  in  this  countr}^  than  statistics  would 
seem  to  indicate.  Its  immediate  cause  is  unknown.  Some  believe  the 
disease  is  a  tropho-neurosis  of  spinal  or  sympathetic  nerve  origin.  It 
certainly  seems  to  be  closely  related  to  progressive  facial  hemiatrophy, 
and  it  is  not  unfrequently  associated  with  Raynaud's  disease,  erythro- 
melalgia,  Addison's  disease,  rheumatic  troubles  and  exophthalmic 
goitre. 

Others  still  continue  to  regard  it  as  a  true  skin  disease,  due  to 
some  local  afifection.  The  old  view  that  it  was  due  to  closure  of  the 
thoracic  duct  or  other  lymphatics  and  a  stagnation  of  the  lymph  has 
not  been  confirmed  by  the  more  recent  examinations. 

Pathology  and  Pathogenesis. — Beyond  the  obvious  symp- 
tomatic changes,  the  pathological  findings  are  not  of  special  significance. 
The  changes  in  the  skin,  the  connective  tissue  over-growth,  the  disap- 
pearance of  the  subcutaneous  fat.  the  increase  of  elastic  fibers,  have 
given  the  name  to  the  disease.  The  vessels  are  numerous,  but  dimin- 
ished in  calibre. 

The  entire  affection  is  in  all  likelihood  a  primary,  connective- 
tissue  hypertrophy  of  nervous  origin  or  disturbance,  ending  in  resolu- 
tion or  atrophy.  The  neurotic  nature  of  the  disease  is  strongly  sug- 
gested by  numerous  observations.  Schwimmer's  cases  revealed  disease 
of  the  peripheral  nerves.  Westphal  saw  significant  changes  in  the 
brain.  Eulenberg  and  others  have  reported  the  association  of  pro- 
gressive facial  hemiatrophy  and  other  tropho-neuroses  with  the  disease. 
In  some  cases  marked  arthritic  changes  have  been  observed  not  unlike 
those  seen  in  the  Charcot  joint. 


THE   NEURONIC   DISEASES 


347 


Symptoms. — In  exceptional  cases  these  begin  with  chills,  fever  and 
-other  signs  of  inflammation.  More  generally,  however,  the  first  symp- 
tom noticed  is  the  growing  stiffness  and  rigidity  of  some  portion  of  the 
skin.  This  slowly  increases  during  months  and  years.  It  is  most 
noticeable  and  often  limited  to  the  upper  extremity,  though  it  may 
appear  in  the  lower.  It  may  occur  in  circumscribed  patches  or  be 
diffused  over  a  very  large  area.  Sometimes  the  spots  are  disseminated 
at  first  and  later  on  run  together.  The  face  and  neck  are  not  unfre- 
quently  involved.  The  trouble  is  usually  bilateral,  but  is  sometimes 
unilateral.  The  lips  may  be  retracted  or  the  gums  exposed.  The 
nose  may  be  greatly  attenuated,  giving  the  physiognomy  a  very  dis- 
agreeable appearance.  The  hands  are  tense  and  glossy,  the  fingers 
thinned  and  club-shaped  and  the  me'tacarpo-phalangeal  articulations 
sometimes  subluxated.  As  the  subcutaneous  fat  atrophies  the  skin 
clasps  the  bone  and  reveals  sharply  its  outlines. 

The  diseased  skin  is  cold,  thick,  rigid  and  hard.  It  feels  like  the 
derma  of  a  frozen  corpse.  It  is  not  sharply  delimited  from  the  normal 
skin,  though  it  often  has  a  hypersemic  tract  around  it.  It  is  swollen 
in  the  neighborhood  or  shrunken.  The  surface  of  the  epiderma  is 
smooth,  shining,  scaly,  whitish  in  color  or  pigmented  in  patches.  In 
the  beginning  it  is  often  merely  cedematous  and  hypertrophic. 

The  mucous  membrane  of  the  mouth  and  vagina  often  exhibit 
similar  alterations. 

Wrinkling,  of  course,  ceases,  and  all  actions  implicating  the  sitm, 
like  laughing,  winking,  breathing,  become  difficult  and  impeded.  The 
■muscles  beneath  are  usually  indurated,  shriveled  and  atrophied.  The 
tones  are  thinned.  Peculiar  constrictions,  mutilations,  even  spon- 
taneous amputations  and  ulcerations  have  all  been  seen.  Sclerodactyly 
or  characteristic  crippling  of  the  fingers  occurs. 

The  sensibility  is  rarely  involved,  though  it  may  be  somewhat 
blunted.  The  tenseness  is  felt  by  the  patient  and  sometimes  pain,  itch- 
ing or  parsesthesia.  Paralytic  symptoms  occasionally  appear.  Hypo- 
chondriacal neurasthenia  usually  exists.  There  is  general  marasmus 
and  the  patient  is  depressed  mentally.  In  some  instances  amyloid  de- 
generation has  been  found  post-mortem  in  the  lungs,  heart  and 
kidneys. 

Besides  the  diseases  mentioned  under  the  head  of  etiology,  sclero- 
derma has  been  complicated  bv  eczema,  acne,  erysipelas,  herpes  zoster, 
variola,  morphoea  and  keloid.    Its  diagnosis  is  not  difficult. 

Prognosis. — Rarely  the  disease  disappears  by  involution.  The 
retrogression  is  gradual,  often  only  in  spots.  The  trouble  is  always 
a  chronic  one,  with  remissions  now  and  then  during  its  long  course. 
Most  cases  go  on  to  the  formation  of  ulcerations,  mortification  and 
other  complicating  conditions,  suffering  all  the  while  wath  pains,  insom- 
nia, bad  nutrition,  and  finally  die  from  marasmus. 

Treatment. — There  is  no  known  cure  for  scleroderma.  Nutri- 
tion, rest,  good  general  hygiene  and  such  general  tonics  as  iron,  qui- 
nine, arsenic  and  cod-liver  oil  are  in  order  in  all  cases.  Salol  internally 
in  fifteen-grain  doses  three  times  a  day  has  seemed  to  have  been  bene- 
£cial  in  a  few  instances.     Improvement  has  occurred  in  many  cases 


348  THE   XEUROXIC   DISEASES 

under  thyroid  medication.  Galvanization  of  the  sympathetic  was 
urged  by  Schwimmer.  and  the  local  application  recommended  by  Pif- 
fard,  Fieber  and  others. 

Ointments  and  local  medication  are  frequently  grateful.  Xaphthol 
salicylate  ointment,  mercurial  and  iodine  soaps  and  preparations,  and 
copper  oleate  are  thus  available.  To  these  should  be  added  local  baths 
and  massage. 

PROGRESSR'E  FACIAL  HEMIATROPHY. 

This  is  a  very  rare  affection  in  which  one  side  of  the  face  under- 
goes a  remarkable  progressive  wasting,  and  is  probably  due  to  a  dis- 
turbance of  the  trophic  functions  of  the  trigeminal  nerve.  The  earliest 
accounts  of  it  were  given  by  Parry  and  Romberg. 

Etiology. — Little  is  known  of  its  causation.  It  prevails  more 
among  women  than  among  men.  It  is  first  recognized  in  early  adult 
years,  though  it  usually  starts  in  childhood  and  in  many  cases  seems, 
to  be  congenital  in  origin.  Being  a  chronic,  progressive  disease,  it  may 
run  on  into  old  age,  but  it  is  rarely  ever  seen  to  start  after  thirty. 
It  has  followed  slight  injuries  to  the  face  and  head,  acute  rheumatism,, 
scarlatina,  diphtheria  and  typhoid  fever.  It  is  not  known  whether  the 
neuralgic  pains  in  the  fifth  nerve  that  sometimes  accompany  it  earl}'  in 
its  course  bear  a  causal  or  symptomatic  relationship  to  it.  A  genei^l 
inherited  neuropathic  taint  has  been  detected  in  some  cases. 

Pathology  axd  Pathogexesis. — The  only  pathological  findings 
that  are  of  any  significance  are  those  which  enter  into  the  symptomatol- 
og\-  of  the  disease. 

The  pathogenesis  of  the  disease  is  almost  wholly  conjectural.  I 
am  inclined  to  follow  Gowers"  view  that  it  is  an  organic  affection  of  the 
fifth  ner\^e  or  its  Gasserian  ganglion.  The  marked  limitation  of  the 
symptoms  to  the  peripheral  area  innervated  by  this  nerve  is  only  ex- 
plainable on  this  basis.  The  trophic  character  of  the  predominant 
symptoms  and  the  implication  of  both  the  sensory  and' trophic  branches 
of  the  nerve  point  to  the  ganglion  as  the  primary  seat  of  the  trouble. 
Its  connection  with  slight  injuries  and  local  infective  processes  are 
highly  suggestive  of  the  nature  of  the  disease  process. 

Most  authors  regard  the  trouble  as  primarily  a  trophoneurosis. 
Those  who  try  to  class  the  disease  with  exophthalmic  goitre  and 
migraine  are  illogical.  In  some  respects  it  resembles  scleroderma  and 
yet  there  is  not  that  sharp  trigeminal  distribution  of  the  manifestations 
in  scleroderma  that  there  is  in  this  disease.  ^loreover  scleroderma 
never  follows  trigeminal  disease  under  any  circumstances  so  far  as  we 
know.     It  is  a  more  general  trophoneurosis. 

Oppenheim  leans  toward  the  sympathetic  hypothesis.  Bitot  thinks 
it  is  a  primary  skin  disease.  IMobius  regards  it  entirely  as  an  infec- 
tive process  following  some  local  injury  or  sore  in  the  neighborhood. 

Symptoms. — The  symptom  of  the  disease  is  described  in  its  name, 
progressive  facial  hemiairophy.  Gradually  there  is  a  diminution  in  the 
general  bulk  of  one  side  of  the  face.  In  this  all  the  tissues  partake, 
the  skin,  the  subcutaneous  elements,  the  muscles  and  e^'en  the  bones^ 


THE   NEURONIC   DISEASES 


349 


The  skin  tightens  down  and  clasps  the  bones  so  as  to  emphasize  their 
■outlines.  The  hairs  fall  off  and  the  sebaceous  glands  shrivel  up.  The 
cartilages  of  the  nose  waste  causing  it  to  be  grossly  distorted.  The 
lips  diminish  on  one  side  and  are  sunken.  The  perspiration  may  be 
•excessive  while  the  local  temperatvire  remains  normal.  The  bones 
are  decidedly  smaller  on  the  affected  side.  One  side  of  the  face  is  full 
and  youthful,  the  other  worn,  haggard  and  aged  looking. 

The  strange  physiognomy  thus  presented,  a  sort  of  double  indi- 
A^idual  as  it  were,  is  so  striking  that  the  diagnosis  can  be  made  at  a 
glance.  The  palate  and  tongue  are  usually  unaffected.  Sometimes, 
"however,  they  also  have  been  wasted  on  the  same  side. 

Not  in  all  cases  are  the  muscles  implicated,  though  the  frequent 
paresis  of  the  pteragoids,  masseter,  temporal,  and  the  fibrillation  and 
tremor  in  them,  point  to  implication  of  the  motor  root.  The  electrical 
reactions  are  usually  preserved,  thus  distinguishing  the  disease  from  a 
true  progressive  myopathy. 

Sensibility  as  a  rule  is  unaffected  though  in  some  cases  intense 
neuralgic  pains  occur  early  and  anaesthesia  or  at  least  hypsesthesia 
later.  The  arteries  and  veins  do  not  seem  to  vary  in  size.  The  saliva 
and  tears  are  permitted^to  flow  as  usual.  The  organs  of  special  sense 
seem  to  be  undisturbed  so  far  as  their  functions  are  concerned.  Bilat- 
eral atrophy  has  been  seen  occasionally  and  once  atrophy  of  the  skin 
and  subcutaneous  tissue  in  the  back  and  arm  of  the  same  side  was 
seen. 

The  disease  progresses  steadily  for  a  number  of  years  and  then 
remains  stationarv^  for  the  rest  of  life, 

Oppenheim  notes  the  occurrences  of  the  disease  repeatedly  with 
neuralgia,  epilepsy  and  the  psychoses,  with  chorea,  spasm  of  the  mus- 
cles of  the  face,  jaw  and  tongue,  once  each  with  tabes,  syringomyelia 
and  disseminated  sclerosis. 

The  diagnosis  must  be  differentiated  from  congenital  inequality 
between  the  two  sides  of  the  face,  fromi  facial  atrophy  in  anterior 
poliomyelitis,  and  in  hemiplegia  of  children  and  adults.  It  must  be 
kept  clearly  apart  from  acquired  facial  hemihypertrophy,  as  described 
by  Montgom.er}',  which  by  contrast  may  lead  to  a  diagnosis  of  hemia- 
trophy of  the  other  side.  And  it  should  be  distinguished  carefully  from 
scleroderma  and  morphcea.  If  it  is  to  be  regarded  as  a  result  of  trige- 
minal neuritis,  according  to  Mendel's  findings,  then  it  should  also  be 
carefully  differentiated  from  atrophy  due  to  nuclear  lesions  and  to 
sympathetic  nerve  paralysis. 

The  gross  diagnosis  is  easy.  The  minute  differential  diagnosis 
is  sometimes  rendered  confusing  because  we  are  ignorant  of  the  exact 
pathology  of  the  disease  and  its  limitations.  Some  authorities  un- 
doubtedly include  more  in  progressive  facial  hemiatrophy  than  oth- 
ers do. 

Prognosis. — Favorable  as  to  life.  Bad  as  to  recovery.  The  dis- 
ease is  chronic  and  progiessive  but  usually  becomes  stationary  after  a 
number  of  years.  The  pains  are  sometimes  wearing  and  the  limita- 
tion of  movements  in  the  muscles  of  mastication  is  sometim.es  annoy- 


350  THE   NEUROXIC   DISEASES 

ing ;  otherwise  the  patients  are  sound  and  well  and  suffer  no  very  great 
discomfort. 

Treatment.- — It  is  not  amenable  to  any  known  form  of  treatment. 

AINHUM. 

This  is  a  disease  of  the  negro  and  is  probably  a  trophoneurosis^ 
It  was  first  described  by  Silva  Lima,  of  Bahia,  but  cases  have  been  re- 
ported by  Hornaday  and  Pittmann,  Duhring,  Shepherd,  and  Morrison. 
It  is  rare  in  this  country  but  has  been  frequently  seen  in  South  Amer- 
ica and  somewhat  in  Asia.  Its  cause  is  not  known.  There  is  a  singu- 
lar constriction  of  the  skin  formed  about  the  base  of  one  or  more  toes. 
Finally  a  deep  furrow  completely  encircles  the  member,  the  bloodves- 
sels are  obliterated  and  amputation  takes  place.  The  little  toe  seems 
to  be  the  favorite  victim.  It  is  a  chronic  trouble  and  the  toe  does  not 
drop  off  often  for  years.  There  is  no  sign  of  inflammation  and  usually 
no  pain  is  connected  with  it. 

ORGANIC  NEURONIC  DISEASES. 

THE    SYSTEM    DISEASES. 

THE  NATURE  OF  THE   SYSTEM  DISEASES   AND  THEIR 
CLASSIFICATION. 

In  the  preceding  chapters  the  neuroses  and  psychoneuroses  have 
been  discussed.  As  coiTMnonly  accepted,  these  are  functional  derange- 
inents  of  the  neurones  or  functionating  part  oif  the  nervous  system. 
Our  present  means  of  scientific  research  is  not  such  as  tO'  enable  us 
to  declare  positively  what  the  nature  of  the  change  is  in  the  neurones 
or  in  their  relationship  to  one  another  whereby  the  alteration  of  func- 
tion, upon  which  we  call  the  condition  one  of  disease,  is  brought 
about.  And  yet  in  regard  to  these  neuroses  and  psychoneuroses,  cer- 
tain facts  stand  out  with  a  most  suggestive  prominence  and  upon  these 
facts  we  can  at  least  frame  a  working  hypothesis. 

In  the  first  place  it  is  to  be  noted  that  heredity,  tox(Bmia,  shock, 
strain,  malnutrition  and  overexertion-  play  the  greatest  role  in  their 
etiology.  These  causes  are  of  a  general  nature  and  presumably  act 
upon  all  parts  of  the  nervous  apparatus  in  the  same  way.  Every 
neurone  is  subjected  to  the  same  deleterious  influence.  The  nervous 
system  is  usually  the  victim  in  toto. 

Another  fact  that  stands  prominently  forth  is  that  no  changes  of 
any  sort,  whereupon  the  symptoms  of  these  diseases  can  be  explained, 
have  ever  been  seen  in  the  nervous  elements.  We  have  to  assume  that 
the  primary  trouble  is  inherent  in  the  neurones  themselves  and  entirely 
beyond  our  ken.  It  is  born  and  has  its  expression  there.  While  we 
cannot  say  whiat  this  inherent  trouble  is,  we  can  very  definitely  declare 
that  it  involves  the  two  primary  functions  of  the  neurones  concerned. 


THE   NEURONIC   DISEASES 


351 


namely,  their  power  of  exhibiting  ncurihty  and  their  power  of  main- 
taining their  own  nutrition.  In  the  very  nature  of  things  the  former 
function  is  dependent  upon  the  latter. 

When  a  neurone  functionates  abnormally,  it  is  mere  truism  to  say 
that  its  power  of  exhibiting  sensibility  is  disturbed.  Whether  this  is 
always  due  to  a  disturbance  of  its  power  of  maintaining  its  own  nutri- 
tion, as  it  undoubtedly  is  in  a  large  nimiber  of  diseases,  or  whether 
shock,  toxaemia,  strain,  etc.,  can  directly  cause  it  to  act  thus  abnor- 
mally without  affecting  in  the  least  its  power  of  self-nutrition,  seems 
to  be  a  debatable  question. 

Change  of  neurility  without  change  of  nutrition  or  structure  would 
indeed  be  a  true  functional  disease.  It  could  hardly  continue  long,  it 
seems  to  me,  without  some  structural  effect  being  produced  upon  the 
intimate  physio-chemical  constituents  of  the  neurone.  So  intimately 
related  are  the  neural  and  nutritional  functions  of  each  individual 
neurone,  that  it  is  all  but  inconceivable  that  one  should  long  be  changed 
without  some  change  in  the  other. 

Underlying  all  functional  diseases,  I  take  it  therefore,  there  is 
sooner  or  later  some  undiscoverable  but  structural  change.  The  change 
may  continue  to  be  undiscoverable  and  the  trouble  continue  to  be 
spoken  of  as  functional. 

There  are  changes  in  the  neurones  in  some  diseases,  however,  that 
are  observable  under  our  present  staining  and  microscopic  methods  of 
examination.  We  speak  of  these  as  degenerative  changes.  Every 
neurone  in  the  body  is  liable  to  them  and  all  parts  of  the  neurone,  cell 
and  process,  may  be  implicated. 

There  are  all  degrees  of  degeneration  from  that  which  is  scarcely 
detectable  down  to  the  complete  atrophy  and  disappearance  of  the  en- 
tire neurone. 

Every  indication  points  toward  the  fact  that  the  degeneration  is 
a  nutritive  change  and  that  it  is  dependent  upon  the  failure  of  the 
nutritional  function  of  the  cell-body.  This  is  called  primary  degen- 
eration. 

When  any  part  of  a  neurone  is  severed  from  its  cell-body,  com- 
pletely or  partially,  that  part  immediately  begins  to  undergo  degen- 
eration. If  the  separation  is  complete,  it  will  disappear  entirely.  This 
is  termed  secondary^  or  Wallerian,  degeneration. 

Two  facts  are  obvious,  therefore,  in  regard  to  all  neuronic  degen- 
eration, namely,  that  though  the  process  be  practically  identical  in  both 
the  primary  and  the  secondary  forms,  in  the  former  it  is  caused  imme- 
diately by  an  inherent  functional  nutritive  disorder  within  the  cell 
bodies  themselves,  and  in  the  latter  by  the  gross  separation  of  the  de- 
generating parts  from  their  centers  of  nutrition. 

The  distinction  is  an  important  one.  The  primary  forms  are  thus 
the  result  of  a  profound  neuronic  deficiency.  In  accordance  with  all 
clinical  evidence,  this  is  largely  due  to  hereditary,  toxaemic,  shock, 
exhaustion  and  straining  influences  just  as  the  functional  deficiencies 
in  the  neuroses  are,  only  more  so.  In  these  cases  the  vigor  of  the 
cause  or  the  limited  resistance  of  the  neurone  constituents  is  such  that 
the  mal-nutritive  process  emerges  from  its  obscurity   and   reaches   a 


352  THE   NEURONIC   DISEASES 

Stage  where  we  can  observe  it  with  our  microscope  and  other  aids. 
When  it  has  reached  this  stage — a  stage,  remember,  which  does  not 
indicate  the  beginning  or  the  end  of  a  new  process,  but  merely  the 
hmit  of  our  powers  of  detection — we  term  the  degeneration  organic. 

A  primary  organic  degeneration  then  is .  merely  a  gross,  observ- 
able deterioration,  of  the  neurone  resulting  from  a  profound  disturbance, 
inherited  or  acquired,  in  the  nutritive  function  of  the  cell-body  of  the 
neurone.  This  would  make  it  appear,  therefore,  that  primary  organic 
degenerative  neuronic  diseases  are  in  close  relationship  to  the  neuroses. 
Per'haps  the  better  way  to  state  it  would  be  tliat  the  neuroses  are  at 
the  beginning  of  the  organic  neuronic  primary  degenerations  or  are 
earlier  forms  of  organic  troubles. 

As  everybody  knows  the  earliest  clinical  manifestations  of  all  de- 
generative diseases  are  functional  or  neurosis-like  in  character.  This 
is  so  common  an  observation  that  it  needs  but  to  be  stated  tO'  be  readily 
acknowledged.  It  is  the  reason  for  most  of  the  diagnostic  mistakes 
that  are  made  in  the  earliest  stages  of  the  organic  neuronic  diseases. 

Two  great  forces  underlie  all  of  these  primary  organic  degenera- 
tions. The  one  is  the  inherited  and  represents  a  diminished  vitality, 
a  lessened  power  of  resistance  ag'ainst  ordinary  stimuli,  or  even  extra- 
ordinary stimuli,  in  the  constituents  of  the  neurones ;  the  other  is  the 
acquired  and  is  revealed  in  the  special  virulence  or  vigor  of  the  exciting 
cause. 

In  most  cases,  both  of  these  forces  are  in  more  or  less  operation 
at  the  same  time,  though  in  some  afit'ections,  like  Friedreich's  disease 
for  instance,  the  one  will  be  the  dominant  factor,  whereas  in  other 
affections,  like  locomotor  ataxia,  the  other  will  be  most  in  evidence. 

For  the  hereditary  factor,  with  all  its  tendencies,  Gowers  has  re- 
cently suggested  the  name  abiotrophy  and  defined  it  as  the  ''degener- 
ation or  decay  of  parts  in  consequence  of  a  defect  of  vital  endurance." 
This  defect  of  vital  endurance  characterizes  practically  all  of  the  pri- 
mary organic  degenerative  diseases  more  or  less. 

The  process  which  seems  to  take  place  in  the  cell  bodies  is  the 
same  as,  or  is  very  closely  related  to,  that  which  is  technically  called 
chromatolysis.  This  term  is  now  employed  to  cover  the  alterations 
in  the  cell-body  whidi  we  can  observe  and  which  are  of  the  nature  of  a 
degeneration.     They  are  not  in  any  sense  of  the  zvord  inflammatory. 

Chromatolysis  is  a  specific  nervous  phenomenon  and  is  not  wit- 
nessed in  any  other  tissue  of  the  body.  There  are  various  degrees 
of  the  process  down  to  complete  atrophy  and  annihilation  of  the  cell. 
The  accompanying  illustrations  show  roughly,  but  forcibly  the  be- 
ginning of  the  chromatolytic  process.  Tlie  causes  of  these  changes 
have  already  been  dwelt  upon  in  speaking  of  the  degenerative  process 
in  general.  Anything  that  profoundly  disturbs  the  nutrition  of  the 
cell  tends  toward  its  chromatoh'tic  modification.  Hence  an  inheritance 
of  poor  vitality,  a  toxsemda  of  marked  virulence,  an  exhaustive  strain, 
or  a  tremendous  shock  may  initiate  it. 

A  certain  degree  of  chromatolysis  usually  occurs  in  cases  of  sec- 
ondary, or  Wallerian,  degeneration,  as  well  as  in  those  of  primary 
degeneration.    The  proximal  end  of  the  neurone  wastes  somewhat  while 


THE  NEURONIC  DISEASES 


353 


the  distal  or  severed  end  is  disappearing.  This  is  especially  seen  after 
amputations  and  in  the  rare  conditions  of  neuromyelitis  and  ascend- 
ing degeneration  of  the  motor  nerves.  This  upsets  in  part  the  Wal- 
lerian  law  that  when  a  nerve  is  severed  from  its  nutritive  center,  the 
distal  or  severed  end  only  undergoes  degeneration;  for  here  we  ob- 
serve the  proximal  end  also  undergoing-  degeneration.  As  early  as 
twenty-four  hours  after  the  damage  is  done  to  the  peripheral  nerve, 

FIGURE  54. 


X 


A. 


A.  Normal  nerve-cell,  stained  by  the  Nissl  method.     (After  Marinesco-Ray- 
mond. 

B.  Disease  of  the  cell  after  section  of  the  peripheral  nerves.     Chromatolj'sis 
with  nuclear  displacement.     (After  Oppenheim.) 

changes  have  been  observed,  chromatolytic  in  character,  in  the  related 
cell  bodies  of  the  medullary  nuclei  and  anterior  cornua.  Restitution 
sometimes  takes  place;  not  infrequently  complete  atrophy  occurs  un- 
der these  remarkable  circumstances. 

The  explanations  offered  for  this  phenomenon  are  all  hypothetical 
though  plausible.  For  example,  it  was  for  a  time  supposed  to  be  a 
sort  of  retrograde  process,  a  backward-going  Wallerian  degeneration. 


354  THE   NEURONIC   DISEASES 

Many  to-day  believe,  however,  with  Marinesco,  Goldscheider,  Len- 
hossek  and  others,  that  in  health  the  nutrition  of  the  cell  is  excited 
and  maintained  by  the  usual  sensory  and  volitional  impulses.  When 
the  cell  is  put  out  of  action,  as  it  were,  by  these  peripheral  degener- 
ative conditions,  it  is  not  called  upon  to  functionate  as  it  was  wont  to 
do,  and  is  therefore  not  made  4he  recipient  of  its  wonted  stimulus.  Its 
nutrition  therefore  flags  and  it  undergoes  a  chromatolytic  deterioration. 

The  observable  phenomena  in  chromatolysis  I  have  briefly  de- 
scribed elsewhere.  They  consist  first  of  a  swelling  and  blurring  of 
the  cell,  then  of  a  shriveling  up  with  a  serration  of  its  edges.  The  nu- 
cleus moves  to  one  side  (decentralization)  and  the  nucleolus  gradually 
disappears.  The  whole  cell  has  its  pov^^er  to  absorb  staining  reagents 
markedly  lessened.  The  chromatin  bodies  move  toward  the  periphery 
and  the  dumbbell-like  bodies  closely  hug  the  edge  of  the  nucleus.  The 
latter  bodies  stain  deeply.  Vacuolation  appears  in  the  cell  substance. 
As  the  process  advances  general  atrophy  of  the  neurone  takes  place 
and  the  latter  finally  disappears.  If  regeneration  should  occur,  the 
reverse  phenomena  obtain,  but  much  more  slowly.  The  space  that  is 
left  vacant  is  then  filled  with  an  overgrowth  of  neuroglia  and  connec- 
tive tissue  (secondary  sclerosis).  In  the  secondary  degenerations  the 
cell-body  undergoes  a  lesser  degree  or  partial  chromatolysis,  though 
sometimes  it  may  be  complete  and  atrophic.  Thte  neuraxoiie,  both  that 
part  of  it  which  has  been  severed  from  the  cell  and  that  which  still  re- 
mains attached,  undergoes  the  well-known  fibre  degeneration;  abso- 
lutely and  completely  in  the  former,  relatively  to>  the  degree  of  the  cel- 
lular chromatolysis  in  the  latter. 

It  is  clear  thus  far  that  neuronic  degeneratiou  is  a  special  patho^ 
logical  phenomenon  and  characterizes  the  nobler  elements,  the  true 
nervous  apparatus.  The  organic  (observable)  neuronic  changes  and 
the  functional  (non-observable)  neuronic  changes  constitute  the  basis 
of  the  true  nervous  diseases,  the  diseases  that  belong  to  the  nervous 
system  per  se. 

These  diseases  in  all  probability  differ,  so  far  as  their  being  or- 
ganic or  functional  is  concerned,  in  degree  rather  than  in  kind.  There- 
fore, I  have  grouped  these  two  great  sets  of  diseases  together  and  made 
a  special  class  of  them,  calling  them  the  neuronic  diseases. 

We  have  just  seen,  however,  that  in  the  subclass  of  neuronic  dis- 
eases, called  the  organic,  the  degenerative  process  is  primary  and  sec- 
ondary in  its  origin.  This  of  course  is  merely  another  way  of  saying 
that  there  are  two  great  groups  of  causes  that  damage  the  nutritive 
function  of  the  neurone  and  its  several  parts.  The  one  group  of 
causes  go  to  the  very  fountain  head  of  nutrition  and  overthrow  it  by 
directly  hurting  the  cell-body.  The  other  group  of  causes  merely  ciit 
off,  compress  or  otherwise  mutilate  the  neurone  and  its  processes  so  as 
to  interfere  v^ith  its  vitality.  Except  in  regard  to  heredity,  we  may 
say  of  both  groups  of  causes  that  they  are  from  without  or  are  extra- 
neural.  A  toxin  that  sets  up  a  primary  degeneration  is  as  much  an  ex 
ternal  disease  affecting  the  neurones  secondarily  as  is  a  stab  wound 
that  severs  the  spinal  cord  and  sets  up  a  secondary  degeneration.  In 
both  troubles  the  degenerations  per  se  are  the  same,  though  their  loca- 


THE   NEURONIC   DISEASES 


355 


tions  and  immediate  causes  are  different.  A  poison  that  initiates  a 
primary  polyneuritis,  so-called,  is  really  as  much  of  an  extraneural 
cause  as  is  a  cerebral  embolus  that  cuts  off  the  blood  supply  of  a  cer- 
tain area  of  cerebral  neurones.  The  peripheral  degeneration,  as  a 
mere  disease  process,  is  as  much  of  a  degeneration  as  that  which  oc- 
curs in  the  central  trouble. 

It  is  obvious,  therefore,  that  our  classification  of  these  degenera- 
tions into  primary  and  secondary  is  quite  artificial  and  is  made  only 
for  coarse  practical  purposes.  This  is  only  too  well  demonstrated,  and 
to  our  chagrin,  when  we  try  to  decide  wdiether  a  certain  degenerative 
disease  is  a  primary  or  a  secondary  one.  We  tacitly  admit  in  such  in- 
stances that  the  degeneration  is  one  and  the  same  but  we  can't  make 
up  our  minds  whether  the  causative  factor  is  the  primary  or  the  sec- 
ondairy  one.  How  often  this  is  the  case !  It  is  perhaps  best  illustrated, 
however,  in  the  development  of  our  ideas  in  regard  to  locomotor  ataxia. 
One  hypothesis  has  declared  that  the  degeneration  of  the  peripheral 
sensor}^  neurone  is  the  direct  result  of  the  syphilitic  virus  in  some  way. 
Another  hypothesis  argues  that  it  is  due  to  a  slow  compression  oi  the 
posterior  nerve  roots  by  the  specifically  inflamed  meninges.  The 
former  explanation  makes  of  tabes  a  primary  degeneration ;  the  latter 
relegates  it  to  a  secondary  degeneration  from  meningitis. 

Take  as  another  illustration  multiple  neuritis.  A  degeneration  of 
the  peripheral  neurones  is  observed  in  practically  all  cases.  In  the 
toxic  cases  it  is  sometimes  a  primary  degeneration  and  due  to  a  polio- 
myelitic  process ;  sometimes  a  secondary  degeneration  and  due  to  a 
compressing  interstitial  inflammation. 

Landry's  paralysis  may  be  an  initial  stage  of  primary  or  secondary 
degeneration  in  the  peripheral  motor  neurones.  Ophthalmoplegia  is 
both  a  primary  and  a  secondare'  degenerative  disease. 

The  point  I  wish  to  emphasize  by  these  and  numerous  other  illus- 
trations that  could  be  cited  is  that  in  these  organic  neuronic  degenera- 
tions we  have  a  sort  of  borderline  group  of  diseases  which  lie  between 
the  purely  inherent  neuronic  troubles,  like  the  functional  diseases,  and 
the  non-neuronic  troubles  like  the  inflammations  and  neoplasms  that 
only  affect  the  neurones  secondarily  and  by  compression. 

Therefore,  it  is  difficult  to  classify  positively  all  of  the  organic 
neuronic  degenerations,  for  sometimes  w^e  behold  them  as  primary  pro- 
cesses, at  other  times  as  secondary  processes.  xA.nd  yet  I  feel  that  the 
best  interests  of  neurology  will  be  subserved  by  a  general  classification 
founded,  so  far  as  present  data  will  permit,  upon  the  distinction  be- 
tween the  primar}^  and  the  secondary  organic  neuronic  degenerations. 

The  two  sets  of  diseases  in  which,  the  primary-  and  secondary 
neuronic  degenerations  respectively  appear  are  so  dissimilar  in  respect 
to  etiology,  prognosis  and  treatment  that  for  this  reason  alone  it  seems 
to  me  most  practical  to  emphasize  the  distinction  by  thus  making  it  the 
basis  of  a  classification.  A  degeneration  of  the  p}Tamidal  tracts  from 
an  intracranial  hemorrhage  may  be  no  less  serious,  as  a  degeneration, 
than  that  which  we  see  in  amyotrophic  lateral  sclerosis,  but  the  sec- 
ondary nature  of  the  former  and  the  primary  nature  of  the  latter  in- 
siPMate  an  important  distinction  between  them  when  it  comes  to  the 


356  THE   NEURONIC   DISEASES 

matter  of  their  prevention  by  early  treatment,  or  to  the  question  of 
prognosis  when  they  first  begin  to  appear.  Primary  degenerations 
are  usually  hopeless,  whereas  secondary  degenerations,  especially  if 
they  don't  implicate  the  nutritional  function  of  the  neurone  bodies,  are 
comparatively  hopeful. 

In  taking  up  what  I  have  termed  the  organic  neuronic  diseases  in 
the  next  chapter,  I  have  in  mind  especially  the  primary  organic  neu- 
ronic degenerations.  The  secondary  degenerations  will  be  incidentally 
referred  to  in  the  latter  part  of  the  book  as  the  expected  or  accidental 
sequelae  of  the  extra-neuronic  diseases  in  which  they  happen  to  ap- 
pear. To  illustrate,  progressive  muscular  atrophy  with  its  atrophic 
paralysis  is  regarded  as  a  primary  degeneration  and  is  therefore  classi- 
fied and  treated  here  as  an  organic  neuronic  disease ;  acute  anterior 
poliomyelitis  with  a  similar  atrophic  paralysis  is  regarded  as  an  in- 
flammatory disease  of  the  spinal  cord  and  is  therefore  classified  and 
treated  elsewhere  as  a  non-neuronic  afifection.  The  neuronic  degener- 
ation here  is  regarded  as  a  secondary  process,  an  early  sequel  as  it 
were,  of  the  infectious  myelitis. 

Where  a  disease  happens  to  be  either  a  primary  or  a  secondary 
degenerative  trouble,  it  will  be  treated  of  most  fully  in  the  section 
wherein  it  would  naturally  fall  by  the  greater  prominence  of  the  one 
or  the  other  of  its  manifestations,  and  it  will  be  only  incidentally  men- 
tioned in  the  other  section.  Moreover  in  this  way,  where  the  classi- 
fication of  the  disease  is  in  doubt  among  the  authorities,  I  will  intimate 
my  own  opinion  in  regard  to  it. 

System  Diseases. — The  sharp  localization  of  the  lesion  and  its 
limitation  to  certain  definite  neurones  is  a  remarkable  characteristic  of 
these  organic  degenerative  diseases.  The  phenomenon  has  always 
aroused  the  greatest  investigative  enthusiasm  among  neurologists,  and 
there  have  not  been  wanting  plenty  of  hypotheses.  To-day,  however, 
we  are  as  much  in  the  dark  as  ever.  Why  such  a  general  cause  as 
heredity  or  toxaemia  should  provoke  a  degeneration  in  a  particular  set 
of  neurones,  and  not  in  others,  is  still  a  profound  mystery.  And  even 
in  the  secondary  degenerations  there  is  no  adequate  explanation  as  to 
why  certain  groups  of  neurones  should  be  more  implicated  than  oth- 
ers. If  the  explanation  is  to  be  found  in  a  biological,  evolutionary 
embryonic  or  developmental  influence  we  are  not  yet  in  a  position  to 
adequately  word  our  explanation.  This  is  the  same  as  saying  that  we 
do  not  know  how  heredity  acts.  T  am  convinced,  however,  that  even 
in  the  inflammatory  troubles  with  their  so-called  secondary 
degenerations,  such  as  acute  anterior  poliomyelitis,  though  the 
location  of  the  inflammation  may  be  accounted  for  in  some 
wav  by  the  peculiarity  of  the  circulation  in  and  through  the 
anterior  horns  of  the  cord  in  this  disease,  the  frequency  with  which 
certain  of  the  cells,  as  those  that  preside  over  the  tibialis  anticus 
muscle,  are  affected,  is  due  to  som.e  hidden  .biological  fact,  some  spe- 
cial susceptibility  conferred  upon  them  by  their  evolution,  their  early 
use  or  their  embryonic  development. 

Certainly  heredity  plays  a  role,  though  perhaps  a  minor  one,  along 
with   the  infection,   in  these  focal,   inflammatorv   troubles   with   their 


THE   NEURONIC   DISEASES 


357 


sharply  localized  secondary  and  permanent  degenerations.  In  the 
purely  hereditary  troubles,  like  Friedreich's  disease,  we  can  go  no 
farther  than  to  say  that  an  inherited  biological  or  embryonal  influence 
is  at  work.  It  would  be  perfectly  useless  to  tr\-  and  imagine  why  the 
brunt  of  the  damage  falls  upon  some  neurones  and  not  upon  others. 
The  fact  is  as  much  of  an  enigma  as  is  the  origin  of  sex. 

In  regard  to  the  organic  degenerative  diseases  that  follow  a  gen- 
eral intoxication,  such  as  locomotor  ataxia,  we  can  make  a  guess,  but 
only  a  feeble  one,  as  to  why  the  lesion  is  confined  to  a  particular  set 
of  neurones.  In  this  case  we  can  reason  behind  the  intoxication,  as 
it  were,  and  found  our  guess  upon  a  biological  and  physiological  basis. 
In  some  of  them  there  is  undoubtedly  a  localizing  influence  exerted 
by  the  heredity,  along  with  the  general  strain  or  intoxication. 

If  in  the  pure  hereditan.-  degenerative  troubles  certain  groups 
of  neurones  are  constantly  broken  down,  it  is  but  a  fair  conclusion  to 
suppose  that  in  some  other  acquired  diseases,  this  same  sort  of  heredi- 
tary influence  may  lie  dormant,  and  does  thus  lie  dormant,  until  it  is 
rendered  eft"ective  by  the  added  presence  of  the  depressing  intoxica- 
tion. The  question  is  often  asked,  for  instance,  why  all,  or  even  more, 
syphilitics  do  not  develop  locomotor  ataxia,  if  syphilis  be  indeed  the 
cause  of  this  disease.  One  legitimate  answer  would  be,  though  it 
would  amount  only  to  an  inference  drawn  from  analogy,  that  in  cer- 
tain individuals  who  acquire  the  infection,  there  is  an  inherited  weak- 
ness in  the  sensory  system.  The  infection  lowers  the  resisting  power 
of  the  sensor}'  neurones  and  immediately  the  hereditar\-  tendency  re- 
veals its  presence  and  force.  Another  answer  to  the  same  question 
could  be  made  in  accordance  with  the  Weigert-Edinger  hypothesis. 
In  this  it  is  assumed  that  those  neurones  or  systems  of  neurones, 
which  are  normally  called  upon  to  do  more  work  than  other  systems, 
have  the  nice  balance  between  their  combustion  and  repair,  their  de- 
structive and  constructive  metabolism,  more  quickly  and  more  pro- 
foundly upset  than  those  which  are  not  subject  to  such  strenuous  du- 
ties. Edinger  argues  that  the  sensory  nen'-ous  apparatus  is,  compara- 
tively speaking,  never  idle  and  that  certain  parts  of  it  are  even  more 
constantly  in  action  than  are  other  parts.  For  example,  in  locomotor 
ataxia  the  peripheral  sensor}-  neurones  of  the  legs  and  eyes  are  the 
chief  points  of  the  localization  of  the  lesion  because  normally  these 
neurones  are  incessantly  in  action  in  all  of  the  performances  of  the 
waking  state,  reflex  and  voluntary. 

Of  these  two  hypotheses,  I  prefer  the  former  for  several  reasons. 
Edinger "s  theor}-  does  not  answer  the  question  why  all  syphiHtics  do 
not  develop  locomotor  ataxia.  It  is  to  be  presumed  that  the  physio- 
logical strain  upon  their  sensory  apparatuses  is  approximately  the  same 
in  all.  Moreover  the  hypothesis  omits  entirely  to  account  for  the  purely 
hereditar}-  cases  and  those  that  begin  to  show  their  sharp  localization 
even  before  the  special  neurones  are  actively  called  upon  to  work. 

If  overwork  is  to  be  employed  in  explaining  the  localization  of 
the  lesion  in  these  acquired  troubles  of  adults,  the  theory  cannot  cer- 
tainly be  laid  aside  entirely  when  the  question  involves  the  sarne  sort 
of  a  lesion  that  appears  early  in  life.     I  can  much  more  readily  un- 


358 


THE    NEURONIC    DISEASES 


derstand  how  heredity,  strong  or  weak,  may  provoke  the  degenera- 
tions in  Friedreich's  disease  and  ordinary  tabes,  though  it  be  the  sole 
cause  in  the  former  and  the  partial  cause  in  the  latter,  than  can  I  con- 
ceive of  a  force  deterniining  a  lesion  in  one  disease  such  as  super- 
function  does,  as  it  is  claimed,  in  tabes,  but  doing  nothing  in  another 
disease  with  a  similar  lesion  such  as  the  posterior  degeneration  ob- 
served in  the  Friedreich  type  of  the  trouble.    Heredity  can  cover  both 


FIGURE  55. 


=^  Corttx 


TiLri.yktTJ.1 

r\ierv<-s 


Schematic  representation  of  the  neuronic  structure  of  the  motor  and  sensory 
pathways.     (Modified  from  Jakob.) 

diseases  in  part  at  least ;  but  super-function  can  only  be  made  to  apply 
to  one  of  them.  If  it  be  a-nswered,  however,  that  in  Friedreich's  dis- 
ease, the  influence  of  excessive  function  is  the  proper  explanation  just 
as  it  is  in  locomotor  ataxia,  then  we  must  assume  that  it  accounts  for 
the  accompanying  pyramidal  degeneration  in  the  motor  tracts  as  well. 
If  this  is  granted,  then  by  analogy  we  ought  to  have  the  motor  neu- 
rones more  often  degenerated  in  locomotor  ataxia  than  we  do. 


THE   XEUROXIC   DISEASES 


359 


On  account  of  these  objections,  I  do  not  think,  therefore,  that  the 
Weigert-Edinger  hypothesis  is  as  well  supported  as  is  the  hereditary 
in  explaining  why  certain  groups  of  neurones  are  so  much  more  liable 
to  degenerate  than  others  are  when  the  same  exciting  causes  are  in 
operation. 

If  the  reader  will  recall  the  preceding  chapter  upon  the  neuronic 
architecture  of  the  nerv'ous  system,  and  the  illustrations  that  accom- 
pany it,  he  will  remember  that  the  neurones  were  grouped  together 
into  various  motor,  sensory,  commissural,  associating  and  storage  sys- 
tems. 

Lying  side  by  side  their  cell-bodies  formed  the  ganglia  while 
their  processes  constituted  the  tracts.     Each  tract  was  made  up  of  an 

FIGURE  56. 


-iie^lex 


Schematic  representation  of  the  neuronic  structure  of  the  sensory  nerve  tracts. 
(Modified  from  Jakob.) 

immense  number  of  neuronic  pathways  along  which  the  individual  im- 
pulses traveled  from  one  end  to  the  other.  In  their  course  we  learned 
that  the  impulses  had  to  proceed  step-like  over  two  or  more  neurones, 
placed  end-to-end,  as  it  were,  by  synaptase,  before  they  reached  their 
journey's  end.  We  analyzed  two  of  the  pathways  about  which  we 
know  the  most,  namely,  the  projection  sensory  and  motor  paths.  AVe 
found  that  the  former  consisted  of  a  number  of  neurones  in  apposi- 
tion, whereas  the  latter  was  made  up  of  only  two,  the  upper  and  the 
lower  neurones. 

Our  acquaintance  with  organic  neuronic  degenerations  is  entirely 
limited  to  the  diseases  of  these  projection  sensory  and  motor  path- 
ways.    Doubtless  there  are  similar  degenerations  in  the  commissural, 


36o 


THE  NEURONIC  DISEASES 


association  and  intercalary  systems  of  the  brain  and  elsewhere  that, 

for  aught  we  know,  underlie  many  obscure  psychic  and  other  troubles. 

We  are  far  from  being  in  a  position  to  affirm  that  we  know  all 

of  the  degenerative  diseases  of  the  motor  and  sensory  projection  sys- 

FTGURE  57- 


Ic  U.S 


M«.scle 


terns.  Even  of  those  we  do  know  we  have  still  much  to  learn.  Never- 
theless as  the  neuronic  construction  of  these  projection  systems,  so 
well  shown  in  the  accompanying  diagrams,  is  such  that  the  division  of 
them  into  brain,  spinal  cord  and  nerve  tracts  is  simply  untenable  from 
the  clinical  standpoint,  we  must,  if  possible,  make  the  lines  of  divis- 


THE   XEUROXIC   DISEASES  361 

ion  correspond  with  the  divisions  between  the  individual  neurones. 
On  the  motor  side  we  can  do  this  much  more  easily  than  we  can  on  the 
sensory  side,  for  the  neurones  that  make  up  the  individual  pathways 
are  much  less  in  number  and  the  points  of  separation  between  the  two 
long-itudinally  related  neurones  are  more  uniformly  and  distinctlv  lo- 
calized. 

The  upper  neurones  of  the  motor  tract  consist  of  a  group  whose 
cell-bodies  lie  embedded  in  the  cerebral  cortex  around  the  fissure  of 
Rolando  and  whose  neuraxones  pass  down  in  a  bundle  through  the 
internal  capsule,  the  crura  cerebri  and  the  direct  and  indirect  pyra- 
midal tracts  of  the  cord.  They  all  terminate  in  arborizations,  but  at 
various  levels,  in  the  column  of  gray  matter  that  makes  up  the  ante- 
rior horns  of  the  cord  and  its  homologous  extension,  the  motor  nuclei 
in  the  medulla  oblongata.  Their  arborizations  surround  the  cell- 
bodies  found  there.  In  this  way,  it  will  be  observed  that  the  cerebral 
cortex  is  brought  into  physiological  communication  with  the  cell- 
bodies  of  the  lower  motor  neurones  lying  in  the  motor  cranial  nuclei 
and  the  anterior  cornua.  These  variously  lengthened  upper  neurones, 
taken  all  together,  constitute  what  is  called  the  Upper  Motor  Segment. 

The  lower  neurones  of  the  motor  tract  are  observed  to  have  their 
cell-bodies  where  the  neuraxones  of  the  upper  segment  terminate  in 
arborizations,  namely,  in  the  motor  cranial  nuclei  and  the  anterior 
cornua  of  the  cord.  Their  neuraxones  pass  out  through  the  motor 
cranial  nerves  and  the  anterior  roots  and  spinal  nerves  respectively. 
They  terminate  in  the  motorial  end-plates  of  the  various  muscles  to 
which  they  are  supplied.  In  this  way  the  entire  somatic  musculature 
of  the  body  is  brought  into  direct  physiological  connection  with  the  an- 
terior horns  of  the  cord  and  motor  cranial  nuclei,  and  into  indirect 
physiological  connection,  through  the  upper  motor  neurones,  ^vith  the 
cerebral  cortex.  These  lower  neurones,  taken  en  masse,  make  up  what 
is  termed  the  Lozcer  Motor  Segment. 

The  functions  of  these  respective  segments,  though  motor,  are 
somewhat  different,  a  fact  which  must  be  remembered  when  their  dis- 
eases are  clinically  considered.  The  lower  segment,  through  its  indi- 
vidual neurones  controls  and  stimulates  the  contractions  of  the  indi- 
vidual  muscles  of  the  body.  It  also  presides  over  their  nutrition.  As 
its  constituent  neurones  spring  from  various  levels  in  the  cord  and 
from  different  motor  cranial  nuclei,  the  location  of  the  lesion  in  a  cen- 
tral disease  can  thus  be  determined  by  the  particular  muscle  or  the 
particular  motor  nerve  that  is  symptomatically  affected. 

Furthermore,  disease  of  this  lower  motor  segment,  or  of  any  of 
its  constituent  neurones,  produces  for  obvious  reasons  a  flaccid  paraly- 
sis, a  muscular  atrophy  and  an  electrical  reaction  of  degeneration. 
Since  these  lower  motor  neurones  serv-e  as  the  efferent  pathways  for 
all  the  reflexes,  their  damage  also  causes  a  diminution  or  loss  of  all 
forms  of  reflex  action. 

The  principal  organic  degenerative  diseases  that  are  limited  to 
the  lower  motor  segments,  that  we  know  of.  and  that  will  be  discussed 
in  the  next  chapter,  are  poliomyelitis,  Wernicke's  superior  and  infe- 
rior polioencephalitis,  the  acute  ascending  paralysis  of  Landr\-.  asthenic 


362 


THE   NEURONIC   DISEASES 


bulbar  paralysis  or  myasthenia  gravis,  and  the  primary  degenerations 
of  the  cranial  motor  nerves,  such  as  the  ocular,  facial,  hypoglossal  and 
motor  branch  of  the  trigeminal. 

FIGURE  58. 


Ulu 


m 


The  upper  segment,  through  its  constituent  neurones,  controls, 
stimulates  and  inhibits  the  activities  of  the  lower  segment.  It  does 
not  influence,  nor  does  it  even  know  of,  individual  muscles.     It  pre- 


THE   NEURONIC   DISEASES  363 

sides  only  over  systematised  physiological  movements.  These  move- 
ments are  produced  by  the  comibined  action  of  a  number  of  physiolog- 
ically related  muscles. 

The  distinction  between  the  functions  of  the  upper  and  lower  seg- 
ments in  regard  to  these  physiological  movements  and  the  individual 
m.uscular  contractions  is  of  immense  importance  in  clinical  practice. 
I  am  in  the  habit  of  teaching  that  the  upper  miotor  neurones  are 
psychic,  so  to  speak,  in  their  activities  and,  like  the  mind,  are  cogni- 
zant of  general  movements  only,  such  as  those  of  the  leg  or  of  the 
hand,  whereas  the  lower  motor  neurones  are  wholly  spinal  and  are 
cognizant  only  of  individual  muscles,  such  as  the  deltoid  or  the  quad- 
riceps femoris. 

The  upper  motor  neurones  do  not  enter  into  the  production  of  an 
ordinary  reflex,  though  by  reason  of  their  inhibitory  control  over  the 
lower  neurones  they  inhibit  the  normal  reflex  somewhat.  They  do 
not  exert  any  special  trophic  influence,  though  it  is  assumed  that  their 
normal  stimulant  action  upon  the  lower  neurones  helps  in  a  measure 
to  preserve  the  latter's  proper  nutrition. 

Remembering  then  the  relationship,  anatomical  and  functional,  of 
the  upper  motor  segment  to  the  lower,  we  are  not  surprised  to  discover 
that  when  it  is  diseased  and  its  inhibitory  controi  is  thus  withdrawn 
from  the  lower  segment,  the  muscles  are  thrown  into  state  of  spastic 
rigidity  or  spastic  paralysis;  that  this  paralysis  implicates  muscle 
groups  which  subserve  the  movements  of  various  parts  of  the  body  like 
the  face,  the  arm,  the  leg  or  the  whole  half  of  the  body,  but  does  not 
implicate  merely  individualized  muscles ;  that  the  reflexes  are  exag- 
gerated; that  there  is  little  or  no  muscular  atrophy;  and  finally  that 
the  normal  electrical  reactions  remain  unchanged. 

The  more  important  organic  diseases  of  the  upper  segment  that 
we  know  of  and  that  will  be  treated  of  here  are  the  spastic  paralyses  of 
adults  and  of  children,  hereditary  spastic  paraplegia,  Erb's  spinal 
paralysis,  soine  secondary  spastic  paralyses  and  briefly  hysterical  spas- 
tic paraplegia.  If  Strumpell's  cortical  polioencephalitis  be  listed, 
though  there  is  some  doubt  as  to  its  existence,  it  will  have  to-  be  in- 
cluded here  among  the  secondary  degenerations. 

There  are  a  number  of  diseases  that  involve  the  entire  motor  tract, 
lx>th  upper  and  lower  segments.  For  obvious  reasons  t-he  dominant 
symptoms  will  be  those  of  the  lower  motor  segment.  To  this,  how- 
ever, there  is  one  exception,  namely,  the  type  of  progressive  muscu- 
lar atrophy  which  Charcot  named  amyotrophic  lateral  sclerosis.  Here 
the  disease  process  seemis  to  begin  in  the  lower  end  of  the  upper  motor 
segment  and  hence  for  a  time  the  dominant  symptoms  are  those  of  an 
upper  motor  segment  disease. 

The  troubles  that  we  usually  classify  as  mvolving  the  whole  mo- 
tor tract  are  the  progressive  muscular  atrophies,  progressive  bulbar 
paralysis,  the  progressive  muscular  dystrophies  and  the  amyotrophic 
lateral  sclerosis. 

The  sensory  tract  is  far  more  complicated  than  the  motor  and  in 
regard  to  its  organic  degenerative  diseases  we  are  not  well  informed. 
We  are  best  acquainted  with  those  that  belong  to  the  peripheral  neu- 


364 


THE   NEURONIC   DISEASES 


rones  of  the  system,  namely,  locomotor  ataxia,  tic  douloureux,  some 
neuralgias  about  which,  however,  there  is  considerable  doubt  and  the 
primary  degenerations  of  the  nerves  of  special  sense,  especiallv  the 
optic. 

FIGURE  59. 


yVci-ve 


The  best  way  to  indicate  the  construction  of  the  various  pathways 
that  make  up  the  sensory  system  will  be  to  trace  an  impulse  along 
them  from  the  skin  to  the  brain.  The  accompanying  diagrams  will 
assist  the  reader  in  following  the  courses  of  the  impulses. 


THE   NEURONIC   DISEASES  365 

Leaving  the  skin  and  passing  first  along  fne  sensory  nerve,  a  stim- 
xilus  arrives  at  the  poisterior  spinal  ganglion  where  the  cell-body  of 
the  respective  neurone  is  found.  Up  to  this  point  the  impulse  has 
Jbeen  traveling  by  way  of  a  long,  modified  dendrite.  After  it  leaves 
the  cell-body  in  the  posterior  ganglion  it  emerges  along  the  neuraxone 
of  the  same  neurone  that  passes  directly  into  the  cord  by  way  of  the 
posterior  root  to  arborize  around  a  group  of  cells  embedded  in  the  pos- 
terior horn.  From  this  second  cell,  and  by  way  of  its  neuraxone,  the 
impulse,  crosses  through  the  anterior  commissure  to  the  lateral  column 
■of  the  opposite  side  where  it  ascends  m  the  antero-lateral  ascending 
tract  of  Gowers  to  finally  pass  through  the  medulla  and  pons  and 
to  arborize  around  the  cell-bodies  nesting  in  the  optic  thalamus.  Con- 
tinuing on  through  this  third  cell  and  its  neuraxone,  it  ultimately 
reaches  the  cerebral  sensory  cortex. 

This  is  what  is  called  a  direct  sensory  path  and  it  consists  of  the 
three  end-to-end  neurones,  the  peripheral,  the  spino-thalamic  and  the 
thalamo-cortical. 

Another  direct  pathway  is  that  up  the  columns  of  Burdach  and 
Goll  to  the  nuclei,  cuneatus  and  gracilis,  at  their  summits,  thence  to 
the  thalamus,  and  so  on  to  the  cortex.  The  peripheral  neurones  in  these 
instances  are  of  enormous  length  and  actually  extend  from  the  skin, 
through  the  posterior  root,  to  the  top  of  the  posterior  columns  of  the 
cord. 

There  are  certain  sensory  impulses  from  the  muscles,  the  joints 
and  the  viscera  that  reach  the  brain  through  a  very  much  more  in- 
direct route  than  the  two  just  outlined.  These  indirect  pathways  are 
not  well  known  and  we  can  only  trace  the  impulses  along  them  in  a 
tentative  sort  of  a  way.  Entering  the  cord  by  way  of  the  posterior 
roots,  the  latter  ascend  the  posterior  columns  to  their  respective  nuclei, 
thence  they  cross  to  the  opposite  side  in  the  sensory  decussation,  some 
ultimately  reaching  the  cerebellar  cortex  where  they  terminate,  others 
continuing  on  from  the  cerebellar  cortex  to  the  red  nucleus,  optic  thal- 
amus and  cerebral  cortex.  Other  impulses  of  this  sort  ascend  to  the 
cells  of  the  column  of  Clarke,  thence  to  the  cerebellum  by  way  of  the 
direct  cerebellar  tracts,  and  so  on  to  the  brain.  These  indirect  paths 
may  be  summarized  thus,  peripheral  sensory  neurone,  spino-cerebellar 
neurone,  cerebello-thalamic  neurone,  and  thalamo-cortical  neurone. 

Along  the  direct  paths  are  supposed  to  pass  all  the  sensations  of 
touch,  temperature  and  pain ;  along  the  indirect  travel  the  impulses 
from  the  muscles,  tendons  and  joints  that  have  to  do  with  coordina- 
tion and  the  maintenance  of  equilibrium  and  the  activities  of  the  vis- 
cera. 

My  excuse  for  introducing  here  this  minute  account  of  the  sen- 
sory pathways  is  that  they  are  all  implicated  apparently  in  the  sen- 
sory system  disease  about  which  we  know  the  most,  namely,  locomo- 
tor ataxia.  Further  details  in  regard  to  the  anatomy  and  physiolog}' 
of  these  various  projection  pathways  will  be  found  in  the  chapters  de- 
voted to  the  physiology  of  the  brain  and  spinal  cord.  The  considera- 
tion of  the  neuronic  structure  of  the  special  sense  systems  will  not  be 


366 


THE   XEUROXJC   IHSEASES 


taken  up  in  detail  here  as  it  belongs  to  the  description  of  the  various 
cranial  nerves  later  on. 

There  are  quite  a  number  of  organic  neuronic  degenerations  that 

FIGURE  60. 


«2^  o-tAr:  ■^/ 


vete^eKum. 


umus. 


'  Sensory  iMerve 
ftoii't    (V\.u.sc  U  etc. 


yAorn'Vjsceri 


occur  in  a  comhincd  way  in  both  the  sensory  and  motor  systems.  Chief 
among  these  are  amaurotic  family  idiocy,  some  forms  of  hereditary 
cerebellar  ataxia,  Friedreich's  disease,  ataxic  paraplegia,  the  primary 


THE   NEURONIC   DISEASES  367 

combined  sclerosis  of  Putnam,  toxic  combined  sclerosis,  progressive 
interstitial  hypertrophic  neuritis  of  children,  multiple  neuritis  and 
neuromyelitis. 

Some  authors  are  perhaps  justified  in  classifying  among  these  or- 
ganic neuronic  degenerative  troubles,  because  of  the  frequent 
prominence  of  their  systemic  manifestations,  syringomyelia, 
infantile  diplegia  from  agenesis,  delirium  grave  or  Bell's 
mania,  and  dementia  paralytica.  I  prefer  for  the  present  not  to  do  so, 
however,  because  it  seems  to  me  that  the  extra-neuronic  manifestations 
are  sufficiently  prominent  to  still  keep  them  entirely  out  of  this  class. 
Their  neuronic  changes,  except  perhaps  in  a  few  exceptional  cases 
of  Bell's  mania  are,  in  my  judgment,  emphatically  secondary. 

DISEASES  OF  THE    AFFERENT    OR    SENSORY    SYSTEM. 
LOCO^IOTOR  ATAXIA. 

Locomotor  ataxia  is  a  better  name  for  this  disease  than  either 
tabes  dorsalis  or  posterior  spinal  sclerosis.  All  three  are  objectionable 
however.  It  is  not  a  motor  trouble,  as  might  be  inferred  from  the  first 
name.  It  is  not  a  wasting  of  the  back,  as  the  second  suggests.  And 
it  is  not  primarily  a  posterior  spinal  sclerosis.  As  the  ataxia,  shcrwn  in 
the  gait,  is  the  most  obtrusive  symptom,  the  name  locomotor  ataxia 
is  perhaps'  the  most  convenient  to  employ. 

The  disease  consists  of  a  slow,  progressive  degeneration  in  the 
peripheral  sensory  neurones,  and  their  related  structures,  with  a  secon- 
dary sclerosis  of  the  sustentacular  tissues.  Clinically  it  is  character- 
ized by  certain  sensory  phenomena ,  incoordination  of  movement,  and 
trophic  disturbances.  It  is  notable  for  the  absence  of  all  true  motor 
symptoms  and  mental  aberrations. 

Etiology. — Since  the  initial  work  of  Fournier,  Erb  and  others, 
the  opinion  has  been  growing  that  syphilis  is  the  cause  of  locomotor 
ataxia.  Tersely  state^d,  the  hypothesis  would  be, — no  syphilis,  no  loco- 
motor ataxia;  or  in  other  words,  every  case  of  locomotor  ataxia  pre- 
supposes syphilitic  infection.  Many  do  not  accept  entirely  this  dictum 
because  no  sets  of  statistics  have  yet  been  brought  forward  in  which  a 
positive  history  of  syphilis  was  obtained  in  every  case.  Even  Four- 
nier and  Erb  admit  this,  but  as  such  a  history  is  obtainable  in  at  least 
75  to  85  per  cent,  of  all  cases,  they  and  others  assume  that  it  has  been 
overlooked  in  the  remaining  15  or  25  per  cent.  This  is  not  improbable 
as  syphilis  is  sometimes  innocently  acquired  and  honestly  denied.  At 
other  times  it  reveals  such  slight  and  evanescent  primary  and  sec- 
ondary manifestations  as  to  be  very  easily  overlooked.  It  is  not  abso- 
lutely true,  however,  as  is  frequently  asserted,  that  it  is  in  this  class  of 
syphilitics  that  locomotor  ataxia  is  most  prone  to  occur.  While  a  con- 
servative opinion  would  not  agree  with  Fournier  that  locomotor  ataxia 
is  parasyphilis  or  metasyphilis,  a  mere  sequel  of  constitutional  syph- 
ilitic infection ;  and  much  less  with  Eesser,  who  believes  that  it  rep- 
resents a  fourth  stage  of  syphilis,  thereby  being  in  no  sense  a  separate 
and  distinct  entity  of  itself,  it  does  accept  the  statement  that  syphilis 
is  far  and  bevond  all  others  a  cause  of  locomotor  ataxia. 


368  THE  NEURONIC  DISEASES 

Some  of  the  conservatives  hold  that  the  specific  infection  serves 
simply  as  a  predisposing  cause  and  in  that  sense  may  underlie  most 
of  the  cases.  Other  causes,  however,  must  come  into  play  along  with 
the  specific  to  provoke  the  disease  under  discussion. 

A  still  larger  number  of  conservatives  argue  that  in  the  15  or  25 
per  cent,  of  cases  in  which  a  history  of  syphilis  is  not  obtainable,  the 
other  causes  may  and  probably  do  produce  tabes  without  the  existence 
of  an  underlying  specific,  predisposing  factor,  such  as  syphilis. 

That  syphilis  precedes  the  appearance  of  tabes  in  a  large  majority 
of  cases  is  undeniable.  That  it  is  an  antecedent  demonstrable  in  all 
cases,  has  not  yet  been  shown.  Therefore,  that  it  is  the  only  cause  of 
locomotor  ataxia  is  still  an  open  question. 

The  other  causes  that  are  believed  to  act  in  conjunction  with 
syphilis  and  in  occasional  cases  possibly  alone,  are  excesses  of  all 
kinds,  especially  excessive  venery,  occupations,  such  as  that  of  the  syph- 
ilitic driver  whose  ataxia  began  in  the  rig"ht  arm,  exposure  to  prolonged 
cold  and  dampness,  strains  of  all  kinds,  such  as  running  a  machine, 
climbing  arduous  steeps,  difficult  parturition  with  hemorrhage,  pro- 
longed lactation,  depressing  emotions,  and  spinal  injuries.  Simple 
traumatic  tabes  is  to  be  regarded  with  doubt. 

Apart  from  syphilis,  other  infections  have  been  credited  with  the 
disease,  namely,  pneumonia,  rheumatism,  typhus  fever.  Most  tabetics 
have  had  gonorrhoea  but  it  is  not  a  cause.  Latent  syphilis  may  have 
been  present  in  all  of  these  cases  for  where  such  causes  are  discov- 
ered apart  from  syphilis  they,  like  ergot  when  used  in  excess,  produce 
an  atypical  form  of  the  disease  or  a  combined  type  of  degenerative 
sclerosis. 

Heredity  does  not  play  a  significant  part  in  the  etiology  though 
it  is  believed  by  many  that  an  inherited  neuropathic  predisposition  goes 
far  toward  explaining  why  some  syphilitics  acquire  locomotor  ataxia 
and  others  do  not. 

Men  are  more  frequently  attacked  by  the  disease  than  women,  in 
the  proportion  almost  of  ten  to  one.  This  may  be  because  of  the  greater 
liability  of  men  to  the  various  causes  spoken  of  above;  and  yet  the 
difference  is  so  marked  that  a  special  susceptibility  is  believed  by  many 
to  belong  to  the  male. 

The  disease  appears  preeminently  in  the  middle  period  of  adult 
life.  More  than  half  of  the  cases  occur  between  the  ages  of  thirty  and 
fifty.  About  thirty-seven  seems  to  be  a  favorite  year  for  its  commence- 
ment. It  has  been  observed  as  early  as  ten  or  twelve  years  of  age, 
and  as  late  as  sixty-five.  It  is  exceedingly  rare,  however,  before  twenty 
and  after  sixty. 

In  some  mysterious,  probably  biological,  way,  race  and  nationality 
appear  to  exert  an  influence  upon  its  development.  In  the  Negro,  the 
Jap,  the  Egyptian,  the  Bosnian  and  the  Herzegovinian,  the  Kirgizh 
and  the  natives  generally  of  East  and  Southeast  Africa,  among  whom 
syphilis  is  rife,  tabes  is  all  but  unknown.  This  has  been  used  as  an 
argument  against  the  syphilitic  etiology  of  the  disease;  but  it  may  be 
counter-argued  that  it  is  because  syphilis  in  these  races  has  effected  an 


THE   NEURONIC   DISEASES  ■  369 

immunity  on  account  of  its  very  excessiveness  and  almost  universality, 
against  its  own  tertiary  accidents. 

Pathology  and  Pathogenesis. — If  syphilis  is  the  cause,  medi- 
ately or  immiediately,  of  locomotor  ataxia,  the  lesions  found  are  not 
those  commonly  recO'gnized  as  syphilitic.  Hence,  tabes  is  not  a  syph- 
ilitic affection  in  the  strict  anatomico-patholog-ical  sense.  The  degener- 
ation that  is  known  now  as  the  primary  process  of  the  disease  is  a 
remote  result  of  the  specific  intoxication,  the  wreckage,  as  it  were, 
after  the  storm.  Most  of  the  syphilitic  cases  reveal  their  first  symptom 
in  from  five  to  fifteen  years  after  the  acquisition  of  the  infection.  In 
a  large  number  of  these  cases  the  signs  of  syphilis  have  been  slight 
and  when  the  tabetic  manifestations  had  begun  to  appear  were  prac- 
tically nil.  Only  the  suspicion  of  an  initial  lesion  can  be  formed  some- 
times. In  women  usually  this  is  wanting.  Erb,  Fournier  and  others 
"have  noticed  that  in  a  few  cases  in  which  no  history  of  syphilis  could 
be  secured,  the  father  was  syphilitic. 

The  term  tertiary  as  applied  to  the  disease  in  the  sense  of  be- 
ing a  late  manifestation  of  syphilis,  is  misleading,  for  the  primary 
infection  may  precede  the  outbreak  of  the  trouble  anywhere  from  one 
to  forty  years. 

The  most  prominent  and  constant  post  mortem  finding  in  loco- 
motor ataxia  is  the  degenerated  appearance  of  the  posterior  spinal 
columns.  Burdach's  columns,  especially  in  the  lumbar  and  dorso- 
lumbar  regions,  and  Goll's  columns  higher  up,  are  seen  to  be  grayer, 
smaller,  harder  and  less  punctated  than  normally.  A  narrow  ventral 
area  just  alongside  the  posterior  commissure  escapes  the  change. 
Clarke's  vesicular  columns,  Lissauer's  tracts,  and  the  posterior  cornua 
are  included  in  old  cases  of  the  disease.  This  can  all  be  readily  ob- 
served with  the  naked  eye.  This  pathodogical  picture  is  what  misled 
the  earlier  investigators  into  giving  the  names  to  the  disease  that  they 
did  and  in  placing  it  among  the  spinal  cord  affections. 

Two  things  are  to  be  distinctly  noted  in  regard  to  the  pathological 
basis  of  locomotor  ataxia,  as  we  know  the  disease  to-day.  They  are, 
first,  that  the  disease  is  not  an  inflammation,  but  a  progressive  degen- 
eration, and  secondly,  that  this  degeneration  occurs  in  the  peripheral 
sensory  neurone,  whose  cell -body  rests  in  the  posterior  root  ganglion 
and  whose  processes  extend  out  into  the  peripheral  nerve  on  the  one 
hand  and  up  into  the  posterior  tracts  of  the  cord  on  the  other.  The 
■degeneration  may  be  looked  for  anywhere  in  the  entire  cutaneo-spinal 
extension  of  this  neurone.  It  is  more  often  found,  however,  in  the 
outer  or  cutaneous  end  and  the  inner  or  spinal  end  than  anywhere  in 
the  middle  or  in  the  cell-body.  It  is  most  frequently  observed  in  the 
spinal  end.  As  these,  spinal  ends  extend  up  into  the  posterior  columns, 
it  is  clear  why  in  the  great  majority  of  cases,  these  columns  are  the 
principal  seat  of  the  disease. 

Microscopically  this  symmetrical,  bilateral  posterior  degeneration 
is  seen  to  originate  in  the  nerve  fibres  and  run  through  the  usual  course. 
The  neuroglia  may  remain  normal  but  as  a  rule  it  proliferates  along 
with  the  connective  tissue.  A  few  remaining  fibres  may  be  seen  run- 
ning through  the  proliferated  tissue.     The  bloodvessels  do  not  exhibit 


370 


THE   NEURONIC   TOSEASES 
FIGURE  6l. 


Locomotor  ataxia.    Cervical  section.    Dorsal  section.    Lumbar  section.    (After 
Jakob. 


THE   NEURONIC   DISEASES  37I 

any  signs  of  congestion,  vascular  irritation  or  inflammatory  change. 
The  degeneration  of  the  nerve  elements,  with  the  secondar}^  sclerosis, 
can  be  traced  into  Clarke's  column  in  some  cases,  into  Gowers',  antero- 
lateral tract  in  others,  and  even  into  the  direct  cerebellar  tract  in  a 
still  smaller  number.  The  posterior  roots  are  often  degenerated  and 
the  posterior  ganglia  also  in  a  few  cases.  The  anterior  roots  are  not 
affected  or  only  so  in  very  late  and  complicated  cases.  In  the  latter 
the  degeneration  is  seen  in  the  pyramidal  tracts  and  other  anterior  and 
lateral  areas  of  the  cord  also.     The  peripheral  nerves,  especially  those 


FIGURE  62. 


..A.^r 


Atrophy  of  the  posterior   root  and  of  the  spinal  ganglion  in  tabes   dorsalis. 
h.  W ,  posterior  root.      (Weigert's  stain.)      (After  Oppenheim.) 


of  the  leg,  in  advanced  cases  exhibit  signs  of  degeneration,  degenera- 
tive atrophy  or  neuritis.  Whether  this  cutaneous  degeneration  is  pri- 
mary or  secondary  is  not  yet  established.  When  the  disease  process 
has  reached  into  the  medulla,  the  degeneration  may  be  observed  in 
ihe  spinal  roots  of  the  fifth  cranial  nerve,  and  often  in  the  solitary 
bundle  and  posterior  vagus  nucleus.  Rarely  the  auditory  and  hypo- 
glossal nuclei  may  be  wasted.  The  nuclei  of  the  third  nerve  have  been 
implicated.  Among  the  cranial  nerves,  however,  the' optic  is  more 
often  the  one  affected.  The  Gasserian  ganglion,  the  nerves  of  the 
ocular  muscles,  the  vagus,  the  recurrent  laryngeal  and  the  hypoglossal 
have  all  been  broken  down  in  some  cases.  The  membranes  along  the 
posterior  surface  of  the  cord  and  around  the  posterior  roots  are  often 
chronicallv  inflamed. 


Z7^'  THE   N)iURONIC   DISEASES 

In  regard  to  the  modus  operandi  of  the  syphilitic  virus  in  pro- 
ducing these  lesions  and  in  Hghting  up  the  degenerative  process  that 
constitutes  the  basis  of  the  disease  we  know  nothing  positively.  Va- 
rious hypotheses  have  been  offered  from  time  to  time" but  none  of  them 
satisfactorily  explain  all  of  the  conditions  present.  Most  of  them  have 
been  entirely  abandoned.  Two,  however,  are  still  regarded  with  some 
favor,  and  to  a  certain  extent  are  yet  on  trial. 

Marie  long  ago  put  forth  the  view  that  the  syphilitic  virus  affects 
the  nutritive  function  of  the  peripheral  sensory  neurones  by  directly 


Sagittal   section  through  the  spinal  ganghon  with  the  posterior  and  anterior 
roots  and  efferent  nerves.     (Weigert's  stain.)      (After  Oppenheim.) 


poisoning,  or  otherwise  damaging,  their  cell-bodies  found  massed  to- 
gether in  the  posterior  spinal  ganglia.  This  being  the  case  the  ends 
of  the  neurones  farthest  removed  from  the  nutritive  centers,  namely, 
the  cutaneous  ends  on  the  one  hand  and  the  spinal  ends  on  the  other, 
naturally  waste  and  degenerate  first.  The  objections  to  this  hypothe- 
sis are  that  tlie  degenerative  process  here  represents  something  more 
than  what  would  be  the  result  of  a  mere  malnutrition  of  the  neurone 
produced  by  a  disturbance  of  the  nutritive  function  of  its  cell-bod\- ; 
that  it  is  not  supported  by  sufficiently  constant  or  uniform  changes 
within  the  posterior  spinal  ganglia ;  and  that  it  fails  to  explain  the 
greater  frequency  of  the  degenerative  process  in  the  spinal  end  of  the 
neurone  and  its  relative  infrequency  in  the  cutaneous  end.     Though 


THE   XEUROXIC   DISEASES  2)73, 

Marie  has  himself  lately  given  up  this  hypothesis  it  still  seems  to  be 
somewhat  in  favor  in  some  quarters. 

Redlich  and  Obersteiner,  noting  the  constancy  and  the  character 
of  the  degeneration  in  the  posterior  roots  and  the  frequency  of  the 
adjoining  meningitis,  propounded  the  theory  that  a  chronic  specific 
meningitis  of  the  posterior  parts  of  the  cord  is  the  primar)^  disease. 
This  meningitis,  by  constricting,  compressing  and  otherwise  injuring 
the  roots  where  they  pass  through  it  sets  up  an  atrophy  in  them  and 
thus  transmits  the  disease  by  contiguity  up  into  the  cord.  This  hvpothe- 
sis  brings  locomotor  ataxia  into  line  with  the  established  form^; 
of  spinal  syphilis  by  making  of  it  primarily  a  vascular  disease,  a  spe- 
cific meningitis.  ]\Iany  of  the  earlier  symptoms,  especially  the  pains, 
are  not  unlike  those  obs€r\^ed  in  meningitis  involving  constriction  of 
the  posterior  roots.  The  objections  to  the  theory,  however,  are  that 
it  fails  to  explain  the  almost  universal  limitation  of  the  meningitis 
and  its  associated  degenerative  sequelae  to  the  posterior  parts  of  the 
cord  (though  Alarie  and  Guillain  have  latelv  invoked  the  peculiar  vas- 
cular and  lymphatic  supply  here  to  solve  this  difficulty )  ;  that  it  ac- 
counts for  a  degenerative  process  that  ought  accordingly  to  appear 
more  frequently  in  other  forms  of  chronic  specific  and  non-specific  men- 
ingitis :  and  that  it  fails  utterly  to  explain  the  not  infrequent  associated 
degeneration  of  some  of  the  cranial  nerves,  as  for  example  the  optic, 
and  the  peripheral  cutaneous  nerves,  and  of  the  posterior  spinal  ganglia. 

Every  explanation  hitherto  advanced  leaves  without  an  answer 
the  question  as  to  why  the  disease,  whether  it  be  syphilitic  or  not  in 
origin,  begins  and  limits  itself  to  the  sensory  neurones,  and 
especially  to  the  lower  sensory  neurones.  Biology,  embry- 
ology, evolution  and  heredity  have  ail  been  invoked  to  show 
that  there  is  a  special,  neuropathic  weakness  in  these  particular  neu- 
rones and  that  therefore  they  yield  to  the  virus  of  the  syphilis.  The 
Edinger  theory  endeavors  to  cover  the  ground.  In  it  the  assumption, 
first  noted  by  W^eigert,  is  made  that  certain  parts  of  the  nervous  appa- 
ratus are  worked  more  than  others  with  consequently  a  more  rapid 
disintegration  and  consumption  of  the  elemental  metabolism.  This 
occurs  in  the  sensory  system  which  is  ceaselessly  transmitting  im- 
pulses from  the  periphery  to  the  brain.  Under  the  stress  therefore  of 
such  a  universal  depressing  agent  as  syphilis,  the  sensory  system  is 
the  first  to  give  way. 

Symptoms. — Xo  case  of  locomotor  ataxia  presents  exactly  the 
same  clinical  picture  as  any  other  case.  The  variations  in  the  combi- 
nation of  symptoms  and  their  character  are  innumerable.  Thus  arbi- 
trary types  of  the  disease  have  been  described,  much  to  the  confusion 
of  its  diagnosis.  There  is,  how^ever,  a  fairly  definite  symptomatology 
and  keeping  well  in  mind  this  typical  picture,  one  can  easily  recognize 
the  slighter  shades  of  variation  v>'hich  it  may  undergo. 

I  will  first  attempt  a  description  of  the  typical  presentation  of 
the  disease  and  then  discuss  a  little  more  in  detail  a  few  of  its  varia- 
tions. It  must  be  remembered  that  the  symptoms  in  all  cases  \Aall  be 
those  that  one  w^ould  naturally  expect  from  a  slow,  progressive  de- 


374  THE   NEURONIC   DISEASES 

generation  here  and   there  in  a   widely  extended,   peripheral   sensory 
apparatus. 

Progressive  sensory  disturbances  form  the  basis  of  the  sympto- 
matology of  tabes.  These  may  begin  and  remain  in  the  legs ;  they  may 
extend  to  the  arms ;  or  the}'  may  commence  in  and  be  limited  to  the 
arms.  They  may  involve  the  sensory  nerves  of  the  head  and  of  the 
viscera.  Later  symptoms  may  diverge  from  the  purely  sensory  type  so 
that  trophic,  motor  and  vasomotor  manifestations  may  be  present.  The 
uniformity  of  the  symptomatology  of  tabes  depends  upon  its  sen- 
sory character  and  upon  its  steady  progressive  course ;  its  variability 
depends  upon  the  variations  in  tlie  location  of  the  degenerative  pro- 
cess. While  the  former  tempts  us  at  times  to  make  a  diagnosis  upon 
the  barest  indications,  the  latter  should  warn  us  not  to  do  so  unless 
two  or  more  symptoms  are  present.  A  mere  pain,  a  mere  diplopia,  a 
mere  loss  of  knee-jerk  or  a  miere  loss  of  vision,  \\athout  any  other  symp- 
tom to  base  a  diagnosis  upon,  even  when  there  is  a  historv'  of  syphilis, 
ought  never  to  more  than  arouse  a  suspicion  of  possible  tabes.  Only 
in  this  way  can  mistakes  be  minimized  in  the  diagnosis  of  a  disease 
which  assumes  sucn  a  variety  of  outward-  forms. 

The  first  indications  of  locomotor  ataxia  usually  make  their  appear- 
ance in  from  five  to  fifteen  years  after  the  contraction  of  the  syphilis. 
Ten  years  is  about  the  average.  The  patient  notices  a  feeling  of  iveak- 
ness  and  tiredness  in  his  legs,  especially  after  a  slight  exertion,  not  un- 
like that  seen  in  neurasthenia.  He  observes  that  in  writing  or  button- 
ing his  clothes  he  has  not  quite  his  usual  control  over  the  fingers. 
Along  with  these  suspicious  manifestations  there  may  appear  here  and 
there  about  the  body  slight  fugitive  momentary  pains  that  are  mistaken 
for  cold  and  rheumatism.  On  the  other  hand,  none  of  these  symptoms 
may  be  present,  but  the  patient  begins  to  worry  about  his  slowly  failing 
eyesight,  with  the  occasional  attacks  of  temporary-  diplopia.  One  or 
both  eyelids  may  droop  slightly.  In  other  cases  even  before  the  above 
warnings  have  arisen,  there  may  have  been  noticed  for  awhile  excessive 
sexual  desire,  satyriasis,  followed  by  rather  rapid  and  alarming  im- 
potence. The  bladder  often  manifests  a  slight  disturbance.  The  urine 
comes  slowly.  The  zveakness,  the  fugitive  pains,  the  bladder  irregular- 
ity, the  sexual  impotence  or  the  failing  eyesight  usually  sends  the  pa- 
tient to  a  physician,  who  makes  a  careful  examination  and  finds  other 
very^  suggestive  and  objective  signs  of  an  incipient  tabes. 

A  convenient  classification  of  the  symptoms  may  be  made  upon 
the  progressive  character  of  the  disease.  We  speak  of  a  pre-ataxic,  an 
ataxic  and  a  paralytic  stage.  These  are  not  by  any  means  sharply 
defined  from  one  another.  They  overlap  and  the  symptoms  of  one  may 
be  found  in  another.  Furthermore,  there  is  nothing  definite  as  to  the 
duration  of  any  one  of  the  stages.  They  are  only  uniform  in  respect 
to  the  successive  relationship  that  they  bear  to  each  other. 

The  pre-ataxic  stage  of  locomotor  ataxia  is  the  all-important  stage, 
both  in  the  interests  of  the  patient  and  to  the  credit  of  the  practitioner. 
In  the  ataxic  stage  the  disease  has  already  progressed  so  far  that  a 
diagnosis  is  comparatively  of  slight  value  to  the  patient  and  of  little 


THE   NEURONIC   DISEASES  375 

honor  to  the  diagnostician.  In  the  paralvtic  stage  it  is  of  no  special 
moment  to  anybody. 

Therefore  the  earhest  manifestations  of  the  disease  are  of  the  great- 
est importance  and  must  be  sought  for  and  studied  with  the  keenest 
acumen. 

The  symptoms,  named  in  the  order  of  their  frequency,  which  par- 
ticularly characterize  the  pre-ataxic  stage  are  loss  of  the  patella-reflex 
(Westphal's  sign),  lancinating  pains,  Argyll-Robertson  pupil,  anas- 
thesia  and  analgesia  and  static  ataxia  (Romberg's  sign). 

Other  symptoms  that  may  appear  in  this  stage,  though  they  are  not 
so  constant  as  those  named,  are  bladder  disturbances,  sexual  weakness, 
diplopia  from  ocular  paralysis,  gastric  and  laryngeal  crises,  paralysis  of 
the  vocal  cords  with  spasmodic  cough,  optic  atrophy  and  even  trophic 
changes  in  the  joints  and  bones. 

My  own  observation  confirms  that  of  most  writers  of  large  experi- 
ence that  the  loss  of  the  knee-jerks  is  a  relatively  constant  and  early 
symptom.  It  is  found  m  about  05  per  cent,  of  the  cases.  It  is  not 
always  the  first  symptom  by  any  means,  though  it  is  the  most  frequent 
among  the  initial  symptoms.  Diminution  and  loss  of  the  knee-jerk 
occurs  in  many  other  diseases,  as,  for  instance,  neurasthenia,  peripheral 
neuritis,  anterior  poliomyelitis,  complete  transverse  myelitis  in  the  dorso- 
lumbar  region.  I  saw  it  absent  once  in  an  unusually  healthy  young 
woman,  though  Oppenheim  doubts  whether  it  is  ever  a  normal  phe- 
nomenon. In  locomotor  ataxia  the  loss  is  usually  complete  from  the 
beginning  and  cannot  be  modified  by  any  known  means  of  reinforce- 
ment. The  ankle  reflex  occasionally  precedes  the  patella  reflex  in  van- 
ishing. When  both  are  gone  the  loss  of  the  ankle-jerk  may  be  more 
absolute  than  that  of  the  knee-jerk.  Both  phenomena  continue  through- 
out the  entire  course  of  the  disease.  They  ma}'  be  observ-ed  for  a  time 
in  rare  instances  upc-n  one  side  only. 

Very  many  authorities  declare  that  the  lancinating  pains  are  the 
first  and  the  most  frequent  symptom  of  locomotor  ataxia  (Brannvell, 
Goldflam  and  others).  The  statistics  of  Mott,  Starr,  Robinson  and 
myself  show  that  they  occur  in  only  about  60  or  80  per  cent,  of  tlie 
cases.  As  Oppenheim  well  points  out,  the  intrinsic  value  of  this  symp- 
tom is  lessened  somewdiat  because  of  its  subjective  character.  Neverthe- 
less, when  the  pains  are  present  their  character  and  distribution  can 
hardly  be  mistaken.  They  are  quick,  sharp  and  distressing.  They  are 
characterized  as  lancinating,  lightning-like,  fulgurating.  They  are  mo- 
mentary in  duration,  appear  in  most  unexpected  spots  and  do  not  follow 
the  anatomical  distribution  of  any  particular  nerve  or  set  of  nerves. 
They  may  be  frequent  and  succeed  one  another  with  great  rapidity  in 
the  course  of  a  number  of  hours  or  days.  Then  they  may  remain  away 
for  many  hours,  days,  weeks  or  even  months,  only  to  reappear  again 
in  all  their  pristine  severity  and  freakishness.  They  have  to  be  endured 
in  any  part  of  the  body,  though  in  the  vast  majority  of  the  cases  they 
occur  in  the  legs.  The  trunk  suflrers  next  in  frequency  with  them,  then 
the  arms,  and  lastly  the  thighs.  Intense  hypcrccsthcsia  is  sometimes 
located  where  the  pains  have  occurred. 

As  the  disease  advances  the  pains  gradually  lessen  and  become 


3/6  THE   NEURONIC   DISEASES 

of  a  dull,  boring  character.  Late  in  the  ataxic  stage,  and  all  during 
the  paralytic  stage,  the}^  are  practically  absent.  When  they  attack  the 
viscera,  the  sexual  apparatus,  the  anus,  most  peculiar  descriptions  may 
be  given  of  them.  They  have  been  known  to  be  present  as  long  as 
twenty-five  years  before  the  onset  of  any  other  manifestation  of  the 
disease.  The  victims  sometimes  become  habituated  tO'  them  and  go 
regularly  about  their  business  in  spite  of  them.  They  are  in  such  cases 
often  imagined  to  indicate  rheumatism,  neuralgia  and  other  painful 
affections.  This  fact  and  their  entirely  subjective  character  suggest 
most  vehemently  that  as  a  single  diagnostic  sign  they  can  awaken 
nothing  more  than  a  strong  suspicion  of  locomotor  ataxia,  though,  on 
the  other  hand,  they  must  never  be  assumed  too  positively  as  the  pains 
of  any  other  disease. 

The  Ar gyll-Robcrtson  pupil,  or  the  pupil  that  is  irresponsive  to 
light  but  readily  responsive  to  convergence  and  accommodation,  is,  in 
importance  as  a  symptom  of  loco'motor  ataxia,  second  only  to  West- 
phal's  sign,  though  it  is  not  so  constant  as  the  latter.  It  is  ofttimes  a 
very  early  symptom  and  may  even  precede  all  the  others  by  a  long 
period  of  time.  The  phenomenon  may  be  observed  in  only  one  eye  or 
it  may  be  more  marked  in  one  eye  than  in  the  other.  Occasionally  it 
is  preceded  by  a  sluggish  or  weakly  responsive  pupil.  It  occurs  in 
about  80  per  cent,  of  all  cases.  Sometimes  it  is  present  when  there  is  a 
lo'SS  of  the  cutaneous  reflex  contraction  of  the  pupil.  Myosis  and,  less 
frequently,  mydriasis  may  accompany  reflex  iridoplegia.  According  to 
Rochon-Duvigneaud  and  Heitz,  myosis  is  regularly  accompanied  by  a 
simple  Argyll-Robertson,  that  is  to  say,  the  contraction  to  convergence 
is  perfect ;  but  mydriasis  is  always  accompanied  by  a  complicated 
Argyll  symptO'm,  or  one  in  which  the  contraction  to  convergence  is  ab- 
sent or  defective.  In  both  the  reaction  to  light,  of  course,  is  totally 
abolished.  Though  this  remarkable  form  of  reflex  iridoplegia  is  some- 
times witnessed  in  general  paresis  and  in  acquired  or  congenital  syphilis, 
it  is  so  much  more  common  in  tabes  that  with  any  other  single  symptom 
it  may  be  adopted  as  the  ground  for  a  po'sitive  diagnosis.  It  may  be  the 
only  important  sign  of  those  present. 

Oppenheim  regards  analgesia,  with  or  without  impaired  sensibility, 
as  one  of  the  four  cardinal  symptoms  of  the  first  stage.  There  is  no 
question  that  disturbances  of  the  pain  sense,  tactile,  temperature  and 
muscular  senses  may  all  appear  early  and  prominently.  In  the  order 
of  their  frequency  these  sensory  phenomena  appear  about 
as  follows :  Various  parcesthesia:  and  numbness,  gi?  die-sensation, 
anesthesia  and  analgesia,  loss  of  muscular  sense.  Various  combina- 
tions, however,  are  exhibited  by  different  patients  of  anaesthesia,  anal- 
gesia, hypsesthesia,  hypalgesia,  hypersesthesia,  hyperalgesia  and  re- 
tardation of  the  sense  of  touch,  pain  and  temperature. 

When  the  cases  come  actually  under  examination  it  is  probably  true, 
as  stated  by  most  authors,  that  tactile  ancesthesia  is  the  most  frequent 
and  constant  sensory  disturbance.  In  the  extremities  it  is  usually  of  the 
blunted,  stocking  or  gauntlet  type.  In  the  trunk  it  consists  of  bands 
or  partial  bands  of  anaesthesia  to  touch  only,  and  not  pain,  also-,  as  is  the 
case  sometimes  in  the  limbs.     Hitzig  first  called  attention  to  this  symp- 


THE   NEURONIC  DISEASES  177 

torn,  but  we  are  indebted  to  Laehr,  Patrick  and  others  for  its  special 
investigation.  The  anaesthetic  area  does  not  correspond  with  the 
cutaneous  distribution  of  intercostal  nerves,  but  with  the  innervation  as 
represented  by  the  spinal  cord  segments.  It  is  more  horizontal  than 
is  the  course  of  the  spinal  nerves.  These  bands  are  of  varying  width 
and  run  from  the  median  line  toward  the  axillary  line.  When  numer- 
ous they  suggest,  considered  together,  a  sort  of  broad  girdle  disturb- 
ance. 

This  trunk  anaesthesia  may  conservatively  be  said  to  occur  in  about 
80  per  cent,  of  all  cases.  According  to  Alott  trunk  anesthesia  is  present 
in  all  cases  with  gastric  crises  and  covers  mostly  the  zones  of  four  or 
five  dorsal  roots.  As  the  upper  cervical  roots  of  the  brachial  plexus 
are  rarely  diseased,  it  seldom  extends  above  the  second  intercostal 
space. 

Thermo-anasthesia  is  far  less  frequently  met  with  than  tactile  an- 
aesthesia and  analgesia. 

The  Romberg  symptom,  or  static  ataxia,  swaying  with  the  eyes 
closed,  belongs  to  the  latter  part  of  the  pre-ataxic  stage.  It  occurs  in 
about  80  per  cent,  of  cases.  It  is  well  brought  out,  and  its  pathological 
origin  well  emphasized,  by  the  simple  manoeuvre,  suggested  by  Oppen- 
heim,  of  having  the  patient,  with  his  eyes  shut,  bend  his  back  and  then 
straighten  himself  again. 

,  The  other  symptoms  that  are  occasionally  observed  in  the  first 
stage  of  the  disease,  with  or  without  one  or  more  of  the  above,  may 
appear  for  the  first  time  in  any  stage  and  so  will  be  discussed  after  I 
have  finished  the  picture  of  the  disease  in  its  entire  course. 

The  first  stage  or  any  particular  symptom  of  the  first  stage  may 
last  many  years  before  the  onset  of  the  ataxic  stage.  There  are  often 
periods  of  quiescence  in  the  course  of  the  disease  or  new  pre-ataxic 
manifestations  make  their  appearance.  As  the  trouble  progresses, 
however,  the  pains  become  more  sharp  and  frequent,  the  sexual  im- 
jx>tence  becomes  complete  the  gait  develops  a  slight  uncertainty,  vis- 
ceral and  laryngeal  crises  become  alarming,  vision  gets  duller,  deep 
numbness  replaces  the  paraesthesiae  and  possibly  slight  changes  begin 
to  be  noticed  in  the  joints.  The  symptoms  that  were  already  present 
become,  as  a  rule,  more  pronounced.  The  disease  shows  decidedly  that 
it  is  progressing. 

When  the  S}'mptoms  have  reached  the  stage  at  which  the  incoor- 
dination of  movement  is  distinctly  noticeable,  the  patient  is  said  to 
have  arrived  at  the  second  or  ataxic  period.  In  this  period  all  of  the 
earlier  manifestations  that  were  present  become  more  marked,  except 
the  pains  and  crises,  which  now  diminish  both  in  severity  and  fre- 
quency. The  ataxia  is  the  great  symptom  of  this  stage  and  so  far  over- 
shadows all  the  others  that  Duchenne  was  led  by  it  to  give  the  name  to 
the  disease  that  he  did.  It  should  not  be  forgotten,  however,  that 
though  the  incoordination  is  the  most  obvious  symptom,  it  is  not  by  any 
means  the  most  important. 

Ataxia  appears  in  the  legs  in  about  75  per  cent,  of  all  cases,  and 
in  the  arms  in  about  8  per  cent.  The  s}'mptom  occur.-;  in  other  affections 
than   tabes,   notably   in    multiple    neuritis,    disseminated    cerebrospinal 


378 


THE   XEUROXIC   DISEASES 


FIGURE  64- 


FIGURE  65 


Trunk  anaesthesia  in  locomotor  ataxia. 


THE   NEURONIC   DISEASES  379 

sclerosis  and  cerebellar  disease.  When  it  has  appeared,  however,  in 
the  course  of  tabes,  the  disease  is  usually  so  far  advanced  that  there  are 
other  indications  present  which  render  the  diagnosis  a  comparatively 
-easy  one.  The  affection  at  this  time  has  reached  its  full  development. 
The  movements  of  the  arm  or  leg  will  be  observed  to  be  full  and  strong. 
In  other  words,  there  is  absolutely  no  motor  paralysis.  In  walking  the 
patient  exhibits  a  decided  uncertainty,  especially  if  the  room  be  dark- 
■ened.  In  fact,  it  is  sometimes  quite  impossible  for  him  to  get  about  at 
all  in  the  night.  Occasionally  the  trouble  is  first  noticed  by  the  patient 
when  he  ascends  or  descends  a  flight  of  steps.  He  stumbles  unaccount- 
■ably.  Not  rarely  it  is  noticeable  objectively  before  the  patient  himself 
is  aware  of  it.  A  momentary  closing  of  the  eyes,  or  a  looking  away 
from  the  floor  or  neighboring  wall  mcreases  the  ataxia  so  much  that  it 
is  all  but  impossible  to  walk.  In  walking  the  patient  lifts  his  leg 
Tiigher  than  it  is  necessary,  rotates  it  slightly  outward,  jerks  it  forward, 
stamps  it  down  upon  the  floor  with  the  heel  first  and  the  toes  last. 
AVhen  he  is  seated  the  ataxia  is  observed  as  soon  as  he  is  asked  to  kick 
the  leg  of  the  table. 

With  the  hand  he  finds  it  difficult  to  perform  the  more  delicate  and 
■complicated  movements,  such  as  writing,  buttoning  his  clothes  or  touch- 
ing the  end  of  his  nose  cjuickly  when  his  eyes  are  shut. 

Ataxia  may  involve  the  facial  and  tongue  muscles,  though  only 
^ery  rarely. 

More  significant  still  are  the  spontaneous  inovements,  which  are 
sometimes  seen  in  the  ataxic  arms  or  legs.  They  are  entirely  involun- 
tary. The  patient  cannot  keep  his  hmbs  quiet.  The  arm  suddenly  rises 
to  an  elevated  position  or  the  hand  is  lifted  up,  and  all  without  the  pa- 
tient's knowledge  if  he  happen  not  to  be  looking.  According  to  Hirsch- 
terg,  these  weird  movements  are  not  the  result  of  a  complication,  but 
are  a  manifestation  of  the  incoordination.  Like  the  latter,  they  are 
increased  when  the  eyes  are  closed. 

The  duration  of  the  ataxic  stage  may  be  many  years  and,  like  the 
preceding  period,  be  characterized  by  intervals  of  apparent  quiescence 
or  slight  remission  in  the  progress  of  the  disease. 

As  the  second  period  draws  towards  its  close  the  incoordination 
"becomes  so  bad  that  it  is  quite  impossible  for  the  patient  to  move  about 
-at  all.  In  a  short  time  he  takes  to  his  bed  and  the  disease  passes  into 
the  so-called  paralytic  stagf,  which,  as  a  rule,  is  much  shorter  than 
•either  of  the  other  two.  'The  pains  have  at  last  ceased.  The  eyesight 
Is  almost  entirely  gone.  The  anaesthesia  and  the  analgesia  are  extensive 
and  profound.  The  bladder  and  the  rectal  functions  are  most  seriously 
•disarranged.  Trophic  disturbances  result  in  obstinate  ulcers,  bed-sores, 
muscular  wasting  and  especially  softening  and  disease  of  the  bones  and 
joints.  Distortions  and  spontaneous  fractures  are  seen  in  this  stage. 
The  muscular  sense  is  lost  and  the  stereognostic  sense  is  gravely  dis- 
turbed. Anosmia  and  deafness  even  may  be  present.  AA'ith  all  this, 
"however,  there  is  still  no  actual  paralysis  if  the  case  is  "an  uncomplicated 
one.  The  mind  unfortunately  remains  clear  as  a  rule,  though  in  some 
-cases  it  happily  becomes  clouded  or  weakened.  The  patient  grows 
abnormallv  emotional.    Thus  bedridden,  foolish,  wasted,  a  physical  and 


38o  . 


THE   NEURONIC   DISEASES 

FIGURE  66. 


Locomotor  ataxia.     From  a  photograph  in  the   Pathological   Museum   of  the 
Med.  Department  of  the  University  of  Illinois. 


THE   NEURONIC   DISEASES  381 

■mental  wreck,  the  victim  lingers  helplessly  on  a  few  months  more  until 
■complete  exhaustion  from  bedsores,  cystitis,  pyonephrosis  or  some  other 
intercurrent  malady  mercifully  puts  an  end  to  the  sad  picture. 

There  are  symptoms  that  ma}'  appear  at  any  time  in  the  course  of 
-a  locomotor'  ataxia  and  be  indicative  of  the  disease ;  but  they  are  not 
as  constant  nor  as  frequent  as  those  just  referred  to.  Though  thev  are 
of  less  value  in  the  establishment  of  the  diagnosis,  they  are  strongly  con- 
iirmatory  when  they  constitute  a  part  of  the  composite  picture.  Oc- 
casionally they  may  appear  alone  or  early  in  the  disease.  Thev  may  be 
unaccompanied  for  a  long  period  of  time  by  any  other  symptom.  Under 
such  circumstances  they  should  always  awaken  a  suspicion  of  tabes 
and  keep  the  attendant  on  the  alert  to  detect  the  slightest  manifestation 
of  any  other  sign  that  will  confirm  the  suspicion. 

Bladder  disturbances  may  be  among  the  earliest  symptoms.  Thev 
occur  in  about  60  per  cent,  of  the  cases.  Among  my  own  cases  this 
was  a  ver\-  frequent  symptom.  At 'first  there  is  a  little  difficulty  in 
micturition.  The  patient  cannot  void  his  urine  when  he  feels  he  ought 
to.  Then  again  he  may  feel  a  desire  to  void  it  too  frequently.  Grad- 
ually the  trouble  increases  until  in  the  later  stages-  of  the  disease  actual 
incontinence  and  retention  occur.  In  some  cases  this  trouble  disap- 
pears in  spite  of  the  progressive  character  of  the  malady.  An  early 
bladder  disturbance  coming  011  several  years  after  syphilitic  infection 
■should  always  be  mistrusted. 

Constipation  usually,  and  for  the  same  reason,  accompanies  the 
"vesical  trouble. 

The  early  satyriasis  and  impotence  I  have  already  referred  to. 
Oppenheim  has  seen  an  involuntary  priapism  continue  for  weeks  at  a 
time.  Nocturnal  attacks  are  not  uncommon.  Impotence  usually  follows 
all  such  manifestations  and  is  generally  complete  inside  of  a  year.  I 
am  convinced,  however,  that  too  much  stress  is  placed  by  the  pro- 
fession upon  the  sexual  disturbances  as  a  sign  of  tabes.  I  saw  a  case 
of  advanced  locomotor  ataxia  with  all  the  typical  symptoms,  early 
pains,  Westphal  sign,  Argyll -Robertson  pupil  and  extreme  ataxia  pres- 
•ent,  which  several  physicians  declined  to  pronounce  tabes  because  there 
was  not,  and  never  had  been,  the  slightest  disturbance  of  the  sexual 
function.  In  women  a  sort  of  nymphomania  sometimes  occurs  par- 
oxysmally  and  is  spoken  of  as  a  clitoric  crisis. 

The  so-called  crises  are  important  phenomena.  They  occur  in  the 
earlier  periods  of  the  disease.  As  their  name  in  part  indicates,  they  are 
sudden,  unexpected,  teroporar}^  disturbances  of  a  more  or  less  violent 
nature  and  sensory  in  origin,  in  the  viscera  and  visceral  functions.  In 
the  order  of  their  frequency  they  may  be  listed  about  as  follows :  Gas- 
tric, rectal,  lar\-ngeal.  pharyngeal,  intestinal,  cardiac,  renal  and  bladder. 

The  gastric  and  laryngeal  crises  are  the  more  important,  the  former 
on  account  of  their  frequency  (36  per  cent,  in  Mott's  cases),  and  the 
latter  on  account  of  their  alarming  character.  All  of  the  other  crises 
are  comparatively  rare.  In  the  gastric  crises  the  patient  experiences  a 
sudden,  twisting,  wrenching  pain  in  the  region  of  the  stomach.  He 
vomits  first  his  food,  then  gall.  He  grows  pale  and  weak,  and  shows 
hy  the  rapidity  of  his  pulse  and  generally  that  he  is  in  great  distress. 


382  THE   XEUROXIC   DISEASES 

The  crisis  passes  after  several  hours,  or  it  may  be  days  or  weeks,  as- 
suddenly  as  it  came  on.  There  is  no  foretelling  when  it  may  reappear. 
Trunk  anaesthesia  can  be  discovered  in  all  cases  with  gastric  crises. 
Usually  these,  as  well  as  the  other  crises,  alternate  with  the  lancinating^ 
pains  and  sometimes  are  accompanied  by  a  slight  fever. 

The  laryngeal  crisis  occurs  much  less  often.  When  seized  by  it  the 
patient  chokes  and  coughs  suddenly  and  for  a  few  minutes  experiences- 
a  paroxysm,  with  cyanosis,  such  as  occurs  in  pertussis.  The  attack  is 
sometimes  very  severe  and  distressing  and  the  victim  feels  as  if  he  were 
about  to  die  from  asphyxia.  The  lar\"ngoscope  discovers  nothing  ab- 
normal. Paralysis  of  the  laryngeal  muscles,  especially  of  the  crico- 
arytenoidei  postici,  has  been  obsen^ed  late  in  tabes. 

A  rectal  crisis  occurred  in  8  per  cent,  of  Mott's  cases.  It  consists 
of  sudden  pain  and  evacuation,  or  of  colic  with  diarrhoea. 

Abrupt  disturbances  of  deglutition  are  regarded  as  pharyngeal 
crises. 

The  implication  of  the  vago-accessorius  nerve  is  shown  by  the  oc- 
casional cardiac  and  respiratory  crises.  There  is  a  sharp,  quick  pain 
near  the  heart,  with  a  sudden  feeling  of  oppression  and  a  rapid,  irregu- 
lar pulse.  Angina  pectoris  is  not  unfrequently  suspected,  so  similar  are 
the  two  phenomena. 

Pain  in  the  chest,  with  disturbances  of  the  respiratory  function,. 
may  occur.  In  a  case  observed  by  Egger  in  Dejerine's  clinic  a  brachyp- 
nnea  had  lasted  at  least  four  years.  The  respirations  were  reduced  to 
seven  or  eight  per  minute  for  two  or  three  hours  after  eating.  Vomit- 
ing, roughness  of  the  voice  and  tachycardia  were  also  present. 

Renal  and  bladder  crises  are  characterized  by  sudden,  sharp  pains 
in  the  region  of  those  organs.  Pel  and  Oppler  have  described  respec- 
tively a  temperature  crisis. 

Optic  nerve  atrophy  probably  occurs  more  frequently  than  some 
collections  of  cases  of  tabes  state.  It  is  a  symptom  that  is  not  objective- 
ly noticeable  and  is  not  often  enough  sought  for.  ^lott  found  it  in 
50  per  cent,  of  the  cases  of  hospital  tabes  examined  by  him.  Among 
Starr's  cases  it  was  found  in  about  9  per  cent.  The  average,  calculated 
from  the  statistics  of  numerous  observers,  is  about  20  per  cent.  It  is 
sometimes  a  very  early  s}'mptom  and  has  been  known  to  precede  all 
other  signs  for  many  years.  It  may  occur  in  any  period  of  the  disease. 
It  is  a  serious  trouble,  as  it  is  often  the  forerunner  of  brain  involve- 
ment. The  absolute  reliability  of  Benedikt's  dictum,  that  tabetic  symp- 
toms usually  recede  or  come  to  a  standstill  when  optic  atrophy  makes 
its  appearance,  is  open  to  grave  doubt,  thoug'h  in  some  instances  it  does 
seem  to  be  true.  The  beginning  atrophic  changes  can  sometimes 
be  detected  with  the  ophthalmoscope  when  the  vision  is  but  little  inter- 
fered with.  The  atrophy  is  of  the  simple,  progressive  type  and  in 
uncomplicated  tabes  is  never  preceded  by  optic  neuritis.  There  is  no 
swelling  or  hypersemia  of  the  disc.  It  generally  is  first  visible  in  the 
temporal  halves  and  gradually  involves  the  whole  field.  At  first  the 
r.cuteness  of  vision  is  good  and  there  are  no  central  scotomata  for  colors 
or  white.  The  ^^sual  field  is  gradually,  concentrically  and  sector-like 
narrowed.     Sooner  or  later  complete  blindness  comes  on :    in  the  ma- 


THE  NEURONIC   DISEASES  383 

jority  of  cases  in  about  three  years.  One  eye  may  be  affected  sooner 
than  the  other,  but  as  a  rule  the  degeneration  is  bilateral. 

Ocular  palsies  are  the  most  frequent  cranial  nerve  symptoms  of 
tabes.  Any  ocular  muscle,  or  muscles,  may  be  involved,  so  that  the 
paralysis  is  never  an  associative  one.  In  the  earlier  period  of  the  dis- 
ease it  is  apt  to  be  transient ;  later  on  it  becomes  chronic  and  permanent. 
Diplopia,  ptosis,  strabismus  and  even  nystagmus  are  met  with.  Oph- 
thalmoplegia may  occur,  as  well  as  myosis  and  w.ydriasis. 

The  trophic  phenomena  that  occur  in  the  course  of  locomotor  ataxia 
are  important.  They  are  late  symptoms  usually,  though  they  have  been 
seen  in  the  pre-ataxic  stage.  Of  these  the  arthropathies,  Charcot  joints, 
are  the  miost  significant  and  occur  in  about  10  per  cent,  of  the  cases. 
The  knee-joint  is  probably  the  most  frequently  affected.  The  phenom- 
ena may,  however,  be  seen  in  the  hip- joint,  the  shoulder,  the  elbow,  the 
ribs,  the  ankle  and  the  spinal  column.  In  many  respects  the  trouble 
resembles  an  arthritis  except  that  the  latter  is  accompanied  by  pain, 
redness  and  fever.  In  the  Charcot  joint  a  sudden  swelling  comes  on, 
with  a  profuse  accumulation  of  fluid;  the  intra-capsular  tissues  are 
destroyed;  the  capsule  loses  its  power  of  contraction;  and  a  condition 
resembling  a  luxation  or  subluxation  supervenes.  New  substance  is 
found  in  the  joint,  and  either  as  an  excrescence  or  free  causes  a  more  or 
less  marked  deformity.  Under  these  circumstances  the  long  bones  are 
brittle  so  that  spontaneous  fractures  are  frequent. 

The  perforating  ulcer,  most  commonly  located  in  the  ball  of  the  foot 
and  often  bilaterally  in  both  feet,  is  a  trophic  tabetic  symptom.  Other 
rare  manifestations  of  this  character  are  spontaneous  gangrene,  spon- 
taneous falling  of  the  nails,  nutritional  disturbance  of  the  skin,  falling 
out  of  the  teeth,  ulceration  of  the  mucous  membrane  of  the  mouth 
with  alteration  of  the  sense  of  taste,  neuroparalytic  keratitis  and  other 
trigeminal  manifestations,  herpes,  facial  hemiatrophy  and  forms  of 
muscular  atrophy.  These  are  all  comparatively  rare  symptoms.  Some 
of  them,  as,  for  instance,  the  muscular  atrophy,  may  be  extensive  and 
involve  the  whole  bocW.  Multiple  neuritis  (Dejerine)  is  probably  the 
cause  of  them,  though  many  hold  that  they  are  true  spinal  cord  symp- 
toms. 

Unilateral  hyperidrosis,  ecchymosis  or  suggillation  and  various 
exanthems  have  been  reported,  though  it  is  questionable  whether  they 
are  true  tabetic  symptoms. 

Cerebral  symptoms  occur  in  the  course  of  tabes,  but  they  are  indica- 
tive of  a  complication.  They  should  be  noted,  nevertheless,  because 
they  often  modify  the  true  tabetic  symptoms.  The  ansesthesia  and  anal- 
gesia are  naturally  different  when  there  are  psychic  aberrations  pres- 
ent, from  what  they  would  be  otherwise.  Sudden  attacks  of  vertigo, 
congestive,  apoplectiform,  epileptiform  and  migrainous  seizures,  acute 
mania  with  slight  changes  of  character,  hallucinations,  even  visual 
hallucinations  with  complete  optic  atrophy,  may  all  occur  in  tabetics. 
They  indicate,  however,  a  cerebral  complication,  such  as  cerebral 
syphilis  or  incipient  dementia  paralytica. 

Diagnosis. — The  diagnosis  of  locomotor  ataxia  is  not  difficult  in 
typical  and  in  advanced  cases.    Only  in  the  early  period  of  the  disease 


384  THE   NEURONIC   DISEASES 

is  c(~>nfusion  encountered.  One  ought  never  to  doom  a  patient  to  so 
hopeless  a  malady  unless  two  or  more  signs  are  positively  present. 
Not  even  an  Arg}'ll-Robertson  pupil  or  a  loss  of  the  patella  reflex  alone 
will  warrant  a  diagnosis.  A  simple,  progressive  optic  atrophy  is  prob- 
ably the  strongest  single  indication  of  a  probable  tabes,  but  even  it 
should  only  awaken  a  strong  suspicion.  Two  or  more  symptoms, 
therefore,  must  be  observed  before  a  positive  diagnosis  can  be  offered. 
The  combinations  that  these  symptoms  may  assume,  the  groupings 
which  they  may  exhibit,  are  almost  innumerable.  Care,  thoroughness 
and  a  recollection  of  the  cardinal,  sensory-trophic  character  of  the  dis- 
ease, if  exercised  in  the  examination  of  every  case,  will  result  in  a 
minimum  amount  of  error  in  diagnosis. 

A  careful  comparison  of  the  symptomatology  of  locomotor  ataxia 
with  that  of  neurasthenia,  hysteria,  h3^pochondriasis,  aberrant  forms  of 
exophthalmic  goitre,  chronic  myelitis,  spinal  tumor  and  hereditary 
ataxia  will  enable  one  to  make  easily  a  differential  diagnosis  between 
these  affections.  The  Westphal  sign,  the  Argyll-Robertson  pupil,  the 
lancinating  pains,  the  analgesia,  the  optic  atrophy,  the  transient  diplopia, 
the  crises  and  the  ataxia  are  all  characteristic. 

Among  the  affections  that  do  give  rise  to  considerable  trouble  may 
be  mentioned  especially  multiple  neuritis,  syphilitic  pseudo-tabes  or 
spinal  syphilis,  multiple  sclerosis  and  general  paresis.  Moreover,  these 
diseases  may  be  associated  with  the  tabes,  a  fact  which  sometimes  adds 
immensely  to  the  difficulty  of  the  diagnosis. 

In  multiple  neuritis  there  is  a  history  usually  of  an  intoxication 
(alcohol,  lead,  arsenic),  or  an  infection  (tuberculosis,  fevers),  rather 
than  of  syphilis.  There  is  a  true,  flaccid  paralysis.  There  are  local 
pains,  elicited  by  pressure  upon  the  nerves  and  muscles.  The  muscle:^ 
exhibit  a  high  degree  of  atrophy  early  and  the  electrical  responses  are 
characteristically  altered.  In  many  cases  of  multiple  neuritis  a  peculiar 
psychosis  occurs  in  which  amnesia,  disorientation,  confabulation  and 
pseudo-reminiscence  are  notable. 

Perhaps  the  greatest  difficulty  is  met  with  in  distinguishing  a 
syphilitic  pseudo-tahcs,  or  spinal  svphilis,  with  simulation  of  tabes,  from 
true  tabes.  Syphilis  and  parasyphilis  are  not  identical  in  the  usual 
acceptation  of  the  terms.  One  is  not  even  a  complication  of  the  other, 
though  they  both  may  be  present  in  the  same  patient.  Nevertheless, 
whether  so  associated  or  not,  they  sometimes  have  many  symptoms  in 
common  and  lead  to  a  confused-  diagnosis.  It  is  probable  that  most 
of  the  reported  cures  or  improvements  in  locomotor  ataxia  that  have 
been  credited  to  heroic  doses  of  mercury  and  iodides  were  made  possi- 
ble because  the  cases  were  really  cases  of  syphilitic  pseudo-tabes  and  not 
of  true  tabes.  Collins  has  ably  pointed  out  that  syphilitic  pseudo-tabes 
may  be  diagnosed  when  one  or  another  symptom  is  of  disproportionate 
severity;  when  the  tendon-jerks  behave  peculiarly,  as,  for  example, 
being  absent  on  one  side,  exaggerated  on  the  other  or  returning  after 
a  period  of  absence;  when  symptoms  of  implication  of  the  lateral  por- 
tion of  the  cord  are  superimposed  upon  those  of  tabes,  especially  when 
such  S5'mptoms  are  associated  with  unilateral  mydriasis  or  unilateral 
reflex  iridoplegia ;    whenever  there  is  considerable  or  permanent  im  - 


THE  NEURONIC  DISEASES  385 

provement  under  antisyphilitic  medication ;  and  finally  whenever  there 
is  an  association  of  motor  paralysis  (save  transient  ocular  palsy)  with 
the  symptoms  of  tabes,  whether  it  be  dependent  upon  brain,  medullar)' 
or  cord  lesion. 

1  once  saw  a  case  of  multiple  sclerosis  diagnosed  as  locomotor 
ataxia  by  able  diagnosticians.  When  the  lesions  involve  the  lumbar 
cord  especially,  the  ataxia,  the  loss  of  patella  reflex,  the  pains  may  all 
be  looked  for.  Under  such  circumstances  search  well  for  intra-cranial 
symptoms  and  note  the  characteristic  involvement  of  the  upper  extremi- 
ties. Sooner  or  later  nystagmus,  dysarthria,  tremor,  paretic  rather  than 
sensory  incodrdination,  intentional  choreiform  jerking  and  increase  of 
tendon  reflexes  in  the  upper  extremities  will  enable  one  to  recognize 
the  case  as  disseminated  sclerosis. 

As  is  well  known,  general  paresis  is  closely  related,  pathologically 
and  symptomatically,  to  tabes.  In  many  cases  of  the  spinal  disease 
the  onset  of  mental  symptoms  indicates  the  complicating  presence  of 
the  cerebral  aflfection.  Sometimes  both  sets  of  symptoms  make  their 
appearance  together  in  the  beginning.  The  diagnosis  has  to  wait  often, 
under  such  circumstances,  before  it  can  be  positively  determined  which 
disease  is  to  predominate.  In  spite  of  the  presence  of  optic  atrophy,  loss 
of  knee-jerks  and  the  Argyll-Robertson  pupil,  the  existence  of  mental 
manifestations,  speech  disturbances,  fibrillary  tremor  of  the  tongue  and 
apoplectiform  attacks  points  to  dementia  paralytica.  As  I  have  said 
under  the  symptomatology,  pure  tabes  may  in  some  cases  be  accom- 
panied by  mental  manifestations.  These,  of  course,  are  not  tO'  be  con- 
founded with  paresis. 

Prognosis. — Locomotor  ataxia  being  a  slow,  progressive,  degen- 
erative disease,  it  is  prolonged  in  its  course  and  its  prognosis,  while 
favorable  as  to  life,  is  exceedingly  bad  as  to  recovery.  There  seem 
to  be  periods  of  quiescence  during  the  course  of  the  malady  and  usually 
the  greatest  hope  that  dare  be  entertained,  either  with  or  without 
treatment,  is  to  bring  on  such  a  temporary  cessation  of  the  general 
advance.  A  large  number  of  cases  terminate  in  about  ten  years.  Somie 
have  lasted  twenty-five  years  or  more.  Death  is  generally  the  result 
of  exhaustion,  cystitis,  pyelonephritis,  decubitus,  infection  or  other  in- 
tercurrent trouble,  as  in  most  of  these  chronic  degenerative  maladies. 

In  the  first  stage  of  the  disease  recovery  as  a  very  rare  event  may 
occur.  The  earlier  the  stage  and  the  less  severe  the  symptoms  the 
better  the  chances.  In  this  stage  many  of  the  cases,  with  proper  care, 
may  become  stationary  and  endurable  for  a  long  time. 

In  the  second  stage  the  prognosis  is  hopeless  so  far  as  any  change 
for  the  better  is  concerned.  Still  this  stage  is  not  always  unbearable. 
The  patient  can  sometimes  get  about  and  even  attend  to  business.  If 
the  disease  continues  quiescent  during  this  stage  or  during  the  greater 
p3rt  of  it,  the  patient  may  carry  on  the  activities  of  a  fairly  useful 
citizen  and  not  be  entirely  unhappy.  Such  a  state  of  afifairs  may  last 
for  years. 

In  the  third  stage  there  is  absolutely  no  more  hope,  but  rather  an 
outlook  for  an  early  termination. 

It  has  been  noticed  that  a  certain  prognostic  value  may  be  placet 


386  THE   NEURONIC   DISEASES 

Upon  particular  symptoms.  For  instance,  an  early  optic  atrophy  usu- 
ally means  a  long  duration  of  the  disease ;  a  quick  development  of 
bladder  trouble  and  ataxia  indicates  a  much  shorter  course,  and  possi- 
bly an  early  death  :  severe  lancinating  pains  and  gastric  crises  produce 
an  exhausting  and  wearing  strain  upon  the  patient's  general  nervous 
system  and  so  hasten  the  end. 

The  disappearance  of  the  pains,  of  the  ophthalmoplegia,  of  the 
crises  and  of  other  symptoms,  notwithstanding  the  onward  course  of 
the  disease,  must  not  deceive  the  physician  in  regard  to  the  prognosis. 

Treatment. — The  treatment  of  locomotor  ataxia  is  limited.  In 
the  early  stages,  before  the  ataxia  has  appeared,  an  attempt  at  a  cure 
may  be  made ;  especially  if  the  tabetic  symptoms  have  shown  themselves 
within  two  years  of  the  primary  specific  infection,  are  not  very  severe 
or  rapidly  progressive,  and  are  associated  with  other  manifestations 
indicative  of  active  syphihs  inside  or  outside  of  the  nervous  system. 
A  few  complete  cures  have  been  reported  under  such  circumstances, 
though  it  is  a  question  whether  the  diagnosis  was  correct  or  whether 
the  cure,  so-called,  was  not  in  the  syphilitic  manifestations  rather  than 
in  the  tabetic.  In  the  large  majority  of  instances  treated  thus  early 
the  most  favorable  result  obtained  was  the  cessation  of  the  course  of 
the  malady.  In  a  disease  that  is  so  steadily  progressive  and  whose 
primary  lesion  is  a  neuronic  degeneration,  even  such  a  result  as  a 
temporarv  cessation  of  the  onward  advance  is  to  be  looked  upon  as  a 
happv  event,  notwithstanding  the  fact  that  such  a  result  is  known  to 
occur  now  and  then  without  treatment  and  thus  divides  the  credit  with 
the  treatment. 

It  is  in  the  first  stage  that  the  most  troublesome  of  all  questions  in 
the  therapy  of  locomotor  ataxia  presents  itself — namely,  whether  or 
not  to  use  antisxphilitic  medication.  I  am  satisfied  that  if  the  symp- 
toms are  entirely  tabetic  and  they  have  appeared  two  years  after  the 
infection,  the  administration  of  mercury  and  the  iodides  will  do  no 
good,  but  may  do  a  great  deal  of  harm.  If  the  lancinating  pains  are 
unusually  severe  and  frequent,  and  especially  if  the  onset  of  the  ataxia 
is  abrupt  and  early,  the  above  remedies  are  absolutely  contraindicated. 
\\'hen  in  doubt  it  is  safer  in  tabes  to  withhold  all  antisyphilitic  medica- 
tion than  to  experiment  with  it.  Even  if  it  be  granted  that  tabes  is 
nothing  but  a  fourth  stage  of  syphilis,  as  some  extremists  are  begin- 
ning to  teach,  and  not  mere  parasyphilis  as  Foumier  used  to  maintain, 
it  is  a  form  of  syphilis  that  seems  to  be  beyond  the  reach  of  mercury  and 
the  iodides. 

All  of  these  suggestions  are  doubly  applicable  to  the  ataxic  stage  of 
the  disease.  In  the  paralytic  stage  they  are  not  even  up  for  considera- 
tion. 

After  the  first  stage  the  treatment  is  entirely  general  and  symp- 
tomatic. Even  in  the  first  stage  symptomatic  measures  have  a  high 
degree  of  applicabilit}'. 

No  treatment  of  locom.otor  ata,xia  is  to  be  commended  in  which 
rest  is  not  an,  important  factor.  It  is  often  a  very  perplexing  question 
as  to  how  much  rest  is  to  be  enjoined.  In  the  earlier  stages  of  the  dis- 
ease I  believe  the  more  the  patient  keeps  quiet  the  better  it  will  be  for 


THE   XEURONIC   DISEASES  387 

him.  In  the  ataxic  stage  it  is  not  always  so  imperatively  necessary. 
In  the  third  stage  it  is  forced  upon  him  by  his  paralytic  condition. 

When  recommending  rest  we  must  be  careful  not  to  alarm  un- 
necessarily by  making  it  too  absolute.  In  fact,  a  certain  amount  of 
exercise,  short  of  the  awakening  of  the  feeling  of  weariness,  a  con- 
tinuation as  far  as  possible  in  the  business  and  social  affairs  of  life, 
an  avoidance  of  the  thought  that  he  is  doomed  to  a  life-long  invalidism, 
are  best  for  his  mental  and  physical  welfare.  He  should  be  urged  to 
lead  a  hfe  of  great  moderation,  regularity  and  even  tenor.  All  forms 
of  stimulation,  excess  and  dissipation  must  be  absolutely  forbidden. 
Sexual  excitement  must  be  prohibited  and  an  early  ataxic  had  better  be 
urged  not  to  marry.  I  saw  a  case  of  advanced  tabes  in  a  married  man 
who  continued  to  hold  intercourse  with  bis  wife  without  any  apparent 
ill  effects.  Shortly  after  her  death  he  consulted  me  in  regard  to  the 
possible  effect  upon  his  ataxia  of  the  continuation  of  his  sexual  activity 
illicitly.  Of  course,  there  could  be  but  one  answer  to  such  a  question. 
Cases  of  this  sort  are  exceptional. 

Alcoholic  stimulants  and  even  tobacco  had  better  be  given  up  in  the 
interests  of  health. 

A  man's  occupation  must  receive  some  consideration.  It  should 
be  changed  if  it  is  confining,  exhausting  or  dangerous.  I  urged  a 
bricklayer  with  only  a  partial  Argyll-Robertson  reaction,  loss  of  knee- 
jerks  and  an  occasional  lancinating  pain,  to  give  up  his  trade  at  once 
for  obvious  reasons.  A  clerk  who  was  obliged  to  sit  all  day  in  a 
cramped  position  was  persuaded  to  seek  some  mild  form  of  occupation 
that  took  him  more  into  the  open  air. 

Monotony,  whether  mental  or  physical,  must  be  avoided.  With 
the  avoidance  of  a  mental  or  physical  form-  of  monotonous  activitv, 
brief  intervals  of  absolute  rest,  lying  prone  upon  a  couch,  should  be 
arranged  for,  especially  during  the  pre-ataxic  stage  and  when  the  pains 
are  frequent  and  lively. 

The  bodily  nourishment  must  be  maintained  at  the  highest  pitch 
by  the  use  of  plain,  nourishing  food,  with  bat  a  modicum  of  tea  and 
coffee. 

Refreshing  sleep,  long  and  often,  should  be  encouraged  in  every 
possible  way. 

Amusements,  entertainments  and  games,  rural  pleasures  and  sum- 
m-er  resort  delights  must  all  be  indulged  in  with  great  moderation  and 
always  without  provoking  too  marked  emotional  excitement.  Moun- 
tain climbing  and  sea  bathing  are  risky  and  had  better  not  be  in- 
dulged in. 

Hot  and  cold  baths  should  not  be  taken,  but  the  regular  use  of 
tepid  bathing  to  keep  the  skin  clean  and  active  is  to  be  favored. 

The  functions  are  all  to  be  looked  after  and  kept  as  near  healthy 
rctivity  as  possible. 

In  a  word,  quiet,  moderation,  abundance  of  fresh  air  and  good  food, 
rnd  all  the  forces  that  go  toward  the  creation  and  preservation  of  con- 
stitutional vigor,  with  alternations  of  moderate  exercise,  with  plenty 
of  rest  and  sleep,  are  the  chief  elements  in  the  general  treatment  of 
tabes.     But  this  is  not  all,  for  the  symptomatic  treatment  is  always  an 


388  THE   NEURONIC  DISEASES 

important  factor  and  often  the  only  part  of  the  therapy  that  the  physi- 
cian is  called  upon  to  exercise  his  special  knowledge  in. 

The  drug  treatment  of  tabes  is  extremely  unsatisfactory.  Many 
remedies  have  been  proposed  and  tried,  but  none  of  them  has  retained 
the  universal  approval  of  the  profession.  ]\lost  of  them  were  sug- 
gested long  ago  when  our  knowledge  of  the  pathology  of  the  disease 
was  scanty.  It  was  thought  that  somehow  they  would  overcome  or  pre- 
vent the  sclerosis  which  was  believed  to  be  the  primary  trouble.  Now 
that  we  know  the  fundamental  process  is  a  slow,  progressive,  paren- 
chymatous degeneration,  we  are  not  surprised  at  the  successive  disap- 
pointments caused  by  one  vaunted  remedy  after  another.  Of  all  these 
general  alteratives  the  nitrate  of  silver  has  remained  in  favor  the  long- 
est. It  may  be  given  by  the  mouth  or  hypodermically.  It  must  be 
given  for  a  long  period  of  time,  with  frequent  intervals  of  rest  to 
prevent  argyria.  The  dose  is  about  a  quarter  of  a  grain  in  pill.  Ergot, 
potassium  iodide,  the  double  chloride  of  gold  and  sodium,  phosphorus, 
belladonna,  arsenic  and  barium  have  been  used.  I  have  not  seen  any 
benefit  that  could  be  clearly  attributed  to  any  one  of  these  numerous 
preparations.  The  nitrate  of  silver  is  the  only  one  of  the  group  that 
I  would  deem  worthy  of  a  trial.  Some  of  them,  such  as  arsenic,  small 
doses  of  phosphorus,  the  tincture  of  iron,  may  be  given  for  their  gen- 
eral tonic  effect.  Erb  counsels  strongly  against  strychnine,  and  most 
justly  so  in  regard  to  the  use  of  it  in  large  or  even  average  dosage. 
On  the  other  hand,  I  believe  that  strychnine  in  very  minute  doses,  not 
over  one  two-hundredth  of  a  grain  three  times  a  day,  when  added  to 
rest  and  other  general  measures,  is  a  most  valuable  remedy.  In  larger 
doses  it  may  be  absolutely  disastrous.  It  must  always  be  employed  with 
caution  and  one  had  better  err  on  the  side  of  giving  too  small  than  too 
large  doses. 

The  use  of  the  extracts  of  gray  matter,  especially  the  gray  matter 
of  the  sheep's  brain,  as  long  ago  recommended  by  Constantin  Paul,  to 
regenerate  atrophied  nerves,  moved  Leyden  to  recall  humorously  the 
similar  experiments  with  products  furnished  by  the  ass  in  Pliny's  time. 
The  same  atmosphere  of  the  comic  surrounds  the  use  of  Brown- 
Sequard's  testicular  fluid,  the  goat  lymph  and  the  other  startling  agents 
now  more  or  less  in  vogue.  These  primary,  degenerative  neuronic  dis- 
eases, progressive  and  hopeless,  ofifer  a  glorious  field  for  the  unscrupu- 
lous catch-penny  and  the  ignorant  quack. 

The  largest  opportunity  for  the  drug  treatment  of  locomotor  ataxia 
is  in  the  management  of  its  special  symptoms.  The  lancinating  pains 
are  the  symptoms  that  the  patient  most  vehem.ently  demands  relief  from. 
They  are  sometimes  excruciating,  they  are  always  wearing  and  ex- 
hausting. Ofttimes  if  they  are  mitigated  but  in  part  he  can  learn  to 
bear  them  and  for  years  may  go  about  his  ordinary  avocations  in  spite 
of  them.  The  remedies  that  have  from  time  to  time  been  recommended 
for  their  relief  are  now  almost  legion.  ^Most  of  them  will  give  rise  to 
disappointment.  Sometimes  one  w'ill  succeed  in  one  case,  only  to  fail 
in  another;  hence  it  is  well  to  have  a  full  armamentarium  ever  at 
hand.  The  opiates  and  morphine  are  to  be  avoided  as  long  as  possible, 
for  fear  of  establishing  a  dangerous  habit :    and  yet  they  are  the  most 


THE  Ni':i  Koxic  i)iS!:.\si:s  389 

effective  agents  we  have  to  combat  the  pains  with.  At  times  they 
must  be  used,  but  always  cautiously  and  for  as  brief  a  period  as  possi- 
ble. After  the  opiates  the  following  remedies  may  be  mentioned  : 
Codeine,  sodium  salicylate,  cantonin,  chloride  of  alummum,  acetanilid,. 
antipyrin,  phenacetin,  methylene  bltte,  analgen,  salipyrin,  lactophenin, 
pyramidon,  exalgine,  phosphorus,  solanin,  cannabis  indica,  neurodin  and 
bicarbonate  of  sodium.  Here  as  elsewhere  the  axiom  holds  true  that  the 
multiplicity  of  remedies  is  in  inverse  proportion  to  the  benefit  obtained 
fro'm  them.  Most  of  the  above  drugs  will  prove  disappointing  in  the 
majority  of  cases.  Exceptionally  this  or  that  one  may  be  found  effica- 
cious. 

The  crises  usually  need  special  attention.  The  local  application  of 
cocaine  for  the  laryngeal  crises,  and  the  hypodermic  injection  of  mor- 
phine for  the  gastric,  are  the  readiest  means  of  affording  relief.  So 
unsatisfactory  are  all  other  measures  that  one  is  disinclined  even  to  try 
them,  and  yet  morphine  must  be  withheld  from  a  tabetic  patient  as 
long  as  his  endurance  holds  out. 

Bladder  and  rectal  pains  may  be  combated  with  suppositories  of 
iodoform  and  belladonna,  codeine,  antipyrin,  ichthyol,  warm  injec- 
tions, etc. 

Morphine  and  oxalate  of  cerium  may  be  used  for  the  attacks  of 
vomiting.     Nothing  will  prevent  their  coming  on. 

For  insomnia  the  usual  remedies,  such  as  the  bromides,  chloral, 
paraldehyde,  hyoscyamus,  are  all  commendable. 

In  a  word,  the  symptomatic  management  of  tabes  is  no  different 
from  the  symptomatic  management  of  any  other  disease.  It  is  only 
somewhat  more  resistant  and  therefore  calls  for  more  powerful  reme- 
dies, such  as  morphine,  which  very  remedies  must  be  avoided.  One 
must  not  employ  his  strongest  agents  too  early  in  the  battle,  but  reserve 
them  until  later  when  the  struggle  grows  fiercer  and  all  other  measures 
have  completely  failed. 

Hydrotherapy  is  highly  commendable  in  all  cases  of  tabes,  if  em- 
ployed intelligently  and  with  a  certain  degree  of  regularity.  The 
chief  benefits  from  the  water-cures  of  this  country  and  of  Europe  are 
due  to  the  systematic  method  of  application  usually  carried  out,  and  not 
to  any  special  medicinal  virtues  in  the  water.  Sometimes  it  is  positively 
dangerous  for  a  patient  to  go  to  one  of  these  establishments,  for,  being 
absent  from  his  regular  attendant  and  under  the  care  of  those  who  are 
responsible  for  a  large  and  varied  assortment  of  patients,  he  is  apt  to  be 
neglected  or  to  urge  forms  of  heroic  treatment  that  may  hasten  the 
onward  progress  of  his  malady.  The  good  that  these  establishments 
afford  can  just  as  well  be  obtained  at  home  if  the  patient  is  tractable. 
For  ten  or  fifteen  minutes  every  day  a  tepid  bath  is  both  grateful  and 
health-giving.  Brine  and  carbonized  baths  are  excellent.  Hot  baths 
must  never  be  taken.  Sweat  and  vapor  baths,  recommended  by  Leyden 
for  early  tabes,  had  better  be  employed  with  great  caution.  Hot  baths 
are  one  of  the  dangers  of  the  springs  and  resorts  that  have  been  recom- 
mended. As  a  rule  the  temperature  of  the  water  should  never  be  above 
95  degrees  F.  Cold  baths  and  cold  douches  are  approved  of  by  some 
authorities.     Erb  treated  nineteen  patients  with  cold  baths,  of  whom 


390  THE   NEURONIC   DISEASES 

sixteen  were  benefited.  It  is  a  question,  however,  whether  the  risk  run 
does  not  outweigh  the  benefit  obtained.  Erb  affirms  that  a  bath  with 
a  temperature  above  58.5  degrees  F.  is  positively  injurious.  Cold  wcl 
cloths  to  the  lower  limbs,  their  immersion  in  cold  water  after  a  pre- 
liminary warming  with  warm,  moist  wrappings,  are  less  objectionable 
than  a  cold  full  bath.  The  water  may  be  from  48  to  66  degrees  F. 
The  time  of  the  immersion  should  be  not  longer  than  a  minute.  The 
limbs  should  be  vigorously  dry-rubbed  and  kept  at  rest  afterwards. 
Stimulation  of  the  cutaneous  circulation  is  the  object  aimed  at  in  this 
manoeuvre.  Cold  spinal  douches  I  would  never  recommend.  They  may 
prove  harmful. 

Electricity  has  been  happily  used  in  some  cases  of  locomotor  ataxia. 
Care  and  moderation  must  be  observed  here  also.  All  forms  of  elec- 
tricity and  all  modes  of  application  have  been  tried.  Central  galvaniza- 
tion of  the  spine  and  general  faradization  is  a  combined  method  that 
exercises  both  a  tonic  and  beneficial  reflex  effect  upon  the  nervous 
structures.  Three  or  four  times  a  week,  eight  or  ten  milliamperes  of 
the  galvanic  current  miay  be  transmitted  through  the  spine  with  one 
pole  at  the  neck,  the  other  at  the  lumbar  region.  No  sitting  should 
be  prolonged  beyond  five  minutes  and  the  treatment  should  be  kept  uj) 
for  many  months.  Static  electricity  and  the  faradic  brush  are  some- 
times acceptable  to  the  patient.  Pains  and  anaesthesia  have  been  re- 
lieved in  this  way.  The  current  should  be  strong  enough  to  provoke 
slight  pain,  but  not  muscular  contraction.  As  a  symptomatic  remedy 
electricity  has  a  wide  field  O'f  usefulness ;  as  a  curative  measure  it  is 
about  as  valueless  as  all  other  remedies.  There  is  danger  in  its  use,  as 
with  all  other  measures,  if  it  is  applied  too  frequently  and  too  heroically. 

The  indication  for  massage  in  tabes  is  as  a  general  tonic.  Massage 
of  the  skin  improves  its  nutrition  and  may  partly  relieve  some  of  the 
sensory  manifestations.  Deep  massage  of  the  muscles  is  useless  and 
debilitating  to  the  patient.  It  is  to  be  employed  only  when  paralysis  and 
atrophy  begin  to  show  themselves  late  in  the  disease.  Passive  motion 
is  contra-indicated  where  the  articulations  are  already  too  mobile,  and 
the  muscles  are  in  a  hypotonic  state.  There  is  not  much  of  a  field  for 
massage  in  tabes  and  v/hen  it  is  tried  it  should  be  very  gentle,  and  the 
seances  very  short.  Exhaustion  is  a  condition  to  be  studiously  guarded 
against  in  tabetics  and  massage  is  most  dangerously  liable  to  provoke 
exhaustion. 

The  suspension  treatment  introduced  a  few  years  ago  by  Motschut- 
kowsky  and  popularized  by  Charcot  has  not  fulfilled  the  promises  it 
first  held  out.  Temporary  effects,  such  as  relief  of  the  pains  and  im- 
provement in  the  gait,  follow  its  application  in  some,  indeed  in  very 
many,  instances.  But  they  all  relapse.  The  modus  operandi  oi  the 
effect  of  the  treatment  upon  the  degenerating  nerve  elements  is  any- 
thing but  clear  and  in  some  respects  the  treatment  is  unscientific  ar^d 
irrational.  However,  it  is  still  used  to  some  extent  under  a  modified 
form,  such  as  drawing  the  legs  forcibly  up  over  the  patient  while  he  is 
lying  on  his  back  (Benedict),  or  approximating  the  patient's  chin  to  his 
flexed  knees  (Blondel),  or  with  the  legs  extended  and  adducted,  bend- 


THE   NEURONIC   DISEASES  39I 

ing  the  upper  part  of  the  patient's  body  forcibly  forward  while  he  is 
seated  on  the  edge  of  a  table  (Gilles  de  la  Toiirette). 

Operative  nerve  stretching,  once  popular,  has  been  completely  dis- 
carded as  a  therapeutic  measure.  The  wearing  of  a  corset  has  relieved 
the  pains  in  some  instances,  and  according  to  Bramwell  tabetics  with 
much  ataxia  sometimes  walk  better  in  India  rubber  soded  shoes. 

Of  all  the  mechanical  measures  used  Franker s  re-education  exer- 
cises are  the  most  in  vogue  to-day  and  indeed  do  seem  to  afford  the  best 
results.  They  relieve,  however,  only  the  ataxia.  Their  psychic  effect 
on  the  patient  is  good  and  they  improve  the  muscular  strength.  They 
are  useful  in  all  stages  of  the  disease.  The  exercises  are  simple  in 
principle,  though  in  details  they  may  be  greatly  elaborated.  Blocks  oi 
wood  placed  on  the  floor,  short  flights  of  steps,  ladders  for  the  practice 
of  the  legs,  keyboards,  simple  buttoning  and  unbuttoning  of  the  clothes, 
picking  up  of  specially  distributed  articles  for  the  exercise  of  the  arms, 
are  some  of  the  simple  forms  of  apparatus  that  may  be  extemporaneous- 
ly arranged.  A  little  ingenuity  will  suggest  means  by  which  the  patient 
for  a  few  minutes  every  day  can  practice  the  function  of  coordination  in 
his  legs  and  arms.  This,  like  all  other  methods  of  treatment  employed 
in  locomotor  ataxia,  must  not  be  expected  tO'  accomplish  too  much.  In 
some  cases  it  seems  to  be  without  any  effect.  It  should  always,  how- 
ever, be  given  a  faithful  trial  in  all  cases. 

Even  hypnotic  treatment  has  been  suggested  in  this  disease.  Beril- 
lon,  of  Paris,  proposed  it  in  1895  because  of  certain  functional  psychical 
factors.  The  proposal  is  not  such  an  absurd  one  in  view  of  the  facr 
that  many  believe  the  benefit  that  temporarily  accrues  from  the  use  of 
suspension,  gymnastics,  Frankel's  exercises  and  other  measures  is 
largely  psychical.  The  restoration  of  confidence,  the  awakening  of 
hope  and  the  anticipation  of  improvement  are  all  beneficial  in  this  dis- 
ease and  doubtless  are  in  part  the  explanation  for  some  of  the  good 
derived  from  treatment,  whether  the  treatment  be  given  by  the  scientific 
physician  or  the  quack.  This,  taken  in  conjunction  with  the  well- 
recognized  characteristic  of  this  disease  to  cease  progressing  at  times, 
leads  to  the  erroneous  reports  of  cures. 

Unfavorable  as  the  prognosis  is  in  this  disease,  it  is  the  duty  of 
the  medical  mian  to  use  all  his  best  efforts  to  keep  its  victims  out  of  the 
hands  of  frauds  and  religio-medical  charlatans.-  He  can  do-  so  by  en- 
couraging the  patient,  keeping  up  his  anticipation  and  strengthening 
his  confidence  in  every  way.  The  cjuack  does  this  for  his  Oiwn  personal 
gain ;  the  physician  should  do  it  as  a  part  of  his  general  management 
of  the  trouble  because  he  will  thus  keep  the  patient  in  the  hands  of 
those  best  able  to  care  for  him — namely,  the  medical  profession,  be- 
cause the  nature  of  the  disease  is  such  as  to  warrant  a  certain  amount 
of  hopefulness,  and  finally  because  such  a  state  of  mind  exercises  a 
certain  degree  of  positive  benefit  in  minimizing  the  symptoms  and  in 
retarding  their  progress. 

OTHER  SENSORY  DEGENERATIVE  DISEASES. 

We  do  not  know  of  any  other  primary  systemic  sensory  degenera- 
tive  troubles.     It  is  not  improbable,  however,  that  they   may     exist. 


392  THE   NEURONIC   DISEASES 

There  are  some  forms  of  psychosis  and  certain  epileptiform  manifesta- 
tions with  pure  sensory  phenomena,  hke  hemicrania  sometimes,  that 
suggest  a  possible  intracranial  sensory  systemic  trouble.  A  degenera- 
tive affection  is  rarely  limited  to  the  sensory  cranial  nerves.  As  a  rule 
such  degenerations  constitute  a  part  of  tabes,  dementia  paralytica,  mul- 
tiple sclerosis,  syphilis  and  other  general  diseases,  or  they  are  a  sec- 
ondary result  of  inflammatory  and  other  extra-neuronic  processes. 
Primary  disease,  however,  has  been  observed,  though  very  rarely,  in 
some  of  the  cranial  nerves.  The  optic  and  the  trigeminal  nerves  have 
probably  illustrated  the  condition  most  frecjuently.  Perhaps  some  few 
instances  of  tic  douloureux  could  be  classified  here.  The  neuralgias, 
however,  as  I  have  shown  elsewhere,  are  something  more  than  mere 
nerve  troubles  of  a  purely  local  character,  and  this  is  preeminently  true 
of  tic  douloureux.  Primary,  bilateral  optic  atrophy  does  occasionally 
occur,  though  it  is  much  rarer  than  secondary  or  associated  atrophy. 
The  auditory  nerve  has  been  supposed  to  have  been  primarily  afifected, 
but  if  so  it  must  have  been  very  exceptional.  Primary  disease  in  the 
glosso-pharyngeal,  pneumogastric  and  sensory  spinal  nerves  is  prac- 
tically unknown.  In  general  toxic  and  infectious  states  they  are  oc- 
casionally degenerated,  especially  the  vagus.  With  secondary  degenera- 
tion they  are  not  infrequently  affected. 

DISEASES    OF    THE    EFFERENT    OR    MOTOR     SYSTEM. 

a.      DISEASES  OF  THE  WHOLE  MOTOR  TRACT. 

\  PROGRESSIVE  MUSCULAR  ATROPHY. 

There  are  a  number  of  affections  in  which  wasting  of  the  muscles, 
with  a  resulting  paralysis,  is  the  dominant  and  often  the  sole  feature. 
Unlike  the  association  of  the  paralysis  and  atrophy  observed  in  acute 
poliomyelitis  and  neuritis,  in  the  diseases  now  about  to  be  considered 
the  combination  is  one  of  atrophy  and  paralysis.  In  other  words,  the 
wasting  in  the  former  follows  the  paralysis,  in  these  the  paralysis 
follows  the  wasting  and  proceeds  pari  passu  with  it.  Many  of  the  for- 
mer diseases,  in  fact  most  of  them,  are  purely  inflammatory  in  character 
and  the  neuronic  degeneration  is  a  mere  secondary  result  or  sequel. 
In  these,  however,  the  degeneration  appears  to  be  a  pure  primary 
process  throughout. 

It  will  be  remembered  that  the  efferent  or  motor  path  extending 
from  the  cerebral  cortex  to  the  musculature  of  the  body  consists  of 
two  anatomically  separated  grand  divisions. 

The  upper  segment  is  made  up  of  a  group  of  neurones  whose  cell- 
bodies  nest  in  the  cerebral  cortex,  while  their  axones,  of  various  lengths, 
extend  downward  through  the  internal  capsule  and  pyramidal  tracts 
to  their  arborizations  around  the  cells  of  the  various  intracranial  motor 
nuclei  and  anterior  spinal  cornua.  This  is  a  compact  segment  and 
formis  the  pyramidal  tracts. 

The  lower  motor  segment  consists  also  of  a  lot  of  neurones  whose 


THE   NEURONIC   DISEASES 


393 


cell-bodies  are  to  be  found  in  the  anterior  horns  of  the  cord,  while  their 
axones  pass  out  through  the  anterior  spinal  roots  and  related  nerves 
to  their  termination  in  the  distant  muscles. 

The  center  of  nutrition  for  each  neurone  resides  in  its  cell-body. 
Therefore  the  tone  and  health  of  the  upper  neurones  are  dependent 
upon  the  integrity  of  the  related  cell  bodies  in  the  motor  cortex;  the 
tone  and  health  of  the  lower  neurones  are  dependent  upon  the  integrity 
of  the  related  cell-bodies  in  the  anterior  horns  of  the  cord.  Each  of 
these  two  sets  of  neurones  exercise  a  nutritive  control  over  the  respec- 
tive structures  below  them  and  with  which  they  are  in  physiological 
relationship.  The  tone  and  health  of  the  lower  neurones  are  to  a  con- 
siderable degree  dependent  upon  the  integrity  of  the  related  cerebral 
neurones ;  the  tone  and  health  of  the  muscular  tissues  are  very  greatly 
dependent  upon  the  integrity  of  the  related  spinal  neurones. 

These  facts  have  been  all  elucidated  and  illustrated  in  an  earlier 
chapter.  They  are  repeated  here  merelv  to  show  how  a  muscular 
atrophy  of  high  degree  may  occur  from  a  diseased  condition  in  the  cell 
bodies  of  the  lower  motor  neurones ;  and  furthermore,  to  make  plain 
how  a  lesser  degree  of  muscular  atrophy  may  occur  from  a  disturbance 
of  the  health  and  functions  of  the  lower  neurones  by  a  disturbance  in 
the  health  and  functions  of  the  upper. 

Every  muscular  atrophy  of  neural  origin  is  due  to  disease  of  the 
lower  or  peripheral  neurones.  This  disease  may  be  primary,  in  which 
case  it  is  an  original  disease  of  the  anterior  gray  matter  of  the  cord ; 
or  it  may  be  secondary,  in  \vhich  case  it  is  due  to  disease  in  the 
pyramidal  tracts.  This  at  once  establishes  two  great  types  of  spinal 
progressive  muscular  atrophy,  the  primary,  or  what  Charcot  used  to 
call  the  protopathic  type,  and  the  secondary,  or  what  he  termed  the 
deuteropathic  type.  As  in  both  there  must  be  always  some  disease  of 
the  lower  motor  neurones,  many  authorities  do  not  recognize  the  dis- 
tinction between  the  two  types  just  mentioned,  but  refer  tO'  them  all 
as  chronic  muscular  atrophy,  progressive  (central)  muscular  atrophy, 
spinal  progressive  multiple  atrophy,  spinal  progressive  amyotrophy. 

In  view  of  the  immediate  pathogenesis  of  the  muscular  atrophy, 
this  contention  that  they  are  all  practically  one  and  the  same  disease 
is  a  strong  one.  However,  there  are  certain  features  in  the  clinical 
picture  of  the  secondary,  or  deuteropathic,  forms  so  unique  and  striking 
that  it  will  perhaps  be  just  as  well  to  consider  the  latter  in  a  section 
by  themselves.  I  will  discuss  them  under  the  head  of  amyotrophic 
lateral  sclerosis. 

There  is  much  better  ground  for  separating  the  amyotrophic  lateral 
sclerotic  cases  from  those  that  are  not  of  this  type  than  there  is  for 
the  separation  of  the  latter  into  such  subclasses  as  progressive  bulbar 
palsy,  progressive  muscular  atrophy  and  progressive  hereditar\-  muscu- 
lar atrophy ;  for  these  all  represent  pathologically  the  same  disease, 
with  a  symptomatology  varied  merely  in  accordance  with  the  gross 
anatomical  location  oi  the  lesion;  whereas  the  former  represents  a 
characteristic  pathology  that  establishes  a  particular  and  distinctive 
clinical  picture. 

Etiology. — In  both  the  Aran-Duchenne  type  of  progressive  miis- 


394  THE   NEURONIC   DISEASES 

cular  atrophy  now  to  be  considered,  and  the  Charcot  amyotrophic  lateral 
sclerotic  typ«  to  be  considered  later,  the  immediate  cause  of  the  atrophv 
is,  as  was  long  ago  shown  by  Levy  and  Lockhart  Clarke,  disease  of  the 
cells  in  the  ventral  horns  of  the  cord.  The  cause  of  this  disease  is 
practically  unknown,  though  Charcot  believed  that  in  amyotrophic 
lateral  sclerosis  it  was  secondary  to  disease  in  the  pyramidal  tracts. 
This  is  doubted  to-day  and  even  in  Charcot's  type  the  deterioration  in 
the  ventral  horns  is  thought  to  be  primary. 

Men  are  affected  more  frequently  than  women  with  progressive 
muscular  atrophy.  In  most  of  the  cases  it  appears  between  the  ages 
of  twenty-five  and  forty-five.  A  hereditary  influence  reveals  itself  in 
a  small  proportion  of  cases  and  in  these  it  seems  to  be  merely  of  a 
neuropathic  character.  In  rare  instances  the  heredity  seems  to  be 
direct.  In  these  cases  several  members  of  the  same  family  may  be 
afflicted  and  the  disease  occurs  at  an  earlier  age  than  usual.  Such 
cases  of  a  hereditary  or  familial  type  of  progressive  muscular  atrophv 
of  spinal  origin  have  been  observed  by  A\' erdnig,  Hoffmann  and  others. 

The  legs  and  back  are  first  affected  and  later  on  the  other  muscles 
of  the  body.  The  disease  advances  slowly  and  terminates  in  the  usual 
way,  even  with  bulbar  symptoms  (W^erdnig)  in  about  four  or  five 
3'ears. 

It  is  not  yet  positively  established  whether  Charcot-AIarie's  type  of 
hereditary  muscular  atrophy  beginning  in  the  leg  is  a  central,  spinal  or 
peripheral  neuritic  malady.  If  it  is  the  former,  as  Dana  and  others 
think,  it  would  seem  unnecessary  to  elcA^ate  it  into  a  special  affection 
and  devote  a  separate  section  to  its  consideration.  If  it  is  a  neuritic 
affection  it  would  naturally  fall  into  the  chapter  on  neuritis.  In  my  own 
opinion  it  is  but  a  form  of  the  disease  we  are  now  considering,  and  I 
will  so  describe  it. 

The  causes  to  which  progressive  atrophy  have  been  attributed  are 
so  numerous  that  one  instinctively  doubts  the  reality  of  any  of  them. 
Nevertheless  mention  must  be  made  of  cold,  dampness,  exposure,  men- 
tal strain,  over-exertion,  trauma,  infection  and  intoxication.  Perhaps 
th€  last  two  have  a  stronger  claim  for  recognition  than  an  v.  At  all 
events  the  disease  is  said  to  have  followed  measles,  typhoid  fever, 
cholera,  rheumatism,  syphilis  and  childbirth.  The  atrophv  of  lead 
poisoning  is  not  strictly  of  the  progressive  type.  This  disease  has  oc- 
curred as  a  senile  form  at  the  age  of  seventy. 

Pathology  AND  Pathogenesis. — A  slow,  non-inflammatory,  de- 
generative process  in  the  anterior  horns  of  the  spinal  cord  constitutes 
the  primary  pathological  basis  of  the  disease.  Usually  this  is  most 
marked  in  the  lower  cervical  and  upper  dorsal  regions.  From  these 
points  it  may  extend  upw^ards  and  downwards  until  the  entire  cord 
is  involved.  The  large  pyramidal  cells,  especially  the  central  and  me- 
dian groups,  are  shriveled  and  wasted,  are  greatly  reduced  in  number, 
or  are  entirely  absent.  The  neuroglia  and  connective  tissue  are  in- 
creased ;  but  there  are  no  distinctive  vascular  changes,  though  here  and 
there  a  blood  vessel  may  be  dilated.  The  processes  from  the  wasted  cells 
are  also  atrophied  where  they  pass  through  the  white  matter  out  into 
the  anterior  roots.  Sometimes  in  the  course  of  the  disease,  and  to  a  lesser 


THE   NEURONIC   DISEASES 


395 


•degree  usually,  the  white  matter  of  the  cord,  particularly  the  pyramidal 
tracts,  participates  in  the  atrophic  process.  All  parts  of  the  lateral 
columns  except  the  direct  cerebellar  and  antero-lateral  tracts,  and  also 
the  antero-lateral  ground  bundle,  may  exhibit  the  atrophic  condition. 
It  was  thought  by  Charcot  that  cases  showing  atrophy  of  the  pyramidal 
tracts  constituted  a  separate  type  of  the  disease,  but  in  this  he  was  in 
error,  for  many  cases  reveal  upon  post-mortem  examination  a  consider- 
able atrophy  of  the  pyramidal  tracts,  which  during  life  manifested  no 
spasticity,  the  symptom  upcn  wdiich  Charcot  largely  founded  his 
aviyotrophic  lateral  sclerosis.  The  latter  is  only  a  clinical  manifesta- 
tion of  the  general  disease.  In  most  of  the  cases  there  is  sooner  or 
later  extension  of  the  malady  into  the  medulla.  In  some  cases  it  seem.s 
to  start  and  terminate  in  the  medulla,  constituting  the  type  known  as 
progressive  bulbar  paralysis.  When  the  disease  advances  from  the  cord 
upwards,  the  homologous  motor  nuclei  show  the  same  general  changes 
as  do  the  anterior  horns.  Along  the  pyramidal  tracts  the  degeneration 
Tias  been  traced  even  as  f^r  up  as  the  cerebral  cortex.  In  the  opposite 
direction  the  degenerative  process  has  extended  out  through  the  anterior 
roots,  into  the  peripheral  r.erves  and  even  into  the  muscular  tissue.  In 
the  latter  the  fibres  are  shrunken  and  diminished,  then'  striations  have 
disappeared,  granulations  and  fat  globules  have  taken  their  place  and  the 
interstitial  connective  tissue  is  increised.  The  entire  muscle  therefore 
is  at  first  soft,  then  hard,  ard  its  appearance  is  pale,  streaked  and  yel- 
lowish. Healthy  fibres  may  continue  here  and  there  among  the  dis- 
-eased  ones  and  the  small  vessels  among  them  may  be  dilated. 

A  primary  degeneration  of  the  entire  neuromuscular  apparatus 
■^with  its  prominent  focus  in  the  anterior  horns  of  the  cord  and  their 
related  structures,  the  muscles,  constitutes  the  pathological  basis  of  all 
forms  of  spinal  progressive  muscular  atrophy.  So  uniform  and  con- 
stant, though  not  necessarily  always  to  the  same  degree  in  all  parts 
of  this  neuromuscular  tract  or  apparatus,  are  these  pathological  changes 
found  that  were  we  to  confine  our  attention  solely  to^  their  anatomical 
side,  all  forms  of  progressive  atrophy  would  be  reduced  to  the  nomen- 
■clature  of  a  single  disease. 

Symptoms. — The  moment  we  begin  to  attempt  a  classification  of 
progressive  muscular  atrophy  from  its  clinical  presentations  alone  wc 
find  that  we  must  speak  of  difi^erent  types,  though  in  general  the  symp- 
tomatology of  all  types  is  about  the  sam,e.  If  simple  muscular  atrophy, 
with  a  paralysis  running  alcng  parallel  with  it,  occurs  vvdthout  any 
•other  manifestation,  we  have  the  pure  form  of  the  disease.  If  spasticity 
accompanies  the  atrophy  and  paralysis,  showing  considerable  involve- 
inent  of  the  pyramidal  tracts,  we  have  Charcot's  amyotrophic  lateral 
•sclerosis.  If  the  simple  muscular  atrophy  with  paralysis  appears  first 
in  particular  groups  of  muscles,  we  have  the  Aran-Duchenne,  the 
peroneal,  the  bulbar,  the  ophthalmoplegic  and  other  localized  types. 

In  all  cases  the  disease  develops  slowly  and  insidiously.  The  pa- 
tient may  be  affected  for  months  and  years,  but  not  being  particularly 
discommoded,  he  either  does  not  notice  the  trouble  or  else  fancies  that 
lie  is  merely  a  little  thinner  than  he  ought  to  be.  I  knew  a  case  where 
the  marked  wasting  of  the  upper  limbs  irduced  the  patient  for  a  long 


396 


TH1<:  NEURONIC   DISEASES 


FIGURE  67. 


^f  FIGURE  6S_ 


FIGURE  69. 


Fig.  67. — Chronic  bulbar  paralysis  with  amyotrophic  lateral  sclerosis.  Sectioix 
through  the  medulla. 

Fig.  68. — Amyotrophic  lateral  sclerosis.  Section  through  the  lower  cervical 
cord. 

Fig.  69. — Spinal  muscular  atrophy.  Section  through  the  cervical  cord. 
(  Striimpell-Jakob.) 


THE   NEURONIC   DISEASES 


397 


lime  to  the  belief  that  she  was  generally  run  down  and  abnormally 
thin  all  over  the  body,  though  as  an  actual  fact  her  lower  limbs  were 
plump  and  normal  in  size.' 

The  disease  shows  itself  first  in,  and  often  remains  limited  to,  the 
upper  extremities.     Sometimes  one  limb  is  affected  more  than  another. 

FIGURE  70. 


_  Progressive  muscular  atrophy.     Age  of  patient  forty-five  years.   (After  Fried- 
Teich. ) 

In  the  beginning  there  may  be  some  slight  zveakness  and  dull,  rheuma- 
toid pain  in  the  muscles  of  the  arm  and  shoulder ;  or  there  may  be  a 
mild  sort  of  rigidity  causing  the  finer  m.ovements  to  reveal  a  trace  of 
awkwardness.  Usually  about  this  time  the  muscles  have  commenced 
to  show  some  degree  of  wasting.    In  the  more  common  Aran-Duchenne 


398  THE    NEURONIC   DISEASES 

type  the  small  muscles  of  the  hanci  are  the  first  to  become  atrophied^ 
The  balls  of  the  thumb  and  of  the  little  finger  flatten ;  the  hollows  be- 
tween the  tendons  on  the  back  of  the  hand  deepen ;  the  lumbricales  and 
interossei  seem  to  disappear  and  the  fingers  are  scrawny  and  prominent 
at  the  joints.  The  entire  hand  gets  flat  and  the  thumb  stretches  parallel' 
with  the  fingers,  giving  it  the  ape  appearance.  The  adductor  longus 
pollicis  is  soon  involved.  Adduction,  abduction  and  flexion  of  the- 
thumb  is  extremely  difficult.  Gradually  the  fingers  are  drawn  back- 
ward and  are  abnormally  flexed  on  accovmt  of  the  extension  of  the  dis- 
ease up  into  the  arm,  thus  giving  them  the  well-known  appearance  of 
the  main-en- griife.  As  the  disease  advances  on  up  the  forearm,  arm 
and  shoulder  it  is  noticed  that  the  anatoanical  nerve  distribution  is  not 
followed,  although  in  many  cases  the  ulnar  nerve  area  is  prominently 
involved. 

x\ll  possible  changes  are  seen  in  the  course  of  the  disease.  One  arm 
may  become  far  advanced  before  the  other  is  attacked.  On  the  other 
hand,  the  trouble  may  appear  in  the  shoulder  first,  particularly  the 
deltoid  muscle,  thence  pass  to  the  biceps,  less  frequently  the  triceps,  and 
so  on  all  the  way  down  the  limb. 

The  appearance  of  the  entire  arm  is  very  characteristic ;  thin^ 
wasted,  with  the  grooves  deepened,  the  bony  prominences  exaggerated^ 
it  hangs  limp  and  gaunt  by  the  side. 

Other  parts  of  the  body  beside  the  arms  may  be  implicated.  In 
fact,  it  is  a  peculiarity  of  the  disease  to  thus  skip  about.  The  entire 
shoulder  girdle  may  suffer  and  with  it  the  deep  muscles  of  the  back. 
The  legs  are  rarely  affected,  and  then  as  a  rule  only  late  in  life.  The 
muscles  of  the  pelvic  girdle,  particularly  the  glutei,  the  extensors  and 
the  abductors  of  the  thigh,  are  occasionally  attacked.  The  diaphragirf 
becomes  involved  and  ultimately  the  intercostals.  Last  of  all  the  mus- 
cles of  the  neck  and  others  under  the  control  of  the  medulla  succumb. 
Involvement  of  this  important  part  of  the  brain  usually  brings  the  case 
to  an  early  termination.  Many  years  and  almost  an  entire  lifetime  may- 
be consumed  by  this  slow  progressing  malady. 

Fibrillary  twitching  usually  accompanies  the  advancing  atrophy,, 
together  with  paralysis.  The  electrical  excitability  shows  a  correspond- 
ing decrease. 

On  account  of  the  absence  or  presence  of  a  slight  rigidity  and 
stiffness  in  the  muscles  two  forms  of  the  disease  have  been  referred 
to — namely,  the  tonic  and  the  atonic.  These,  as  I  have  intimated  before,, 
are  confusing  and  artificial  distinctions.  All  that  is  necessarj'  to  note 
in  regard  to  this  is  that  in  some  cases  the  pyramidal  tracts  may  be  suffi- 
ciently implicated  to  provoke  a  mild  degree  of  spasticity  and  give  the 
case  a  resemblance  to  that  still  more  pronoimced,  though  arbitrarily 
separated  clinical  type,  amyotrophic  lateral  sclerosis. 

There  are  no  objective  sensory  symptoms  in  progressive  muscular 
atrophy  and  the  subjective  phenomena,  like  numbness  and  other  mild 
parsesthesige,  areinfrequent  and  inconsequential. 

Some  authors  refer  to  other  symptoms  which  are  either  of  minor 
significance  or  indicate  extension  of  the  disease  to  the  medulla.  Such 
are  sweating,  local  congestion  and  some  other     vasomotor     troubles ; 


THE   NEURONIC   DISEASES 


399 


inequality  of  the  pupils  from  irritation  of  the  ciliospinal  center ;  weak- 
ened sexual  power  ;  urinary  abnormalities. 

There  is  a  form  of  the  disease,  the  Chaycot-Marie  peroneal  type, 
in  w^hich  heredity  plays  a  striking  role  and  the  atrophy  begins  in  the 
leg.  It  appears  usually  under  twenty  years  of  age.  The  trouble 
ascends,  involving  successively  the  peronei  muscles,  the  extensors  of 
the  foot,  the  calf  and  ultimately  the  thigh.  After  many  years  even 
the  upper  extremity  may  be  involved.  The  foot  and  hand  frequently 
escape.  Pains  are  complained  of  by  many  patients.  This  disease  for 
the  most  part  resembles  an  ordinary  progressive  atrophy.  In  other 
respects  the  type  simulates  an  ascending  neuritis.  Hoffmann  and 
others  believed  it  was  such  and  named  it  the  neural  type  of  progressive 
muscular  atrophy.  There  are  many  good  reasons  for  not  regarding  it 
as  primarily  neuritic  in  origin,  but  rather  as  poliomyelitic,  like  all  the 
other  spinal  atrophies.  A  polyneuritis  in  which  the  foot  and  hand  so 
unifomily  escape  would  certainly  be  anomalous,  and  moreover  hereditv 
is  not  an  influential  factor  in  the  production  of  peripheral  nerve  degen- 
erations.. On  the  other  hand,  it  is  a  fact  that  in  all  forms  of  progressive 
spinal  atrophy  more  or  less  degeneration  does  occur  in  the  peripheral 
nerves  or  outer  ends  of  the  diseased  lower  neurones.  This  would 
account  for  the  diseased  nerves  observed  in  this  type  of  the  trouble  by 
Virchow,  Friedreich  and  others.  The  other  symptoms  upon  which 
the  neural  theory  of  the  disease  is  based,  as,  for  instance,  the  pains,  are 
too  insignificant  to  have  much  weight  when  placed  in  contrast  with 
the  many  other  manifestations  which  seem  so  strongly  to  ally  it  to  the 
ordinary  progressive  muscular  atrophy.  The  work  of  Dana,  j\Iarinesco 
and  others  has  confirmed  the  belief  that  the  primary  cause  of  the 
peroneal  type,  as  in  all  other  forms  of  progressive  atrophy,  is  a  lesion 
of  the  anterior  horns  of  the  cord. 

Diagnosis. — In  typical  cases  progressive  muscular  atrophy  is  easy 
of  diagnosis  if  close  attention  be  given  to  the  onset,  distribution  and 
slow  progress  of  the  atrophy.  jMuscle  groups  rather  than  individual 
muscles  or  the  whole  limb  is  the  predominant  area  of  distribution.  The 
atrophy  precedes  and,  as  it  were,  controls  the  paralysis.  Sensory  symp- 
toms are  wanting  except  to  a  slight  extent  in  the  so-called  neural,  or 
Charcot-^Iarie  peroneal  type  of  the  disease.  A  slight  muscular  stiff- 
ness and  fibrillary  twitching  are  frequently  present.  The  progress  of 
the  trouble  is  slow%  skipping  from  muscle-group  to  muscle-group,  often 
with  temporar}'  remissions,  but  always  steadily  onward. 

Clinically  it  is  always  wise  to  attempt  a  differential  diagnosis  be- 
tween progressive  muscular  atrophy,  amyotrophic  lateral  sclerosis  and 
chronic  anterior  poliornyelitis,  though  many  authors  insist  upon  refer- 
ring to  all  three  as  practically  the  one  disease. 

In  amyotrophic  lateral  sclerosis  the  marked  spasticity  with  the  com- 
paratively slight  atrophy,  the  commencement  of  the  trouble  in  the  arms, 
and  the  bulbar  manifestations,  are  all  highly  indicative. 

In  chronic  anterior  poliomyelitis  the  symptoms  appear  more  sud- 
denh^,  reach  a  climax,  and  then  recede,  leaving  a  permanent  paralysis 
in  individual  muscles.  The  paralysis  always  precedes  the  atrophy  and 
is  accompanied  early,  as  a  rule,  by  changes  in  the  electrical  reactions. 


400  THE   NEURONIC   DISEASES 

At  times  it  must  be  admitted  the  differential  diagnosis  is  all  but  im- 
possible. In  such  cases  time  will  show  the  slow  extension  of  the  atrophy 
to  other  muscles  and  parts  of  the  body.  \A'hen  bulbar  symptoms  come 
on  late  to  complicate  the  clinical  picture  the  diagnosis  of  progressive 
muscular  atrophy  is  assured. 

Other  diseases  from  which  a  dift'erential  diagnosis  may  sometimes 
have  to  be  made  are  the  muscular  dystrophies,  peripheral  neuritis, 
anthritic  neuritis,  cervical  pachymeningitis  hypertrophica,  syringo- 
myelia, general  gliosis,  spinal  caries  and  the  occupation  neuroses. 

From  these  progressive  atrophy  is  best  differentiated  by  exclusion. 
Each  one  has  some  characteristic  s}  mptom  or  symptoms  that  do  not  be- 
long to  progressive  atrophy  and  by  this  sym.ptom  the  separation  is  made 
even  though  the  atrophy,  the  paralysis  and  the  course  of  the  malady  are 
the  same.  The  heredity,  the  age  of  the  patient,  the  prominent  distribu- 
tion of  the  wasting  and  paralysis  in  the  lower  truncal  and  pelvic  muscles, 
the  leg  and  face,  the  existence  of  some  hypertrophy  or  pseudo-hyper- 
trophv  and  the  absence  of  stift'ness  and  bulbar  manifestations,  indicate 
a  muscular  dystrophy. 

Multiple  neuritis  begins  abruptly,  spreads  upward  on  the  limbs 
and  from  the  legs  to  the  arms,  exhibits  ataxia,  late  atrophy,  loss  of  the 
deep  reflexes,  electrical  changes  and  marked  local  sensory  phenomena, 
such  as  pain  and  hypassthesia 

Arthritic  muscular  atrophy  is  always  in  and  around  the  diseased 
joint  and  dees  not  extend  to  the  entire  limb  or  pick  out  special  muscles 
or  groups  of  muscles.  The  paralytic,  electrical  and  reflex  phenomena 
that  accompany  the  classical  form  of  muscular  atrophy  do  not  appear 
with  the  arthritic  wasting.  Moreover,  the  latter  recovers  rapidly  after 
the  joint  trouble  has  disappeared. 

In  the  cervical  hypertrophic  type  of  pachymeningitis  the  symptoms 
seem  to  select  the  median  and  ulnar  nerve  areas  for  their  manifesta- 
tion and  there  are  the  usual  darting,  radiating  pains  of  posterior  root 
irritation.  The  dissociation  of  the  pain  and  touch  sense,  and  the  other 
trophic  characteristics,  besides  the  muscular  atrophy,  will  help  to 
determine  the  syringomyelia. 

Spinal  caries  is  dift'erentiated  by  the  pressure  symptoms,  the 
meningitic  pains  and  local  tenderness,  the  spinal  deformity  and  the  use 
of  skiagraphy. 

The  history  of  overuse  of  a  special  set  of  muscles,  the  limitation 
of  the  trouble  sharply  to  those  muscles  and  its  tendency  to  get  well 
under  simple  rest,  or  at  least  its  indisposition  to  spread,  points  very 
clearly  to  an  occupation  neurosis. 

PROGNOSis.-r-Being  a  slow,  progressive  disease,  the  prognosis  of 
muscular  atrophy  is  bad  so  far  as  a  cure  is  concerned.  The  lost  neural 
elements,  upon  which  the  disease  depends,  cannot  be  restored  by 
human  power.  The  cases  run  on,  ho\\"ever,  for  many  years,  sometimes 
remit  and  become  stationary,  or  in  a  small  percentage  undergo  what 
may  be  termed  a  partial  recovery.  The  possibility  of  such  an  event 
can  be  held  out  to  the  patient,  but  it  dare  not  be  promised  or  anticipated. 
The  more  symmetrical  in  distribution  the  atrophy  is  the  better  the  hope 
for  a  partial  recovery.     The  more  marked  the  type  of  the  disease  is, 


THE   NEURONIC   DISEASES  4GI 

as,  for  instance,  the  hand,  the  leg  or  the  amyotrophic,  the  more  apt  is 
it  to  be  permanent.  The  condition  met  with  at  the  end  of  six  months  or 
a  year  cannot  be  bettered  in  any  way.  Cessation  at  that  point  is  the 
most  than  can  be  hoped  for.  The  chances  are  that  it  will  progress  and 
extend.  Death  usually  results  from  bulbar  involvement,  general  ex- 
haustion and  marasmus,  or  some  intercurrent  malady. 

Treatment. — It  must  be  evident  from  the  description  of  the  nature 
of  this  disease  that  treatment  is  of  little  avail.  Hygienic  and  symp- 
tomatic measures  are  about  all  that  can  be  recommended.  Over-exer- 
tion should  be  carefully  guarded  against  and  it  is  always  wise  to  rec- 
ommend frequent  and  prolonged  rest.  All  stimulants,  general  as  well 
as  local,  alcohol,  tobacco,  sexual  mdulgence,  cold  baths,  vigorous  mas- 
sage, active  or  passive  exercise  and  electricity  had  better  be  refrained 
from,  or  used  very  cautiously.  Arsenic  and  thyroid  extract  may  be 
tested,  but  they  do  not  promise  very  much.  Gowers,  Sanger  Brown 
and  others  have  tried,  with  some  degree  of  success,  the  subcutaneous 
daily  injection  of  the  nitrate  of  strychnia  in  doses  of  about  1-25  grain. 
The  treatment  may  be  kept  up  for  six  weeks,  then  stopped  for  two 
weeks,  then  renewed  again,  and  so  on  until  several  courses  are  taken. 
It  is  a  waste  of  time  and  money  for  a  patient  to  seek  new  climates,  hot 
springs  and  highly  advertised  sanataria  in  the  hope  of  a  cure.  Rest, 
quiet  and  good  nourishment  at  home,  under  the  careful  observation 
of  his  medical  adviser,  is  the  safest  regime  for  his  adoption. 

AMYOTROPHIC  LATERAL  SCLEROSIS. 

Our  knowledge  of  this  disease  dates  from  Charcot's  descriptions  of 
it  in  1869  and  later.  Other  investigators  have  added  much  to  this 
knowledge  and  cleared  up  some  doubtful  points  in  Charcot's  original 
definition. 

Clinically  the  affection  is  revealed  by  a  spastic  paralysis  with  a 
distinct  muscular  atrophy  and  absence  of  sensory  phenomena.  Patho- 
logically it  is  a  degenerative  sclerosis  of  the  upper  and  lower  motor 
neurones.  It  is  usually  classed  among  the  progressive  muscular 
atrophies  of  spinal  origin,  because  it  exhibits  all  of  the  symptoms  and 
post-mortem  findings  of  these  affections,  in  which  the  disease  process 
is  located  in  the  anterior  horns,  anterior  roots,  and  their  extensions  out 
into  the  peripheral  nerves.  In  addition  to  this,  however,  amyotrophic 
lateral  sclerosis  is  a  disease  process  in  the  lateral  columns  of  the  cord, 
especially  the  pyramidal  tracts.  Charcot  believed  that  the  degeneration 
of  the  pyramidal  tracts  was  primary,  causing  a  degeneration  in  the 
cells  of  the  anterior  horns  and  associated  anterior  root  fibres  secondarily. 
It  is  more  probable,  from  the  latest  investigations,  that  the  two  proc- 
esses, that  in  the  pyramidal  tract  and  that  in  the  anterior  horns,  are 
merely  coincident  and  are  dependent  upon  the  same  cause.  As  the 
degeneration  has  been  traced  all  the  way  up  to  the  cortex,  it  is  now 
the  accepted  opinion  that  amyotrophic  lateral  sclerosis  is  a  degenerative 
disease  of  the  entire  motor  path. 

Etiology. — We  know  very  little  about  this.  Heredity  does  not 
seem  to  enter  as  a  factor,  though  it  is  more  than  probable  that  a  con- 


402  THE   NEURONIC   DISEASES 

genital  neuropathic  condition  is  responsible  to  a  certain  extent  for  its 
occurrence  in  certain  individuals.  It  appears  with  about  the  same  fre- 
quency in  both  sexes,  though  Charcot  and  Marie  were  of  the  opinion 
that  females  were  more  prone  to  it  than  males.  It  is  a  disease  of  mid- 
dle adult  life.  Alost  cases  show  themselves  between  the  ages  of  thirty- 
five  and  forty-five,  though  they  have  been  seen  to  occur  at  any  time 
between  the  ages  of  sixty  and  thirty.  j\lany  exciting  causes  for  the 
disease  have  been  enumerated  by  the  authorities,  chief  among  which 
are  exposure  to  wet  and  cold,  mental  strain,  physical  exhaustion,  dissi- 
pation, sexual  excesses,  traumatism,  etc.  Syphilis  does  not  seem  to 
particularly  predispose  to  the  disease,  but  it  has  been  observed  in 
s}^hilitics.  The  etiology  may  well  be  summed  up  by  saying  that  the 
predisposing  cause,  a  neuropathic  constitution,  being  present,  almost 
any  exciting  cause  in  the  way  of  a  shock  or  intoxication  may  start  the 
degenerative  process  in  the  motor  path. 

Pathology  and  Pathogenesis. — The  latest  and  most  carefully 
made  post-mortem  examinations  show  that  this  disease  is  pathologically 
a  degeneration  of  the  entire  cortico-muscular  condncting  path.  The 
degeneration  of  the  peripheral  motor  neurone  is  identical  with  that  of 
the  myelopathic  form  of  progressive  muscular  atrophy.  The  anterior 
horns  are  the  only  part  of  the  spinal  gray  matter  that  is  degenerated. 
The  pyramidal  tracts,  both  crossed  and  uncrossed,  reveal  degeneration 
and  the  disease  process  has  been  traced  up  through  the  medullary  motor 
paths,  the  peduncles  of  the  brain,  the  internal  capsule  and  even  into  the 
motor  areas  of  the  cortex.  In  the  cord  other  structures  have  been  found 
degenerated  by  Spiller,  Mott,  Probst  and  others,  though  these  cases 
have  been  exceptional.  The  dorsomedian  columms  of  Goll  were  wasted, 
likewise  Clarke's  columns  and  the  direct  cerebellar  tracts. 

In  the  medulla  the  degeneration  attacks  the  motor  paths  and  the 
motor  nuclei  and  "the  roots  of  the  motor  cranial  nerves — nameh^,  the 
hypoglossal,  the  facial,  the  vago-accessorius  and  the  motor  fifth.  In 
one  or  two  instances  the  nuclei  of  the  ocular  nerves  have  been  im- 
plicated. 

In  the  brain  the  degeneration  was  observed  in  almost  the  entire 
motor  cortex,  the  corpus  callosum,  the  middle  region  of  the  posterior 
limb  of  the  internal  capsule,  and  the  tangential  fibres  and  the  parts  of 
the  centrum  ovale  anatomically  and  physiologically  connected  wdth  the 
cortical  motor  areas.  The  large  pyramidal  cells  were  diminished  in 
number  and  the  remainder  were  pigmented  and  atrophied. 

Spiller  has  detected  a  degeneration  in  the  peripheral  nerves  even, 
side  by  side  with  undegenerated  fibres. 

No  degeneration  was  regularly  found  in  any  of  the  sensory  paths, 
in  the  intramuscular  nerve  fibres  or  the  muscle  spindles. 

Symptoms. — The  typical  form  of  am.yotrophic  lateral  sclerosis 
exhibits  certain  cardinal  symptoms.  These  are  spastic  paralysis  and 
atrophy  in  the  upper  extremities,  and  zveakness  and  rigidity  with  slight 
atrophy  in  the  lower;  Hhrillary  tremor  in  some  of  the  wasting  muscles; 
exaggeration  of  the  deep  reiiexes;  more  or  less  alteration  of  the  elec- 
trical reactions;    certain  bulbar  symptoms  showing  involvement  of  the 


:he  neuronic  diseases 


403 


cranial  nerves  from  the  seventh  to  the  twelfth ;  and  complete  absence 
of  all  sensory  and  mental  disturbances. 

There  are  types  of  the  disease  that  vary  slightly  from  this  general 
clinical  picture,  according  to  the  location  and  predominence  of  the 
lesion  and  the  resulting  preeminence  of  one  or  more  groups  of  symp- 
toms. For  example,  in  the  majority  of  cases  the  trouble  first  shows 
itself  in  the  upper  extremities  and  later  on  in  the  lower,  but  there  are 
rases  in  which  the  reverse  order  of  events  takes  place.  Occasionally  a 
case  will  first  announce  itself  by  slight  bulbar  symptoms,  a  glosso- 
labio-laryngo-pharyngeal  paralysis,  the  extremities  not  being  implicated 
until  later. 

In  most  of  the  cases  spasticity  and  an  exaggerated  myotatic  re- 
sponse precede  for  a  time  the  muscular  wasting  and  even  continue  along 
with  it  pari  passu.  There  are  cases,  however,  where  the  disease  in  the 
lower  motor  neurones  antedates  for  some  time  the  disease  in  the 
pyramidal  tracts,  and  having,  for  the  time  being,  all  the  usual  signs  of 
a  chronic  poliomyelitis  or  even  progressive  muscular  atrophy  of  the 
Aran-Duchenne  type,  cannot  be  distinguished  from  the  latter  diseases. 
It  was  for  this  reason,  in  a  large  measure,  that  Gowers,  Leyden  and 
even  Charcot  believed  amyotrophic  lateral  sclerosis  to  be  a  mere  form 
of  spinal  progressive  atrophy,  though  the  last  author  did  subdivide  the 
muscular  atrophies  of  spinal  origin  into  the  primary  or  protopathic 
variety,  in  which  the  disease  is  limited  to  the  lower  motor  segment,  and 
the  deuteropathic,  or  amyotrophic  lateral  sclerosis  type,  in  which  the 
disease  is  in  both  the  lower  and  upper  segments.  In  this  latter  type 
Charcot  taught  that  the  degeneration  of  the  anterior  cornua  was  a  sec- 
ondary result  of  the  degeneration  of  the  pyramidal  tracts, 

A  cardinal  symptom  of  amyotrophic  lateral  sclerosis  is  spasticity 
of  the  muscles.  This  appears  before  the  atrophy,  usually  in  the  arms 
first,  except  in  those  very  rare  cases  where  the  disease  in  the  lower 
motor  neurones  has  gone  so  far  in  advance  of  that  in  the  pyramidal 
tracts  that  they  cannot  be  differentiated  clinically  at  all  from  Charcot's 
protopathic  type.  Even  in  those  cases  where  the  symptoms  show  them- 
selves first  in  the  lower  extremities  there  will  be  found  upon  careful 
examination  a  slight  degree  of  rigidity,  with  zveakness  in  the  arms  and 
hands. 

In  all  typical  cases,  therefore,  of  amyotrophic  lateral  sclerosis  the 
arms  will  be  observed  to  be  strongly  adducted,  the  forearm  flexed,  the 
hand  pronated  and  the  fingers  more  or  less  fixed  in  the  claw  position. 
In  the  legs  the  stiffness  is  shown  in  the  walk.  The  patient  steps  slowly, 
more  or  less  rigidly,  and  with  short  strides.  Later  on  he  seems  only 
to  be  able  to  push  himself  along  on  the  tips  of  his  toes.  This  spasticity 
is  the  result  of  muscular  tension,  active  contraction  and  atrophic 
paralysis. 

Equally  important  as  the  spasticity  in  the  symptomatology  of 
amyotrophic  lateral  sclerosis,  though  not  synchronous  with  it,  is  the 
progressive  atrophy  of  the  muscles.  Individual  muscles  and  groups  of 
muscles  may  be  attacked,  simultaneously  or  one  after  the  other,  accord- 
ing to  the  location  and  extent  of  the  lesions.  It  would  be  useless  to 
attempt  to  describe  all  of  the  types  of  atrophy  that  can  appear  in  the 


404 


THE   XEUROXTC   DISEASES 


course  of  this  affection.  Suffice  it  to  say  that  the  wasting  of  the  mus- 
cles, which  usually  is  observed  from  a  few  months  to  many  years  even 
after  the  appearance  of  the  spasticity,  is  never  quite  as  marked  as  it  is 
in  the  ordinary  forms  of  anterior  poliomyelitis  or  progressive  muscular 
atrophy,  and  that  furthermore  it  is  more  pronounced  in  the  upper  than 
in  the  lower  extremities.  In  these  it  begins  most  frequently  in  the 
hand,  gradually  involving  the  shoulder  and  radial  regions  later.  The 
muscles  of  the  lips,  the  tongue,  the  jaw  and  the  face  may  all  become 

FIGURE  71 


Attitude  of  the  hand  in  amyotrophic  lateral  sclerosis.      (After  Charcot.) 

Stiff  and  atrophied.  The  trunk  muscles,  as  a  rule,  escape  or  are  not 
so  profoundly  implicated  as  are  those  of  the  extremities.  In  the  final 
stages  of  the  disease  the  diaphragm,  the-  internal  muscles  of  respira- 
tion, and  even  the  visceral  muscles  may  all  become  more  or  less  affected. 

At  an  early  period  the  deep  reflexes  are  exaggerated,  as,  for  exam- 
ple; those  of  the  quadriceps,  gastrocnemius,  patella,  Acliilles,  biceps,  tri- 
•ceps,  scapular.  A  masseter  clonus,  elicited  by  gently  tapping  the  edge 
'Of  the  lower  jaw,  was  first  studied  by  Beevor  and  Morris  Lewis.  The 
Babinski  sign  may  be  present,  and  later  on  contractures  with  threat- 
ening cardiac  and  respiratory  phenomena.  Early  in  the  disease  the 
electrical  reactions  are  not  far  from  the  normal.  As  the  atrophy  ad- 
vances, however,  the  reflexes  diminish  correspondingly  and  the  elec- 
trical phenomena  assume  irregularly  the  characteristics  of  the  reaction 
of  degeneration. 

At  times  a  characteristic  -fibrillary  tremor  or  twitching  may  appear 
in  advance  of  the  atrophy  or  it  may  even  form  the  first  objective  svmp- 
tom  of  the  disease. 

The  motor  weakness  that  is  present  is  not  the  result  of  the  atrophv 
and  contractures,  but  is  an  independent  phenomenon. 

That  amyotrophic  lateral  sclerosis  is  a  disease  of  the  efferent  or 
motor  path  is  clinically  shown  by  the  complete  absence  of  all  sensor}^ 
S}TTiptoms.     In  a  few  cases  a  slight  parjesthesia  has  been  noticed.     A 


THE   NEURONIC   DISEASES  405 

primary  degeneration  of  tiie  columns  of  Goll,  with  slight  sensory  phe- 
nomena, has  been  recorded  by  Hektoen ;  and  Mills  has  reported  a  case 
of  associated  tabes  and  amyotrophic  lateral  sclerosis.  Such  cases,  while 
constituting  the  link  between  this  disease  and  progressive  muscular 
degeneration  on  the  one  hand,  and  locomotor  ataxia  on  the  other,  should 
probably  be  looked  upon  as  instances  of  combined  sclerosis,  rather  than 
as  examples  of  amyotrophic  lateral  sclerosis  with  a  mere  complication. 

Likewise  there  are  no  mental  symptoms  in  this  disease,  though 
Spiller,  Probst  and  Sarbo  have  recorded  instances  in  which  some  mental 
disturbance  was  present.  These  were  probably  mixed  cases  and  may 
well  be  accounted  for  by  the  wide  extension,  in  a  few  individuals,  of  the 
degenerative  process. 

Amyotrophic  lateral  sclerosis  as  a  typical  disease  is  therefore 
clinically  a  motor  degenerative  paralysis,  and  is  characterized  only  by 
the  symptoms  spasticity,  atrophy  and  paresis. 

Late  in  the  disease,  and  usually  as  its  terminal  phenomena,  bulbar 
paralysis  occurs.  Dysarthria  proceeds  to  anarthria.  Deglutition  be- 
comes difficult  and  even  impossible.  The  lips,  the  tongue,  the  palate 
and  the  cheeks  are  paralyzed,  atrophied  and  electrically  altered.  Drool- 
ing from  the  mouth  occurs,  the  speech  is  blurred  and  "laliing"  in 
character,  and  aphonia  supervenes.  Finally  after  the  disease  has  run 
its  course  in  from  two  to  four  years,  the  end  comes  as  the  result  of 
inanition,  asphyxia  or  aspiration  pneumonia. 

Diagnosis. — A  typical  case  of  amyotrophic  lateral  sclerosis  is  not 
hard  to  diagnose,  for  it  presents  a  strikingly  characteristic  group  of 
symptoms — namely,  spasticity,  paresis,  atrophy  and  absence  of  all  sen- 
sory and  mental  phenomena.  When  the  disease  process  in  the  peripheral 
motor  spino-muscular  system  precedes  for  some  time  the  disease 
process  in  the  central  cortico-pyramidal  system,  it  may  be  impossible  to 
differentiate  it  clinically  from  the  myelopathic  type  of  progressive  mus- 
cular atrophy.  In  such  cases,  however,  some  slight  degree  of  spasticity 
can  be  detected  upon  careful  examination  in  some  muscles  later  on  that 
have  escaped  the  first  onset  of  the  malady.  Cases  in  which  other  de- 
generations are  associated  with  those  of  the  amyotrophic  may  give 
much  trouble  in  the  diagnosis.  A  most  careful  weighing  and  compar- 
ing of  the  various  symptoms  of  the  associated  affection  with  those  of 
Charcot's  disease  can  alone  render  a  differentiation  at  all  possible. 
Bearing  in  mind  the  characteristic  traits  referred  to  elsewhere,  amyo- 
trophic lateral  sclerosis,  with  its  peculiar  features,  ought  not  to  cause 
much  trouble  in  differentiating  it  from  progressive  muscular  atrophy, 
bulbar  and  spinal  chronic  poliomyelitis,  syringomyelia,  focal  spinal 
pachymeningitis  or  cervical  hypertrophic  pachymeningitis,  multiple 
neuritis,  the  cortical  encephalitis  of  Striimpell,  disseminated  sclerosis, 
the  muscular  dystrophies  or  diffuse  myositis. 

Prognosis. — This  is  bad,  as  the  disease  invariably  terminates 
fatally  in  a  few  years. 

Treatment. — The  treatment  is  limited  and  unsatisfactory.  Tonics, 
fresh  air  and  good  nutrition  should,  of  course,  be  given.  Though 
Cowers  recommends  injections  of  strychnine,  and  others  have  suggested 
electricitv,  a  trial  of  the  ;e  measures  has  not  seemed  to  materially  modify 


406  THE   XEUROA'IC   DISEASES 

the  course  or  termination  of  this  progressive  and  profound  degenera- 
tion, 

PROGRESSR'E  BULBAR  PARALYSIS. 

This  disease  was  first  described  by  Duchenne  in  i860,  and  ten 
}ears  later  its  lesion  was  accurately  located  by  Charcot  and  Leyden. 
It  is  sometimes  called  progressive  glosso-labio-laryngeal  paralysis. 

It  is  a  primary,  degenerative  disease  of  the  bulbar  cranial  nerves 
of  motion.  These  nerves  are  the  analogues  of  the  spinal  motor 
nerves,  and  their  nuclei  in  the  floor  of  the  fourth  ventricle  are  the 
homologues  of  the  anterior  horns  of  the  cord.  This  form  of  progres- 
sive, primary  degeneration  in  them,  therefore,  is  nothing  more  nor  less 
than  another  view  of  progressive  muscular  atrophy.  That  this  is  so 
is  further  proved  by  the  fact  that  on  the  one  hand  bulbar  paralysis 
almost  constantly  appears  sooner  or  later  in  the  poliomyelitic  type  of 
progressive  muscular  atrophy  and  the  amyotrophic  type,  and  on  the 
other  hand  degeneration  in  the  pyramidal  tracts  and  in  the  spinal  an- 
terior horns  is  almost  invariably  found  in  the  late  cases  of  this  dis- 
ease. In  other  words  glosso-labio-laryngeal  paralysis  of  the  progres- 
sive type  is  progressive  muscular  atrophy  prominently  appearing  in  the 
medulla  oblongata.  For  this  reason  I  classify  and  describe  it  here 
rather  than  under  the  head  of  diseases  of  the  medulla.  It  is  not  a  dis- 
ease of  the  medulla  in  the  true  sense  of  the  word.  It  is  merely  a  phase, 
a  unique  manifestation,  of  progressive  muscular  atrophy.  The  symp- 
tomatology of  it  may  suggest  an  independent  classification,  but  its 
pathology  binds  it  down  as  one  of  the  unique  localization  types  merely 
of  the  general  disease  of  the  entire  motor  tract  known  as  progressive 
muscular  atrophy.  Only  in  symptomatology  therefore  does  bulbar 
paralysis  of  the  progressive  type  stand  forth  independently. 

Etiology. — What  has  been  said  of  the  etiology  of  the  two  pre- 
ceding affections  is  strictly  applicable  here,  for  all  three  diseases  are 
one  and  the  same. 

It  is  rare  and  occurs  mostly  in  late  adult  life.  It  is  all  but  un- 
known before  the  fortieth  year  of  age.  In  a  few  instances  it  has  been 
reported  as  having  occurred  in  children,  though  there  is  some  doubt 
about  the  exact  pathological  similarity  of  these  cases  with  the  typical 
disease.  I  do  not  regard  the  infantile  hereditary  and  familial  types 
of  progressive  bulbar  paralysis  as  corresponding  exactly  with  the  type 
now  under  consideration.  They  are  more  strictly  bulbar  diseases,  con- 
genital nuclear  atrophies,  and  not  a  mere  part  of  a  general  progres- 
sive motor  atrophy.  They  will  be  referred  to  again  under  the  head  of 
diseases  of  the  lower  motor  segment  more  particularly. 

As  in  the  other  manifestations  of  the  disease,  a  neuropathic  tend- 
ency is  here  present,  responding  to  such  exciting  causes  as  cold,  exces- 
sive emotion,  shock,  traumata  and  over-exertion  of  the  muscles,  such 
as  those  of  the  lips,  tongue  or  larynx. 'that  are  innervated  bv  the  me- 
dulla. 

Pathology  and  Pathogenesis. — To  describe  this  I  would  but 
have  to  repeat  what  I  have  said  under  the  head  of  progressive  muscu- 


THE    NELROMC   DISEASES 


407 


lar  atrophy.  The  changes  are  the  same,  but  in  this  instance  they  have 
started  first  in  the  nuclei  of  the  motor  cranial  nerves,  namely,  the 
facial,  the  motor  branches  of  the  glosso-pharyngeal  and  vagus  and 
the  hypoglossal.  The  spinal  accesssory,  of  course,  is  a  spinal  nerve  in 
reality  so  that  it  escapes  in  bulbar  paralysis,  and  the  limited  nosol- 
ogy does  not  include  implication  of  the  ocidar  motor  nuclei.  The  motor 
branch  of  the  fifth  nerve  is  occasionalh'  included  in  the  disease  process. 
The  pyramidal  tracts  may  atrophy  in  some  cases  before  the  gray  nu- 
clei, or  accompany  it  or  be  entirely  absent.  The  same  is  to  be  said 
of  the  degeneration  in  the  anterior  horns  of  the  cord. 

Symptoms. — It  is  due  almost  entirely  to  its  symptomatologv  that 
progressive  bulbar  paralysis  owes  its  disti-nction  as  a  separate  sort  of  a 


FIGURE  72 


Normal  h>TX)glossal  nucleus.  Atrophic  hypoglossal  nucleus  in  bulbar 

paralysis,    g,  blood-vessel. 
(After  Oppenheim.) 

disease.  A  progressive,  atrophic  paralysis  involving  both  sides  of  the 
face  and  destroying  the  speech,  the  deglutition,  the  phonation  and  the 
mastication  constitutes  the  sum  total  of  the  clinical  manifestations  of 
the  disease. 

Usually  the  speech  is  the  first  function  to  be  affected.  Words  and 
sentences  with  many  dentals  and  Unguals  and  linguo-palatal  letters  in 
them  are  hard  to  utter  and  soon  tire  the  patient.  He  cannot  close 
the  lips  as  tightly  as  he  should  to  utter  the  explosives  p  and  b.  On 
account  of  the  added  nasal  tone,  he  sounds  these  letters  as  if  the}'  were 
mp  or  mb.  To  say  smoothly  the  sentence,  "Peter  Piper  Picked  a  Peck 
of  Pickled  Peppers,"  or  "Round  the  Rugged  Rock  the  Ragged  Ras- 
cal Ran,"  is  almost  impossible.  Dysarthria  with  a  nasal  twang  is  thus 
an  early  and  characteristic  manifestation.  There  is  a  suggestion  in  the 
speech  as  if  something  were  in  the  mouth,  so  much  so  that  a  mother 
in  a  certain  case  constantly  asked  her  daughter  for  a  long  time  to  take 
what  she  had  in  her  mouth  out  before  she  addressed  her,  much  to  the 
annoyance  of  the  daughter,  who  of  course,  had  to  regularly  deny  the 
allegation.     Exhaustion  increases  the  speech  difficulty. 


408  THE   NEURONIC   DISEASES 

Xext  the  tongue  is  seen  to  be  paralyzed.  It  rests  limp,  shriveled 
and  immovable  on  the  floor  of  the  mouth.  The  mucous  membrane 
on  it  is  thrown  into  folds.  At  first  there  are  marked  fibrillary  twitch- 
ings  and  tremors  in  its  muscle.  The  lingual  muscles  are  markedly 
atrophied.  On  account  of  all  this  the  food  bolus  cannot  be  pushed 
back  into  the  pharynx  and  deglutition  thus  becomes  positively  im- 
paired. There  is  regurgitation  of  fluids  up  into  the  nostrils  and  down 
into  the  larynx.  This  of  course  provokes  choking  and  coughing.  The 
saliva  accumulates  and  drools  out  of  the  mouth  over  the  edges  of  the 
paralyzed  lips.  \'omiting  not  infrequently  occurs  as  a  result  of  the 
disturbances  of  and  efiforts  in  swallowing.  At  length  there  is  com- 
plete aphagia.  or  inability  to  swallow  any  solid  or  fluid. 

Later  on  in  the  disease  uiasticafion  is  difficult  and  sometimes  im- 
possible. 

The  involvement  of  the  laryngeal  muscles  eventuates  in  first 
dysphonia  and  finally  aphonia,  the  respiration  suffering  at  the  same 
time.  There  is  in  the  early  stages  a  v.eakening,  a  softening,  a  monot- 
ony of  the  voice.  Choking  spells,  coughing,  shortness  of  breath,  and 
towards  the  end  alarming  and  distressing  dyspncea  are  observed.  The 
laryngeal  paralysis  is  not  usually  as  severe  as  that  of  the  lips  and  tongue 

The  movements  of  all  the  muscles  of  the  various  functions  just  re- 
ferred to  are  gradually  and  slowly  restricted.  The  muscles  themselves 
are  also  distinctly  degenerated.  This  and  the  fibrillary  tremor  and 
the  electrical  reaction  of  degeneration  are  all  characteristic  of  progres- 
sive atrophy.  The  reflexes,  notably  the  jaw  and  pharyngeal,  are  abol- 
ished. 

The  facial  expression,  as  may  well  be  imagined  from  this  descrip- 
tion of  the  limitation  of  movements  and  muscular  wasting,  is  unique. 
The  folds  are  shallow  or  wanting,  the  mouth  stands  partially  open, 
the  lower  lip  hangs  down  and  the  saliva  drools  over  it.  There  is  a 
fixed,  expressionless  countenance,  a  sort  of  dead,  listless,  waxy  ap- 
pearance. All  of  this  involves  mostly  the  lower  half  of  the  face,  the 
upper  half  being  comparatively  intact  and  showing  by  its  greater 
mobility  the  retention  of  the  patient's  mental  activities.  This  relative 
freedom  of  the  upper  part  of  the  face  distinguishes  this  form  of  bul- 
bar paralysis,  in  part,  from  the  infantile  form  where  the  brow  cannot 
be  corrugated  nor  the  eyes  tightly  closed. 

Naturally  this  condition  would  cause  a  high  degree  of  emotion- 
alism in  these  patients,  but  this  emotionalism  is  to  a  certain  extent  a 
symptom  and  not  a  mere  sequel  of  the  disease.  It  is  a  part  of  the  neu- 
ropathic complex  and  enters  mto  its  clinical  presentation. 

With  what  has  already  been  said  in  regard  to  this  disease  being 
but  progressive  muscular  atrophy  in  a  particular  part  of  the  motor 
tract,  it  hardly  needs  to  be  repeated  that  there  are  absolutely  no  sen- 
sory symptoms.  Furthermore  it  is  to  be  expected  that  in  some  cases, 
as  in  the  amyotrophic  types,  there  will  be  a  certain  degree  of  spasticity 
of  the  muscles  and  an  exaggerated  condition  of  the  reflexes.  Spinal 
manifestations  of  the  disease  may  also  appear  in  conjunction  with,  or 
later  than,  the  bulbar  symptoms.  Thus  the  arnT^  ^nd  hands  may  ex- 
hibit the  atrophic  parah  '^is. 


THE   NEURONIC   DISEASES 


409 


Diagnosis. — If  the  symptoms  of  this  disease  be  closely  watched, 
there  ought  to  be  very  little  chance  of  a  mistake  in  diagnosing  it.  In 
the  early  or  beginning  paralysis,  a  lesion  of  the  lozver  motor  cortex 
might  be  thought  of  by  mistake.  In  bulbar  palsy  the  symptoms  are 
always  bilateral,  whereas  in  cerebral  trouble  they  are  rarely  so.  Atrophy 
occurs  in  the  former,  not  in  the  latter.  Polioe^icephalitis  is  somewhat 
more  acute  and  less  progressive  in  its  symptomatology  than  is  this 
disease.  There  are  acute  bulbar  paralyses  that  sometimes  offer  con- 
siderable confusion.  The  reader  is  referred  to  them  in  the  section  on 
diseases  of  the  medulla  oblongata.  Medullary  tumor  is  accompanied 
by  the  usual  pressure  symptoms  of  all  intracranial  growths,  does  not 
produce  bilateral  symptoms,  nor  does  it  pick  out  the  nuclei  and  limit 
its  effects  to  them  and  their  nerves  as  does  this  disease. 

A  careful  distinction  must  be  made  between  this  type  of  progres- 
sive bulbar  paralysis  and  the  hereditary  or  familial  type  spoken  of 
under  the  head  of  diseases  of  the  medulla.  The  latter  occurs  always 
in  children  in  whom  there  is  a  degenerative  heredity.  Consanguinity 
in  the  parentage  is  sometimes  in  the  history.  The  child  exhibits  mark- 
ed stigmata  of  degeneracy.  The  atrophic  paralysis  begins  in  the  upper 
part  of  the  face  and  continues  there  during  the  involvement  of  the 
lower  part.  Ptosis  is  present.  The  ocular  muscles  are  usually  in- 
volved. There  are  no  signs  of  atrophic  paralysis  in  the  extremities 
or  trunk.  The  facial  expression  is  that  of  dementia.  Death  occurs 
usually  in  two  or  three  years.  The  cases  are  rather  hereditary  develop- 
mental anomalies,  closely  related,  in  some  of  them  at  least,  to  the  facial 
and  oculomotor  diplegias. 

Prognosis. — Bulbar  paralysis  is  a  fatal  disease,  ending  always 
in  death  after  two  or  three  years,  rarely  more.  It  is  caused  by  the 
respiratory  disturbance  as  a  rule  which  appears  in  the  form  of  an  as- 
piration pneumonia,  or  an  asphyxia.  Inanition  also  is  present.  It  is 
the  appearance  of  bulbar  symptoms  that  often  foretells  the  early  de- 
mise of  the  victims  of  the  other  forms  of  progressive  muscular  atrophy. 
Very  rarely  the  disease  runs  on  several  years,  slow  and  progressive, 
but  with  remissions. 

Treatment. — The  disease  is  incurable  and  the  treatment  there- 
fore useless.  Nitrate  of  silver,  strychnine,  arsenic,  potassium  iodide 
and  galvanism  are  all  suggested.  I  have  never  heard  of  any  case  be- 
ing modified  for  the  better  by  any  of  these. 

Symptomatic  treatment  may  be  called  for.  Thus  the  drooling  of 
the  saliva  can  be  checked  somewhat  by  the  restriction  of  its  secretion 
with  the  administration  of  atropine.  The  patient's  nourishment  may 
have  to  be  kept  up  by  artificial  feeding  through  a  stomach  tube.  There 
are  no  prophylactic  measures  to  be  recommended,  because  we  do  not 
know  why  the  disease  appears. 

PROGRESSIVE  MUSCULAR  DYSTROPHY. 

The  muscular  dystrophies,  Erb's  dystrophia  muscular  is  progres- 
siva, are  related  clinically  to  the  progressive  muscular  atrophies.  They 
are  not  nervous  affections  and  strictly  ought  not  to  be  considered  in 


410  THE   NEURONIC   DISEASES 

a  work  of  this  sort.  They  are  primary  diseases  of  the  muscular  tis- 
sues and  are  largely  the  result  of  heredity  and  developmental  defects. 
It  will  not  be  amiss,  however,  to  consider  them  here,  for  their  clin- 
ical presentation  is  in  man}-  respects  so  like  the  spinal  atrophies  that 
for  diagnostic  purposes,  and  until  our  knowledge  is  more  exact,  they 
can  be  placed  side  by  side. 

Many  histologists  and  physiologists  take  the  broad  view  that  the 
lower  neurone  and  its  related  muscle  is  a  single  mechanism,  a  uni- 
form, composite  organ,  and  that  disease  of  the  neural  or  muscular  part 
of  this  apparatus  is  merely  a  question  of  location  and  not  of  essential 
pathology.  Neural  disease  affects  the  muscles ;  the  muscle  disease  re- 
acts upon  the  neural  tissue.  For  aught  we  know  positively  the  latter 
may  be  due  to  some  minute  form  of  neural  trouble,  cellular,  mole- 
cular or  physio-chemical,  too  fine  for  our  coarse  means  of  investigation. 
As  heredity  always  plays  its  most  brilliant  role  in  connection  with  the 
nervous  system  and  as  it  is  such  an  important  factor  in  the  muscular 
dystrophies,  the  last  suggestion  is  not  such  an  illogical  one. 

Clinically  these  diseases  have  been  divided  into  separate  types, 
though  it  must  be  kept  in  mind  that  etiologically  and  pathologically 
they  are  all  the  same.  The  types  are  founded  upon  the  age  of  the 
patient,  the  muscles  attacked,  the  presence  of  hypertrophy  or  pseudo- 
hypertrophy and  the  prominence  of  the  heredity.  Erb  makes  two  grand 
divisions  of  them  into, 

L  The  infantile  cases  (dystrophia  mnscularis  progressiva  iiifan- 
tum),  and 

II.  The  cases  that  occur  in  youths  and  adults  (dystrophia  inus- 
cularis  progressiva  juvenum  vel  adult  arum). 

Class  I.  is  further  subdivided  into  the  hypertrophic  and  atrophic 
forms.  Of  these  the  hypertrophic  cases  may  be  truly  hypertrophic  or 
only  pseudo-hypertrophic,  while  the  atrophic  cases  may  begin  with 
primary  involvement  of  the  face  or  without  involvement  of  the  face. 

The  shaded  figures  illustrate  roughly  the  early  localization  of  these 
various  types.  After  discussing  the  main  features  of  progressive  mus- 
cular dystrophy,  the  clinical  types  that  have  been  recognized  will,  un- 
der the  same  head,  receive  brief  notice. 

Etiology. — The  first  thing  preeminently  obvious  in  the  etiology 
of  the  muscular  dystrophies  is  the  influence  of  heredity.  The  trouble 
is  not  merely  congenital,  but  genuinely  hereditar}-.  The  influence  is 
transmitted  through  the  mother  and  is  often  pure  and  direct.  The 
ovum  carries  the  impress  which  it  obtains  from  being  a  part  of  her 
own  constitution.  Its  further  development  is  affected  by  this  im- 
press. Therefore  it  is  that  the  muscular  deterioration,  which  may  not 
begin  to  show  itself  in  the  child  until  the  end  of  the  first  or  the  middle 
of  the  second  decennial  period  of  life,  is  the  result  of  a  developmental 
defect  and  not  of  an  acquired  disease.  The  mother  usually  exhibits 
the  same  disease  as  her  child.  Brasch  saw  a  case  in  which  the  mother, 
forty-two  years  of  age,  developed,  after  the  birth  of  her  dystrophic 
child,  a  hypertrophic  form  of  the  trouble. 

In  some  cases  a  marked  neuropathic  tendency  is  traced  in  the 
maternal  ancestry.     Syphilis,  alcoholism,  consanguinity  do  not     seem 


THE   NEURONIC   DISEASES  4II 

to  be  of  any  great  significance.  What  the  impulse  is,  or  how  far  back 
in  the  ancestry  it  began,  we  are  totally  ignorant  of.  Some  authors  men- 
tion traumata  and  acute  diseases  as  provocative  causes.  Boys  are 
jnore  frequently  affected  than  girls,  and  most  of  the  cases  begin  be- 
iore  the  age  of  ten. 

Heredity  then  is  the  one  great  factor  that  distinguishes  the  etiology 
■of  these  muscular  anomalies.  The  age  and  sex  are  probably  mere  sub- 
sidiary factors. 

Pathology  and  Palhogenesis. — The  essential  element  in  the 
pathology  is  a  change  in  the  muscular  tissues,  primary  in  origin  and 
nature,  whereby  a  hypertrophy  alternates  with  an  atrophy.  The  change 
is  clearly  due  to  an  inherent  developmental  weakness  in  the  muscular 
•elements  themselves  and  seems  to  select  first  those  muscles  generally 
that  were  the  latest  to  have  developed  embryologically.  The  biological 
importance  of  the  latter  fact,  as  indicating  the  hereditary  developmental 
nature  of  the  trouble,  can  hardly  be  over-estimated. 

All  the  muscles  are  not  equally  attacked  in  the  same  way.  This 
■constitutes  the  misleading  basis  upon  which  the  various  types  of  the 
■disease  have  been  erected.  The  legs  especially  seem  to  be  the  loca- 
tion for  the  changes  to  be  especially  marked  in  ;  next  the  muscles  of  the 
pelvic  girdle  and  lower  part  of  the  trunk  ;  and  lastly  those  of  the  face, 
shoulder  and  arm.  On  account  of  the  hypertrophic  condition  in  some 
muscles  and  the  atrophic  in  others  the  general  contour  of  the  part  is 
greatly  altered.  Sometimes  a  part  of  a  muscle  may  be  so  enlarged  as 
to  produce  a  remarkable  intumescent  or  tumor-like  appearance.  In 
one  case  I  saw  the  calves  so  excessively  enlarged  that  the  appearance 
of  the  patient,  when  standing,  was  positively  ludicrous.  The  outline 
of  the  altered  tissue  is  quite  sharp  in  most  cases ;  in  others  it  fades 
away  into  the  normal  tissue. 

There  are  reasons  for  suspecting  that  the  changes  in  the  mus- 
cles undergo  a  more  or  less  regular  and  uniform  process.  There  are 
■early  signs  of  irritation  such  as  sivelliiig  of  the  riuscle  fibre,  prolifera- 
tion of  the  nuclei  and  connective  tissue  and  splitting  and  breaking  up  of 
the  muscular  strands.  The  areolar  and  connective  tissues  undergo  hy- 
pertrophy and  the  muscular  fibres  become  actually  hypertrophied.  This 
of  course  enlarges  the  entire  muscle  mass.  Gradually,  however,  the 
true  muscle  fibres  waste,  diminish  and  disappear.  The  associated  tis- 
sues do  not  waste.  In  this  way  the  muscle  mass  remains  enlarged 
Avhile  the  true  muscle  tissue  is  actually  diminished.  This  is  the  pseudo- 
hypertrophic condition  so  characteristic  of  the  dystrophies.  Fatty  de- 
posits occur  in  the  muscles  and  even  vacuoles  are  formed.  As  the 
muscular  fibres  continue  to  diminish  and  disappear  and  the  connec- 
tive tissue  increases  and  fills  in  the  vacancy,  the  muscle  becomes  hard 
and  dense.  It  assumes  a  condition  of  myosclerosis.  After  a  long  time 
nothing  is  to  be  seen  but  dense  connective  tissue  and  atrophied  fibres. 
With  all  this  change  in  the  muscles,  the  nerves  and  spinal  cord  re- 
main normal.  In  some  cases  secondary  changes  have  been  observed 
of  a  neuritic  and  poliomyelitic  character. 

It  would  be  rash  to  affirm  that  these  dystrophies  are  in  any  way 
-directly  dependent  upon  neural  changes.     In  the  present  state  of  our 


4T2 


THE   XEUROXIC   DISEASES 


FIGURE  72,- 


Jtcveni  (e    'yj'e- 


y\rdr\-J)LLckcnTie 


luscular   atrophy. 


THE  ^EURO^;lc  diseases 


413 


FIGURE  74- 


Muscular    atrophy. 


414 


THE   NEURONIC   DISEASES 


THE  NEURONIC  DISEASES 


415 


knowledge  we  must  be  content  to  regard  them  as  primary,  develop- 
mental defects  in  the  muscular  elements.  And  yet  when  the  sym- 
metrical distribution,  which  not  infrequently  obtains,  is  taken  into  ac- 
count, when  it  is  remembered  that  in  many  cases  neural  changes  are 
observed  which  cannot  positively  be  asserted  to  be  always  secondary 
to  the  muscular  changes,  and  when  finally  the  close  biological  and 
physiological  relation  between  the  nervous  and  muscular  apparatuses 
is  considered,  it  is  not  so  unreasonable  a  suspicion  to  hold  that  even 
the  muscular  dystrophies  may  be  due  to  some  minute  physio-chemical 
nutritive  disturbance  in  the  spinal  nerve  cells,  which  our  present  means 


FIGURE  78. 


FIGURE  79. 


Pseudo-hypertrophic  paralysis.      (After   Duchenne.) 


of  research  cannot  detect,  but  which  may  be  the  immediate  cause  of 
the  muscular  deterioration.  This  of  course  is  only  a  conjecture  and 
must  not  yet  be  assumed  as  true.  It  is  so  much  more  desirable  a 
hypothesis  in  accounting  for  the  many  similarities  between  the  mus- 
cular dystrophies  and  the  progressive  muscular  atrophies  than  is  the 
hypothesis  of  a  primary  muscular  degeneration  in  accounting  for  their 
few  differences,  that  it  is  worthy  of  much  consideration  and  if  pos- 
sible of  future  establishment  b)'^  pasitive  proof  and  demonstration. 

Symptoms. — Instead  of  symptoms,  one  might  truthfully  say  that 
the  symptom  of  this  disease  is  hypertrophy  or  atrophy  of  the  muscfcs. 
All  muscles  of  the  body  may  be  affected,  though  the  change  appears 


4i6 


THE   NEURONIC   DISEASES 


more  frequently  in  some  than  in  others.  Both  hypertrophy  and  atrophy 
may  appear  simultaneously  in  different,  and  even  in  distant,  muscles, 
or  in  different  parts  of  the  same  muscle.  There  is  no  rule  about  the 
matter  and  the  pathology  cannot  be  made  a  basis  for  the  separation 
of  the  malady  into  types.  On  account  of  these  muscular  alterations 
certain  forms  of  paralyses  occur,  deformities  appear,  and  alterations  in 
the  bodily  movements  take  place.  There  are  )io  distinctive  sensory 
symptoms. 

\\'ith  the  atrophy  a  parallel  paralysis,   loss   of  reflex  action   and 
slight  electrical  changes  take  place,  but  none  of  these  are  as  pronounced 

FIGURE  80. 


Attitudes  assumed  in  pseudo-hypertrophic  paralysis   during  attempts   to   rise. 
(Gowers.) 


or  characteristic  as  they  are  in  the  true  neural  atrophies.  Coldness, 
discoloration  and  other  general  vasomotor  disturbances  are  liable  to 
appear  in  the  aft'ected  limbs.  The  general  nutrition  remains  normal. 
The  sphincters  continue  active.  The  sexual  function  is  diminished  or 
lost.    The  mind  remains  clear. 

I  will  now  briefly  consider  the  varieties  of  the  disease  that  have 
been  artificially  established  on  the  basis  of  the  particular  distribution  of 
the  predominant  symptom.  In  doing  so  I  will  at  the  same  time  be  giv- 
ing a  more  or  less  complete  clinical  picture  of  the  entire  affection. 

Pseudo-hy pertropliic  Muscular  Paralysis  (Muscular  Pseudo-hyper- 
trophy; Lipomatous  Muscular  Atrophy).  In  this  form  of  the  disease 
there  appears  in  the  child  usually  a  weakness,  followed  by  enlargement 
of  the  calves  of  the  legs.  A  peculiar  waddling  gait  is  thus  noticed 
and  there  is  some  difficulty  experienced  in  climbing  the  stairs.  Some- 
times the  child  falls  unexpectedly,  and  has  considerable  difficulty   in 


THE   NEURONIC   DISEASES 


417 


getting  up.  It  is  noticed  that  when' laid  upon  his  back  on  the  floor  he 
first  rolls  over  on  his  face,  draws  himself  together,  keeping  his  hands 
and  knees  upon  the  floor,  and  then  with  a  hand  on  each  of  his  legs 
climbs  up  upon  himself,  sliding  his  hands,  and  grasping  his  legs  one 
after  the  other  at  successive  levels,  until  he  has  attained  the  erect 
position.  This  manoeuvre  in  getting  up  is  so  characteristic  that  it  is 
almost  pathognomonic.  It  is  well  illustrated  in  the  accompanying  pic- 
tures from  Gowers.  As  the  disease  progresses  the  extensors  oi  the  leg 
and  the  flexors  of  the  thigh  become  so  weak  that  the  attitude  grows 
characteristic.  The  spine  sags  forward  with  a  marked  concavity  open- 
ing backwards.    This  lordosis  is  always  seen  when  the  patient  is  stand- 

FIGURE  81. 


Progressive  myopathy.  Advanced  case  with  marked  lordosis  in  sitting.     (After 
Souques-Brissaud. ) 

ing  and  sometimes  when  seated.  In  certain  mild  cases  it  may  disappear 
in  the  sitting  posture.  It  is  a  feature  of  the  lumbar  part  of  the  spine 
and  causes  a  marked  protrusion  of  the  abdomen  forwards  and  of  the 
shoulders  backwards.  At  this  stage  of  the  disease  the  legs  are  usually 
enlarged,  ofttimes  remarkably  so,  and  are  barrel-shaped.  The  muscles 
about  the  hips  and  in  the  lumbar  region  exhibit  considerable  atrophy 
with  here  and  there  a  curious  lipomatous-like  swelling.  The  front  of 
the  thigh  has  bulged  in  this  way  and  one  hip  has  been  more  pro'minent 
than  the  other.  After  the  leg  and  lumbar  muscles,  perhaps  the  shoul- 
der and  upper  arm  muscles,  are  the  most  frequently  implicated.  Tlie 
infraspinatus,  the  deltoid,  the  lower  part  of  the  trapezius,  the  pectoralis 
major,  the  serratus  anticus  major,  the  rhomboids,  the  biceps,  the  brachi- 


4l8  THE   XEUROXIC   DISEASES 

alis  internus  and  the  supinator  lonous  may  ail  or  any  one  of  them  be 
weak  and  paralytic.  Alternations  of  hypertrophy  and  atrophy  may  be 
observed  in  them.  The  attitude  and  movements  of  the  shoulders,  the 
elevation  of  the  arms,  and  the  stationary  position  of  the  scapulce  are 
all  distinctive.  In  the  lower  part  oi  the  body  the  glutei,  the  latissimus 
dorsi,  the  quadriceps  femoris,  the  adductors,  the  calf  and  peroneal  mus- 
cles exhibit  the  characteristic  change  and  debility.  The  tongue  in  rare 
instances  is  hypertrophied.  The  distal  parts  of  the  extremities,  par- 
ticularly the  forearms,  the  neck  and  face,  are  rarely  included  in  the 
disease  process. 

Thus  we  note  that  pseudo-hypertrophic  paralysis  is  a  widespread 
afifection,  though  the  changes  in  the  leg  muscles  and  the  gait  are  the 
most  constant  and  obtrusive  symptoms. 

In  the  Juvenile  type  of  Erb,  the  scapula-humeral  form  of  the  dis- 
ease, the  dystrophy,  as  its  latter  name  indicates,  is  most  prominent  at 
first  in  the  muscles  that  make  up  the  shoulder  girdle.  The  same  gen- 
eral process  takes  place  that  has  already  been  described  for  all  forms  of 
the  disease.  Gradually  it  extends  down  the  arm  and  very  late  in  the 
course  implicates  the  forearm  and  the  legs.  The  beginning  of  the  case 
is  the  only  feature  in  which  it  differs  from  the  other  types.  As  it  is 
slow  and  progressive  it  ultimately  comes  to  have  all  the  general  quali- 
ties in  regard  to  the  muscular  hypertrophy  and  atrophy,  the  gait,  and 
the  curvature  of  the  spine  that  they  have. 

The  Facio-Scapiilo-Humeral  type  of  Landouzy  and  Dejerine  is 
often  spoken  of  as  the  infantile  form  because  it  so  often  appears  earlier 
than  the  others.  It  may,  however,  show  itself  at  the  same  age.  Tlie 
implication  of  the  face  with  the  shoulder  and  arm  is  its  dominant  trait. 
The  weakness  and  wasting  are  particularly  observable  in  the  orbicularis 
palpebrarum  and  the  orbicularis  oris,  so  that  the  eyes  cannot  be  closed 
completely  and  the  lips  protrude  tapir-like.  The  involvement  of  the 
buccinators  causes  difficulty  in  eating  and  chewing,  and  a  puffing  of  the 
cheeks  in  talking.  The  disease 'of  the  risorius  and  zygomaticus  major 
renders  smiling  all  but  impossible.  As  the  face  in  these  cases  is  usu- 
ally where  the  trouble  manifests  itself  first,  the  patients  not  infrequently 
declare  that  from  early  childhood  they  have  been  told  by  their  friends 
that  they  never  smiled  or  closed  their  eyes  as  they  should.  So  slow  and 
insidious  is  the  extension  of  the  disease  down  into  the  shoulder  girdle 
that  many  of  its  victims  fatuously  imagine  they  are  merely  constitu- 
tionally thin.  Ultimately  these  cases,  like  those  of  the  other  types, 
develop  the  same  general  appearances  in  other  parts  of  the  body. 

The  myopathic  fate  with  non-implication  of  the  ocular  muscles  or 
the  muscles  of  mastication  and  deglutition,  and  the  prominence  of  the 
atrophy  in  the  shoulder  and  arm,  is  the  sign-manual  oi  this  infantile 
form  of  muscular  dystrophy. 

There  is  a  markedly  hereditary  form  in  which  the  symptoms  begin 
in  the  lower  part  of  the  back  and  legs.  It  is  not  sufficiently  unique, 
however,  clinically  or  pathologically,  though  it  is  slightly  so  etiologi- 
cally,  to  warrant  its  further  detailed  description. 

Diagnosis. — As  our  knowledge  will  increase,  it  is  not  improbable 
that  these  muscular  dystrophies  will  be  seen  to  be  closely  related  to. 


THE   XEUROXIC   DISEASES 


419 


FIGURE  82. 


Muscular   atroph\^ 


420  THE   XEUROXIC   DISEASES 

if  not  identical  with,  the  progressive  nuiscular  atrophies.  For  the 
present,  however,  it  is  safe  and  convenient  to  recognize  a  distinction 
between  the  two,  for  in  a  general  way  the  dystrophies  possess  certain 
preeminent  traits  apart  from  those  of  the  progressive  spinal  atrophies. 
They  may  be  roughly  enumerated  as  pronounced  heredity,  early  onset 
of  the  symptoms,  a  peculiar  and  characteristic  distribution  of  the  mus- 
cular changes,  the  simultaneous  association  of  atrophy,  hypertrophy 
and  pseudo-hypertrophy,  an  absence  of  fibrillary  twitchings  and  of  the 
electrical  reactions  of  degeneration. 

Many  of  the  dystrophies  do  not  conform  absolutely  to  all  of  these 
requirements,  while,  on  the  other  hand,  occasionally  a  case  of  pro- 
gressive muscular  atrophy  assumes  a  remarkable  likeness  to  a  dystrophy. 
These  enumerated  traits,  nevertheless,  are  important  in  aiding  in  the 
drawing  of  the  distinction. 

There  are  a  number  of  diseases  in  which  muscular  atrophy  occurs 
which  must  not  be  confused  with  the  trouble  now  under  consideration. 
Chief  among  them  are  multiple  neuritis,  anterior  poliomyelitis,  pro- 
gressive muscular  atrophy  and  cerebral  atrophy. 

In  multiple  neuritis  the  abrupt  onset  of  the  malady,  its  rise  to  a 
climax  and  its  tendency  to  subside,  the  marked  sensory  phenomena,  the 
ataxia,  the  disproportion  between  the  paralysis  and  the  atrophy,  the 
absence  of  heredity  with  the  presence  of  infection  or  intoxication,  will 
readily  enable  one  to  make  the  correct  dififerential  diagnosis. 

Anterior  poliomyelitis  exhibits  more  or  less  febrile  phenomena,  is 
acute  or  subacute,  is  not  progressive,  but  rather  regressive  up  to  a 
certain  point,  and  is  devoid  of  practically  all  of  the  distinguishing  traits, 
except  perhaps  the  atrophy  of  the  dystrophies.  ^Moreover  the  electrical 
reactions  are  marked  in  poliomyelitis. 

The  cerebral  atrophies  are  not  typical  as  are  the  spinal  or  the  dys- 
trophic. They  are  monoplegic  or  hemiplegic  in  distribution,  are  pre- 
ceded by  the  paralysis,  possess  all  the  usual  signs  of  hemiplegic  de- 
generation of  the  upper  motor  tract,  and  are  notably  wanting  in  the 
characteristic  traits  and  mode  of  development  of  the  d}-strophies. 
Hysteria,  epilepsy,  idiocy,  tabes  and  poliomyelitis  may  complicate  a 
dystrophy  and  so  render  the  diagnosis  difiQcult,  especially  if  the  appear- 
ance of  the  muscles  is  not  very  different  from  the  normal,  on  accoynt 
of  the  nice  balance  between  the  atrophy  and  the  hypertrophy. 

Prognosis. — The  course  of  the  disease  is  apt  to  be  a  prolonged 
one,  with  periods  of  quiescence  and  even  of  remission.  In  the  late  cases, 
such  as  occur  among  the  juvenile  types,  there  may  even  be  partial  re- 
covery. Once  started,  the  disease  never  disappears.  Most  of  the 
patients  die  young  from  implication  of  the  muscles  concerned  directly 
in  the  maintenance  of  the  vital  processes,  as,  for  instance,  the  dia- 
phragm :    also  from  general  marasmus  and  intercurrent  affections. 

Treatment. — The  treatment  is  of  no  avail.  General  hygienic  and 
symptomatic  measures  exhaust  the  entire  theme.  Exercises  must  be 
moderate  and  the  mechanical  treatment  with  baths,  electricity  and 
massage  must  be  undertaken  very  cautiously  and  tentatively.  Tenotomy 
and  other  orthopzedic  measures  may  lighten  the  existence  of  some  of 
these  patients. 


THE   NEURONIC   DISEASES  421 

b.       DISEASES   OF    THE   UPPER    MOTOR    SEGMENT. 

SPASTIC  PARAPLEGIA  OF  ADULTS. 

For  our  knowledge  of  this  affection  we  are  indebted  chiefly  to 
Seguin,  Erb  and  Charcot.  They  named  it  respectively  tetanoid  para- 
plegia, spasmodic  spinal  paralysis  and  spasmodic  dorsal  tabes.  It  is 
better  identified  clinically  than  it  is  pathologically.  While  much  differ- 
ence of  opinion  still  exists,  it  will  nevertheless  be  well  to  recognize 
it  as  a  clinical  entity  and  to  await  further  data  in  regard  to  its  exact 
pathology. 

There  is  an  infantile  and  an  adult  form  of  the  disease.  Most  of  the 
infantile  cases,  commonly  referred  to  as  Little's  disease,  are  really  not 
paraplegic,  but  hemiplegic.  They  are  cerebral  double  hemiplegias,  or 
cerebral  diplegias  due  to  vascular  disease  and  will  be  found  discussed 
under  the  head  of  extra-neuronic  brain  diseases.  A  pure,  primary 
spastic  paralysis  of  spinal  origin  in  childhood  is  a  great  rarity,  if  it  oc- 
curs at  all.  Van  Gehuchten,  Souques,  Raymond,  Erb  and  Dejerine  all 
believe  that  it  does  exist. 

Questionable  as  are  the  adult  and  infantile  forms  of  pure  primary 
spinal  spastic  paralysis,  still  more  questionable  are  the  hereditary  forms. 
The  assumption  is  made  in  regard  to  all  forms  that  there  is  a  degen- 
erative sclerosis  limited  entirely  to  the  pyramidal  tracts.  In  a  large 
number  of  cases  both  the  clinical  and  pathological  evidence  is  not 
wanting,  some  time  or  other,  to  show  that  the  lesion  is  not  so  well  de- 
fined. The  elasticity  of  the  name  lateral  sclerosis,  which  is  occasionally 
employed  to  designate  the  disease,  gives  it  an  advantage  over  spastic 
spinal  paralysis,  which  represents  only  one  symptom  and  presupposes  a 
narrow  and  doubtful  pathology. 

Etiology. — The  cause  of  this  disease  is  obscure.  This  applies  to 
the  hereditary  as  well  as  to  the  acquired  forms.  Jn  the  hereditary  form 
several  members  of  a  family  may  be  attacked  and  the  symptoms  first 
appear  at  about  the  age  of  five.  Nothing  is  known  as  to  the  condition 
of  the  ancestry  in  these  cases.  It  is  not  improbable  that  in  the  acquired 
forms  there  inay  be  a  slight  neuropathic  heredity,  whereby  certain 
neurones  are  rendered  less  able  to  resist  active  influences  of  a  deleteri- 
ous sort.  These  cases  are  first  observed  between  the  ages  of  twenty 
and  forty,  and  in  the  majority  of  instances  follow  some  sort  of  intoxi- 
cation. Syphilis  has  been  credited.  I  have  considered  this  syphilitic 
form  of  the  disease  under  the  head  of  spinal  syphilis  and  have  there 
stated  my  doubt  as  to  its  existence.  Trauma  was  thought  to  have  been 
the  cause  in  -some  cases.  From  the  etiological  as  well  as  from  the 
pathological  side,  the  more  extensive  character  of  the  disease  than 
what  is  assumed  in  the  mere  sclerosis  of  the  pyramidal  tracts  is  hinted 
at ;  for  while  most  cases  reveal  upon  post-mortem  examination  ap- 
pearances that  suggest  secondary  degeneration  from  transverse 
myelitis,  multiple  sclerosis,  or  cerebral  disease,  these  conditions  are 
just  the  ones  to  be  initiated  by  the  etiological  factors  to  which  spinal 
spastic  paralysis  is  frequently  attributed — namely,  trauma,  the  puer- 
perium,  the  infections,   lead   intoxication,  poisoning     from     different 


422  THE   NEURONIC    DISEASES 

forms  of  lathyrus,  etc.  Westphal  was  of  the  opinion  that  only  in 
dementia  paralytica  did  such  a  strictly  limited  primary  sclerosis  of  the 
pyramidal  tracts  ever  occur  as  is  assumed  in  this  disease. 

From  the  little  that  we  know  as  yet  in  regard  to  its  etiology, 
spastic  spinal  paralysis  in  its  pure  form  is  probably  a  result  of  a 
general  agenesis  and  therefore  is  more  or  less  hereditary ;  or  it  is  the 
residual  secondary  degeneration  from  other  and  more  diffuse  diseases 
of  the  brain  and  spinal  cord.  In  a  word,  the  etiology  such  as  we  know 
it  to-day  does  not  favor  the  view  that  spastic  spinal  sclerosis  is  a  limit- 
ed primary  degenerative  sclerosis  of  the  pyramidal  tracts. 

Pathology  and  Pathogenesis. — Not  much  need  be  said  on  this 
score,  since  we  know  so  little  positively.  Elsewhere  I  have  shown  that 
the  degeneration  of  the  pyramidal  tracts  noted  in  Little's  type  of  spastic 
paralysis  is  a  double  hemiplegia  and  is  therefore  a  cerebral  trouble  pri- 
miarily.  In  these  as  well  as  in  the  cases  due  to  a  general  hereditary 
agenesis,  the  cord  lesion  may  be  sharply  limited  to  the  pyramidal  tracts, 
but  it  is  a  secondary  manifestation  dependent  upon  brain  defects. 

In  spinal  spastic  paralysis  it  is  presumed  that  there  is  a  primary 
degenerative  sclerosis,  limited  solely  to  the  pyramidal,  and  especially 
to  the  crossed  pyramidal,  tracts.  Most  of  the  cases  of  this  slow  and 
long  running  disease  that  come  to  autopsy,  show  lesions  elsewhere  than 
those  of  these  tracts.  There  is  always  an  open  question,  therefore,  as 
to  the  priority,  importance  and  inter-relationship  of  these  various 
lesions,  in  their  bearing  upon  the  pathogenesis  of  the  particular  dis- 
ease under  consideration.  It  is  this  that  casts  a  doubt  upon  the  exist- 
ence of  the  pure  type  of  spastic  spinal  paraplegia.  It  is  but  just  to  say, 
however,  that  in  a  few  cases  examined  by  Dejerine  and  Sottas.  Striim- 
pell  and  others  a  degenerative  sclerosis  was  found,  confined  absolutely 
to  the  pyramidal  tracts.  Whether  this  was  merely  an  advanced  lesion 
in  a  more  general  disease  process,  and  whether,  if  the  patients  had  lived 
longer,  they  would  have  developed  other  areas  of  sclerosis  as  a  part  of 
the  same  general  disease  process,  no  one  can  yet  affirm  or  deny. 

Symptoms. — The  symptoms  of  the  hereditary  and  acquired  forms 
of  the  disease  are  the  same,  assummg  the  above  limited  pathology.  In 
most  of  the  so-called  hereditary  forms  the  secovdary  nature  of  the 
spinal  trouble  is  intimated  in  the  frequent  presence  of  cerebral  symp- 
toms and  other  indications. 

In  the  classic  type  of  the  disease  the  only  symptom  is  the  spastic 
paralysis  with  its  usual  accompaniments  of  muscular  rigidity,  reflex 
exaggerations  and  contracinres.  This  symptom  appears  gradually, 
passing  through  an  early  stage  of  weakness ;  then  progressing  steadily, 
it  continues  to  be  the  sole  manifestation  to  the  end.  It  appears  first  and 
advances  farther  in  the  legs  than  in  the  arms.  Often  it  remains  in  the 
lower  limbs.  Sometimes  it  implicates  one  leg  more  than  the  other. 
The  extremity  feels  tense  and  stiff  at  first,  as  if  the  tendons  were  con- 
tracted or  were  too  short.  Rapid  movements  become  difficult.  Grad- 
ually the  gait  assumes  a  characteristic  manner.  Rigidity  is  observed 
in  all  passive  as  well  as  active  movements.  The  reflexes  now  manifest 
a  high  degree  of  exaggeration.  The  slig'htest  tap  on  the  patella  tendon 
evokes  a  violent  jerk.     The  cutaneous  reflexes  are  also  greatly  height- 


THE    NEURONIC   DISEASES 
FIGURES  83  AND  84. 


423 


FIGURE  85.  FIGURE  86. 

Spastic  paraplegia  of  an  adult.  Strumpell's  case.  Fig.  83,  section  through  the 
medulla.  Fig.  84,  cervical  section.  Fig.  85,  mid-dorsal  section.  Fig.  86.  lumbar 
section.      (After  Jakob.) 


424  THE   NEURONIC   DISEASES 

ened.  The  muscles  are  undiminished  m  size  and  the  electrical  responses 
remain  normal.  Gradually  a  distinct  spastic  paresis  comes  on  until 
walking  is  practically  impossible,  or  only  possible  with  short,  laborious 
sliding  steps  on  the  balls  of  the  toes.  The  legs  incline  toward  strong 
adduction  and  the  progression  becomes  "cross-legged." 

With  all  this  serious  motor  trouble  in  the  legs,  and  sometimes 
even  to  a  less  degree  in  the  arms,  there  are  absolutely  )io  sensory  symp- 
toms, no  trophic  manifestations,  no  involvement  of  the  sphincters.  In 
fine,  there  is  nothing  abnormal  about  the  patient  but  this  one  manifesta- 
tion, spastic  paralysis,  though  this  is  so  protean  that  it  represents  a 
most  profound  sort  of  disabilit}".  Late  in  the  disease,  even  after  many 
years,  the  sphincters  sometimes  become  involved,  sensory  SA'mptoms 
appear  and  even  ocular  troubles  supervene.  It  is  a  question  then 
whether  such  manifestations  do  not  remove  the  case  at  once  from  the 
classical  type  of  primary  spastic  paralysis.  They  certainly  would  if 
they  showed  themselves  earher. 

The  diagnosis  of  primary  spastic  paralysis  is  always,  therefore,  a 
provisional  one,  and  at  best  is  always  questionable.  The  disease  may 
unmask  itself  at  any  time  and  reveal  the  symptoms  of  another  trouble, 
such,  for  instance,  as  multiple  sclerosis,  myelitis,  amyotrophic  lateral 
sclerosis,  vertebral  tumor  or  hydrocephalus. 

As  a  clinical  entity  the  spastic-paretic-symptom-complex  may  last 
very  many  years  and  progress  so  slowly  as  to  interfere  for  a  long  time 
but  slightly  with  the  patient's  usual  avocation.  It  may  even  come  to  a 
complete  standstill. 

The  mind  is  never  affected.  The  infantile  cases  in  which  epilepsy, 
mental  deterioration  and  other  cerebral  symptoms  occur  do  not  belong 
here.    They  fall  into  the  group  of  the  cerebral  palsies  of  childhood. 

Diagnosis. — -The  diagnosis  of  spastic  spinal  paralysis  is  essentially 
the  diagnosis  of  a  mere  symptom-complex.  It  is  easy  in  typical  cases. 
In  atypical  cases  it  must  include  the  larger  disease  of  which  the  spastic 
paraplegia  is  but  one  indication.  Elsewhere  under  the  heads  of  myelitis 
and  other  cord  diseases,  and  the  various  cerebral  troubles  in  which 
secondary  spastic  paraplegia  may  occur  as  a  residual  condition,  the 
diagnosis  will  be  touched  upon. 

Spastic  paraplegia  sometimes  is  witnessed  in  hysteria.  It  is  rarely, 
however,  the  only  symptoin.  As  a  hysterical  concomitant  it  appears 
abruptly  and  is  subject  to  psychical  influences.  Care  must  be  exer- 
cised not  to  mistake  a  spastic  paraplegia  for  the  hysteroid  manifesta- 
tions that  may  occur  sometimes  in  incipient  disseminated  sclerosis. 
There  is  a  treacherous  similarity  at  times  between  multiple  sclerosis 
and  hysteria.  Spastic  paraplegia,  organic  in  the  one  case,  psychic  in 
the  other,  is  not  an  uncommon  phenomenon  in  both.  Further  details 
in  regard  to  the  differential  diagnosis  may  be  gathered  from  the  discus- 
sion elsewhere  of  these  two  aft'ections. 

Treatment. — The  treatment  of  the  disease  is  an  ungrateful  task. 
Care  as  to  the  nutrition,  avoidance  of  exhaustion,  massage  and  gym.- 
nastic  exercises  constitute  about  all  that  we  can  do.  Contractures  and 
deformities  are  to  be  managed  on  general  orthopaedic  principles.  The 
younger  the  patient,   so  much  the  more  promising  are  the  results  to 


THE   XEURONIC   DISEASES 


425 


be  expected  from  these  general  measures.  These  patients  often  enjoy 
excellent  general  health  and  live  many  years.  They  must  be  taught 
to  exercise  patience  and  to  make  the  best  of  a  very  chronic  state  of 
invalidism.  ^Medicines  are  of  no  avail,  and  as  there  is  little  real  suf- 
fering beyond  the  inconvenience  of  locomotion,  symptomatic  treatment 
is  rarely  called  for. 

SPASTIC   PAR.\PLEGL\   OF  CHILDHOOD.     LITTLE'S   DIS- 
EASE. 

The  infantile  form  of  spastic  paraplegia,  as  usually  described  in 
the  books,  is  a  double  hemiplegia.  It  is  a  question  whether  such  a  name 
as  paraplegia  cerehralis  spastica  should  not  be  dropped  entirely.  A 
paraplegia  has  come  to  mean  technically  a  spinal  cord  trouble,  there- 
fore to  speak  of  a  cerebral  paraplegia  is  not  only  misleading,  but  is  a 
contradiction  of  terms.  Neither  symptomatically  nor  pathologically  are 
these  diplegias  of  childhood  spinal  cord  affections.  Including  Little's 
disease,  they  are,  so  far  as  the  spinal  changes  are  concerned,  merely 
secondary  degenerations  of  cortical  origin.  They  bear  a  symptomatic 
resemblance,  to  be  sure,  to  the  primary  spastic  paraplegia  of  adults. 
The  reflexes  are  highly  exaggerated,  but  the  spasmodic  jerk  is  not  so 
vigorous  as  it  is  in  the  adult  disease.  Foot  clonv.s  may  sometimes,  but 
very  rarely,  be  obtained. 

In  some  cases  the  nniscular  po\yer  is  not  much  diminished,  but 
walking  is  quite  difficult  on  account  of  the  contractured  condition  of  the 
calf  muscles,  the  strong  adduction  of  the  legs  and  the  tendency  in  the 
gait  to  the  "crossed-legged  progression."  There  is  no  true  muscular 
atrophy,  though  the  legs  do  not  develop  and  grow  as  they  should. 
Some  of  the  cases  may  resemble  Charcot's  amyotrophic  lateral  sclerosis 
in  its  early  appearance,  and  then  exhibit  a  certain  amount  of  true  mus- 
cular atrophy.  Amyotrophic  lateral  sclerosis  is  an  adult  disease,  how- 
ever, rarely,  if  ever,  occurring  before  ten  years  of  age ;  it  involves  the 
arms  most  extensively ;  and  is  distinguishable  from  infantile  spastic 
paraplegia  by  other  signs.  It  was  the  more  or  less  limitation  of  the 
paralysis  to  the  lower  limbs,  and  the  absence  of  all  cranial  symptoms, 
that  led  the  earlier  authorities  to  attribute  the  symptoms  and  the  entire 
disease  to  the  spinal  cord.  In  the  arms,  however,  there  may  be  observed 
choreic  phenomena  and  usually  a  considerable  degree  of  athetosis. 
These  arm  symptoms  are  slight  in  the  cases  that  may  fairly  be  denom- 
inated "spastic  paraplegia." 

The  entire  question  as  to  the  classification  of  these  cases  depends 
upon  the  primary  or  secondary  nature  of  the  spinal  cord  changes.  If 
the  cord  changes  are  primary,  a  condition  which  would  be  very  ex- 
ceptional and  in  my  own  opinion  extremely  doubtful,  there  is  no  need 
of  creating  a  new  disease  out  of  what  would  then  be  an  ordinary  pri- 
mary spastic  paraplegia,  merely  on  account  of  the  age  of  the  victim. 
Granting  that  Van  Gehuchten,  Souques,  Raymond  and  Erb  are  justi- 
fied in  their  belief  that  a  primary  infantile  spastic  paraplegia  of  cord 
origin  does  exist,  and  that,  as  Dejerine  has  found,  there  is  evidence  of 
cervical  degeneration,  with  secondary  degeneration  of  the  pyramidal 


426  THE   NEURONIC   DISEASES 

tracts,  occurring-  during  fetal  life,  the  point  is  still  more  strongly 
emphasized  that  there  is  no  need  of  writing  a  new  section,  and  describ- 
ing these  infantile  cases  apart  from  the  general  description  of  the  ordi- 
nary or  adult  form  of  the  trouble.  On  the  other  hand,  if  the  cord 
changes  in  these  cases  are  secondary  to  the  cortical  lesion,  as  shown  by 
the  frequent  epilepsy,  cranial  nerve  palsies  and  psychical  disorders  in 
addition  to  the  pathological  findings,  there  is  again  no  need  of  elevat- 
ing the  condition  into  one  of  a  special  and  unique  form  of  disease. 
It  is  then  but  a  particular  manifestation  of  double  hemiplegia,  a  diple- 
gia, and  falls  naturally  into  the  discussion  of  brain  diseases. 

SECONDARY  SPASTIC  PARALYSES. 

The  many  hemiplegia  quadriplegic,  diplegic  and  paraplegic  condi- 
tions that  follow  intracranial  and  mtraspinal  lesions  arismg  in  the  non- 
neuronic  tissues  are  not  strictly  to  be  considered  here,  for  the  degenera- 
tion is  of  the  secondary  or  rather  Wallerian  type,  and  the  primary 
disease  which  is  really  of  extra-neuronic  origin  is  the  prominent  feature. 
Thus  inflammatory  conditions,  neoplasms,  compressions,  vascular 
lesions  of  all  sorts  are  commonly  followed  by  de.generation  of  the 
descending  type  in  the  neurones  caught  in  the  damaging  processes. 
This  degeneration  is,  as  it  were,  a  sort  of  a  sequel  of  the  disease.  It 
has  its  own  prognosis  and  treatment,  but  they  are  not  the  prognosis  and 
treatment  of  the  disease  in  which  they  occur. 

These  secondary  neuronic  degenerations  will  be  considered  in 
detail  elsewhere  in  connection  vi'ith  the  diseases  out  of  which  they 
spring. 

Sometimes  it  is  very  difficult  to  distinguish  the  primary  spastic 
paralyses  from  the  secondar}^  A  sharp  distinction  between  the  two, 
thus  made  in  the  classifications,  will,  it  seems  to  me,  help  toward  the 
making  of  the  differentiation  m  the  diagnosis.  At  all  events  it  will 
emphasize  the  difiterences  between  the  prognosis  and  the  treatment  of 
the  two  sets  of  diseases. 

Primary  neuronic  degenerations  are  apparently  diseases  sui  generis 
and  are  hopeless  in  their  outlook  and  unsatisfactory  in  their  treat- 
ment. 

Secondary  neuronic  degenerations  are  the  sequels  of  diseases 
which  are  hopeful  and  satisfactory  to  treat  in  spite  of  the  hopelessness 
of  the  secondary  results. 

C.      DISEASES   OF   THE   LOWER    MOTOR   SEGMENT. 

The  degenerations  involving  the  lower  motor  neurones  are  in- 
numerable, but  they  are  both  primary  and  secondary  in  origin.  The 
former  we  know  less  about  than  we  do  of  the  latter.  All  severe  lesions 
that  damage  the  cranial  nuclei,  the  anterior  horns  of  the  cord,  and  the 
peripheral  nerves  may  cause  the  neurones  in  their  vicinity  to  undergo 
a  progressive  degeneration.  In  this  way  the  polioencephalitic,  polio- 
myelitic  and  peripheral  neuritic  diseases  are  all  more  or  less  followed 
by    degenerative   paralysis.      This    paralysis,    however,    is    virtuallv    a 


THE   XEUROXIC   DISEASES 


427 


sort  of  a  sequel  of  the  disease.  It  may  be  very  prominent  and  demand 
its  own  consideration,  as  in  acute  anterior  poliomyelitis,  for  instance, 
but  it  is  not  the  disease  itself.  Its  prognosis  should  not  be  confounded 
for  a  moment  with  the  prognosis  of  the  affection  out  of  which  it  has 
sprung.  It,  of  course,  like  all  neuronic  degenerations,  is  svstemic  in 
its  distribution.  I  see  no  reason,  however,  for  employing  it  as  a  basis 
for  the  classification  of  the  disease.  It  is  a  false  classification,  it  seems 
to  me,  that  includes  among  the  system  diseases  chronic  poliomyeHtis 
and  not  cerebral  embolism.  It  would  be  a  still  more  unreliable  classifi- 
cation that  would  consider  either  as  a  systemic  neuronic  disease. 
Poliomyelitis  is  an  inflammation  with  certain  secondary  neuronic  de- 
teriorations, even  as  cerebral  embolism  is  a  vascular  trouble  with  like 
secondary  neuronic  wasting.  Of  these  secondary  atrophies,  the  one 
is  below  in  the  spinal  anterior  cornual  neurones,  the  other  is  above  in 
the  cerebral  cortical  neurones.  All  such  degenerations  should  be 
considered  merely  as  one  of  the  results  of  the  primary  disease  and 
should  in  no  way  be  made  the  basis  of  their  classification. 

It  is  frankly  admitted  that  there  are  many  degenerative  conditions 
in  the  lower  motor  segment  that  we  cannot  yet  afiirm  positivelv  to  be 
either  primary  or  secondary.  Most  of  them  are  undoubtedly  secondarv. 
The  few  that  seem  to  be  primary  will  be  briefly  referred  to  here. 

OPHTHAL^IOPLEGIA. 

The  nuclei  of  the  motor  nerves  of  the  eye,  the  third,  the  fourth  and 
the  sixth,  lying  along  the  aqueduct  of  Sylvius  are  the  homologues  of 
the  anterior  horns  of  the  cord.  They  contain  the  cell-bodies  of  the 
neurones  that  innervate  the  ocular  muscles,  just  as  the  horns  contain 
the  cell-bodies  of  the  neurones  that  pass  out  of  the  anterior  roots  and 
innervate  the  muscles  of  the  body.  These  nuclei  undergo  the  same 
.sort  of  degenerative  and  inflammatory  processes  that  the  horns  do 
and,  like  the  latter,  they  can  give  rise  to  an  atrophic  paralysis  that  may 
pick  out  individual  ocular  muscles.  This  is  termed  oplithalnioplegia, 
which  for  clinical  convenience  is  divided  into  internal  ophthalmoplegia, 
when  the  internal  ciliary  muscles  and  iris  are  involved,  and  external 
ophthalmoplegia  when  tlie  external  recti,  the  oblique  and  palpepral 
muscles  are  implicated. 

A  bilateral  external  ophthahnoplcgia.  v/ith  intact  ciHary,  iris  and 
lid  muscles,  is  pathognomonic  of  a  nuclear  lesion,  for  no  peripheral 
ner\^e  trouble  could  hardly  present  such  a  clinical  picture.  The  nuclear 
disease  may  be  acute  and  vascular.  It  would  be  described  then  as  a 
particular  form  of  polioencephalitis,  often  as  a  part  of  \\  ernicke's  type 
of  acute  hemorrhagic  polioencephalitis  stiperior,  mentioned  elsewhere 
tinder  inflammations  of  the  brain. 

Infection  and  intoxication  are  the  chief  causes  of  acute  ophthal- 
moplegia. This  form  of  the  disease  may  or  may  not  have  a  discover- 
able pathological  change  as  its  anatomical  basis,  according  to  the 
virulence  of  the  toxin  and  the  duration  of  its  action. 

The  prognosis  is  not  very  favorable  in  the  alcoholic  cases,  though 


428  THE   XEUROXIC   DJSEASES 

recoveries  often  occur  in  the  influenza  and  other  toxic  cases.  This^ 
of  course,  is  a  secondary  degenerative  process. 

Chronic  opIitJialmopIegia  is  a  slow,  progressive  degenerative  dis- 
ease which  ahgns  itself  easily  with  the  progressive  muscular  atrophies. 
In  fact,  it  is  not  infrequently  the  precursor  of  various  degenerative 
system  diseases,  such  as  tabes,  progressive  bulbar  paralysis,  progres- 
sive muscular  atrophy,  etc.  It  occurs  also  as  a  part  of  the  combined 
diseases  of  the  cord,  of  multiple  sclerosis  and  of  progressive  paralysis. 
It  is  associated  with  psychic  disorders.  It  has  been  seen  as  a  con- 
genital trouble,  as  a  part  of  an  mherited  familial  degeneration.  Op- 
penheim  is  convinced  that  syphilis  can  provoke  the  degenerative  process. 
A  slow  hemorrhagic  cause  may  be  possible. 

Pathologically  the  disease  is  a  primary  degeneration  of  the  neit- 
rones  of  the  nuclei  of  the  ocular  motor  nerves. 

Symptoms. — These  come  on  gradually  and  often  are  not  remarked 
until  the  disease  is  well  advanced.  The  vision  of  the  eyes  individually 
is  not  affected,  and  as  the  trouble  is  so  slow  and  insidious,  when  the 
lines  of  vision  are  disarranged  on  account  of  the  palsy,  the  patient 
becomes  habituated  to  a  monocular  vision.  Graduallv  the  loss  in  the 
mobility  of  the  eyeball  is  noticed.  There  is  a  slight  strabismus,  more 
frequentl}-  divergent.  Examination  with  the  moving  finger  reveals 
the  limited  excursion  of  the  eyeball  in  attempting  to  follow  it.  The 
eyelids  droop  and  what  is  termed  the  "Hutchinson  face"  is  presented. 
Sometimes  amblyopia  is  complained  of.  The  pupil  as  a  rule  is  intact 
and  reacts  well  to  both  accommodation  and  light. 

Progxosis. — The  disease  is  a  very  chronic  one  and  the  prognosis- 
is  unfavorable.  Sometimes  it  becomes  stationary.  Optic  atrophv  often 
combines  with  it,  especially  when  it  is  a  part  of  some  general  systemic 
degenerative  trouble. 

Treatment. — For  the  acute  cases  the  treatment  is  along  general 
antiphlogistic  lines  and  includes  purgation,  baths  to  provoke  sweating, 
ice  bags  and  temporal  bloodletting.  A  history  of  syphilis  points  out  the 
proper  therapy  to  resort  to,  while  in  all  cases  the  causative  factor,  if 
such  can  be  found,  must  receive  the  brunt  of  the  attack.  Galvanism  has 
been  reccmniended ;  upon  what  ground  it  is  hard  to  conceive.  Reme- 
dies that  have  been  used  and  are  still  recommended,  but  are  generally 
ineffectual,  are  strychnia,  arsenic,  potassium  iodide,  phosphorus  and 
general  tonics. 

Primary  Degeneration  of  the  Other  Cranial  Xerves  is  exceedingly 
rare  as  an  isolated  process.  A  few  congenital  bilateral  facial  palsies 
have  been  seen,  and  unilateral  nuclear  disease  of  the  hypoglossal  has 
been  reported.  Such  cases  are  -always  unique  and  we  have  no  knowl- 
edge of  their  true  anatomical  basis.  Alost  of  the  primary  degenera- 
tions of  these  nerves  belong  to  the  bulbar  palsies  and  will  be  described 
under  that  head  for  the  sake  of  convenience,  or  to  the  bulbar  manifesta- 
tions merely  of  other  more  general  troubles,  such  as  progressive  mus- 
cular atrophy,  general  intoxications  and  specific  infections,  where  they 
will  receive  their  appropriate  consideration. 

Of  primary  degeneration  of  the  spinal  motor  nerves  we  know 
nothing,  if  indeed   it  ever  occurs.      Some  forms   of  toxic   peripheral 


THE   NEURONIC   DISEASES 


429 


neuritis  may  be  primarily  degenerative  and  for  aught  we  know  be 
limited  to  the  motor  neurones.  It  is  doubtful,  however,  as  in  these 
-cases  inflammatory  and  sensory  symptoms  are  often  present. 

MYASTHENIA  GRAVIS. 

This  is  believed  to  be  a  bulbar  disease,  as  is  indicated  in  the  names 
asthenic  bulbar  paralysis  and  bulbar  paralysis  imthout  discoverable 
anatomical  lesion;  but  its  functional  neuronic  character  depending,  as 
most  authorities  think,  upon  a  dynamic  disturbance  in  the  lower  motor 
neurones,  it  may  for  the  present  be  classified  here.  A  number  of  cases 
of  the  disease  have  now  been  reported.  I  can  add  to  them  one  that  I 
was  recently  consulted  about,  which  has  since  died  after  presenting  for 
several  months  a  very  typical  clinical  picture,  and  which  seemed  to 
follow  an  aborted  attack  of  scarlet  fever. 

Etiology. — Middle-aged  and  young  persons  are  usually  selected 
as  victims.  Chlorosis  and  a  hereditary  taint  were  noted  in  one  case 
"by  Oppenheim  and  Bruns.  Toxaemia  was  strongly  suggested  in  my 
case.  The  man  was  a  teacher  in  a  college  where  there  had  been  a 
slight  epidemic  of  scarlet  fever.  He  had  a  faint,  evanescent  rash  and 
5igns  of  an  aborted  attack.  Later  on  he  assisted  in  the  formaldehyde 
fumigations  and  shortly  after  this  showed  the  first  signs  of  weakness. 

Pathology  and  Pathogenesis. — There  is  nothing  known  of  this, 
as  no  anatomical  lesions  have  been  found. 

Symptoms. — As  the  name  myasthenia  gravis  indicates,  the  prom- 
inent symptom,  of  this  disease  is  the  profound  muscular  weakness, 
with  remarkable  remissions  in  the  weakness.  The  disease  lasts  often 
many  months  and  in  that  time  the  patient  has  spells  of  such  weakness 
that  he  will  keep  his  bed ;  and  yet  he  will  recover  so  much  that  hopes 
will  be  awakened  that  he  has  fully  gotten  well  again.  The  hopes  are 
soon  seen  to  be  fallacious,  for  on  comes  the  weakness,  almost  paralysis, 
again.  And  thus  he  goes,  up  a  few  weeks,  then  down  again,  the 
weakness  disappearing  from  this  group  of  muscles,  to  reappear  later 
on  in  another  group.  The  muscles  supplied  from  the  medulla  are  so 
frequently  aifected,  and  so  often  are  the  cause  of  the  patient's  death  by 
asphyxia,  that  the  name  asthenic  bulbar  paralysis  has  been  given  to  the 
disease.  Other  muscles  of  the  body,  however,  are  usually  implicated. 
Ptosis  is  particularly  common.  It  was  almost  the  first  symptom  in 
my  case.  The  muscles  of  the  trunk  and  extremities  are  affected.  All 
acts  and  all  movements  are  restricted.  The  patient  feels  as  though  he 
could  walk  as  well  as  any  one,  but  the  moment  he  gets  up  he  begins 
to  weaken  and  he  is  chagrined  to  find  that  the  feeblest  efforts,  the 
shortest  walks,  completely  exhaust  him.  Talking  becomes  a  tremen- 
dous task.     Sometimes  he  can't  masticate  and  swallow  his  food. 

A  remittent,  chronic,  progressive  glosso-labio-laryngeal  paralysis, 
with  weakness  and  palsy  in  other  parts  of  the  body,  constitute  the 
motor  side  of  this  singular  malady.  Sometimes  the  bladder  and  rectal 
functions  are  also  implicated.  The  muscles  are  normal  in  size  and  do 
not  reveal  any  abnormal  electrical  reactions.  Noticeable  variation  of 
the  weakness,  from  a  moribund  state  almost  to  complete  health,  and 


430  THE   NEURONIC    DISEASES 

then  back  again  to  a  moribund  state,  and  marked,  almost  dangerous 
exhaustion  are  the  striking  features  in  the  course  of  the  disease.  There 
are  no  sensory  symptoms  and  the  mind  continues  clear. 

Diagnosis. — This  must  be  made  from  the  character  of  the  weak- 
ness and  palsy,  the  remissions  durmg  the  progress  of  the  disease,  the 
absence  of  organic  muscular  changes,  the  absence  of  sensory  and  men- 
tal symptoms  and  the  probable  etiology.  Hysteria  can  be  differentiated 
by  the  presence  of  sensory  and  mental  phenomena.  Poliomyelitis,  or 
rather  polioencephalomyelitis  and  muscular  dystrophy,  do  not  remit  as 
this  disease  does,  and  they  exhibit  org-anic  muscular  signs  such  as  the 
muscular  atrophy  and  electrical  changes.  There  are  some  things  about 
this  disease  that  lead  one  to  compare  it  with  Landry's  syndrome.  The 
latter  has  even  appeared  first  with  the  bulbar  coniplexus  of  symptomiS. 

Prognosis. — The  malady  is  almost  universally  fatal,  though  a  few 
cases  have  gotten  well.  The  trouble  appears  acutely  or  insidiously, 
but  it  generally  runs  a  remittent,  clironic  course.  It  is  a  dangerous  dis- 
ease, as  one  can  never  tell  when  death  may  come.  The  latter  usually 
results  from  asphyxia  or  exhaustion. 

Treatment. — Rest  and  quietude  in  bed  is  about  the  best  we  can 
do.  There  is  a  strong  temptation  to  use  electricity,  but  it  is  a  danger- 
ous procedure.  Moreover,  it  could  hardly  be  expected  to  do  any  good, 
from  the  nature  of  the  trouble.  When  the  patient  cannot  swallow  a 
stomach  tube  may  be  used,  but  it  involves  a  great  risk.  Oppenheim 
lost  a  case  during  the  manipulation.  If  there  is  the  slightest  degree  of 
spasm  from  the  introduction  of  the  tube,  the  treatment  had  better  be 
desisted.  Simple  tonics  and  a  mild  diaphoretic  treatment  might  prove 
available,  for  it  is  probable  that  the  basis  of  the  trouble  is  an  intoxica- 
tion or  infection  of  some  sort. 

"OCCUPATION     MUSCULAR    ATROPHY.      CRAFT     PALSY. 
PROFESSIONAL  PALSIES. 

This  is  a  borderline  degeneration  which  in  some  cases  is  undoubt- 
edly primary,  while  in  others  it  is  secondary  and  is  associated  with  a 
neuritis. 

The  constant  use  of  certain  nerves  and  muscles  in  one  monotonous 
manoeuvre,  demanded  by  certain  occupations,  sometimes  leads  the  lat- 
ter to  undergo  an  atrophic  paralysis.  Oppenheim  mentions  a  weaver 
who  had  to  extend  his  forearm  about  twenty  thousand  tiriies  a  day 
and  who  thereupon  suffered  from  an  atrophic  paralysis  in  the  right 
triceps  muscle.  In  this  way  locksmiths,  paper-glazers,  blacksmiths, 
cabinet-makers,  g"old-polishers,  oarsmen,  cigar  rollers,  drummers  have 
been  afflicted.  Of  course,  the  trouble  is  mostly  seen  in  the  upper  ex- 
tremity. Potato-pickers,  seed-sowers  and  those  who  kneel  a  great  deal 
may  have  the  trouble  in  their  lower  limbs.  Ballet  dancers  have  thus 
had  their  calf  muscles  affected. 

These  cases  must  not  be  identified  with  the  occupation  neuroses, 
which  are  due  to  a  disturbance  in  the  central  coodinating  apparatus. 
These  cases  are  to  be  attributed  to  over-exertion,  pressure,  even  lacera- 
tion of  the  nerves  in  which  run  the  lower  motor  neurones.     There  is  an 


THE   NEURONIC   DISEASES  43 1 

atrophic  condition  started  in  this  way  in  these  neurones  which  in  most 
instances  is  quickly  recovered  from  if  the  member  is  placed  at  rest. 
This  wasting,  however,  has  in  a  number  of  instances,  in  spite  of  the 
use  of  all  preventive  measures,  gone  on  to  the  production  of  a  pro- 
gressive muscular  atrophy.  General  intoxication  with_  alcohol,  lead, 
infection  from  influenza,  general  marasmus  and  a  previous  history  of 
acute  anterior  poliomyelitis  seem  to  favor  this  unfortunate  turn  to  the 
paralysis.  In  some  cases  there  have  been  slight  parsesthesiae,  and  pains 
and  other  sensory  manifestations  that  have  suggested  an  interstitial 
neuritis.  In  still  other  cases  the  trouble  is  probably  due  entirely  to  the 
muscle  and  not  at  all  to  the  nerve,  in  this  way  intimating  what  we  have 
long  been  suspecting — namely  that  there  is  no  sharp  line  of  division  to 
be  drawn  between  the  atrophies  and  the  dystrophies. 

Most  of  these  craft  palsies  get  well  under  favoring  conditions,  for 
the  atrophy,  whether  primary  or  secondary,  does  not  go  on  to  the 
stage  of  incurability.  When,  however,  it  passes  into  the  progressive 
form,  the  prognosis  is  hopeless. 

The  treatment  consists  of  rest,  the  careful  use  of  galvanism, 
hypodermics  of  strychnia  and  a  general  tonic  and  health-producing 
regimen. 

ACUTE  ASCENDING  PARALYSIS.    LANDRY'S  PARALYSIS. 

Landry  described  in  1859  a  form  of  motor  paralysis  in  which  there 
were  no  sensory  symptoms,  no  muscular  wasting,  no  electrical  reac- 
tions, no  bedsores  or  other  trophic  manifestations,  no  involvement  of 
the  bladder  or  rectal  functions.  The  paralysis  was  flaccid  in  character, 
ascended  rapidly  up  the  body  and  usually  terminated  in  death  in  a  few 
days  or  a  week,  from  respiratory  involvement  and  other  bulbar  symp- 
toms. There  were  no  post-mortem  findings  and  so  Landry,  Westphal 
and  others  attributed  the  trouble  to  some  form  of  acute  poisoning. 
Later  on  when  it  was  found  that  some  cases  of  acute  ascending  paralysis 
exhibited  slight  sensory  symptoms,  and  a  mild  degree  of  muscular 
atrophy,  with  a  loss  of  the  deep  reflexes  and  with  certain  electrical 
changes,  it  was  believed  that  Landry  had  described  merelv  a  form  of 
multiple  neuritis.  Comparisons  were  drawn  between  it  and  the  symp- 
toms produced  often  by  such  forms  of  intoxication  as  alcohol,  curare, 
lead  and  the  infections.  It  soon  became  clear  that  Landry  had  not 
described  a  new  disease,  but  a  symptom-complex  often  observed  in  the 
early  stage  of  virulent  forms  of  intoxication.  In  one  sense,  therefore, 
the  term  acute  ascending  paralysis  covers  more  than  the  term  Landr}-'s 
paralysis,  while  the  latter,  in  its  original,  narrow  definition,  is  but  one 
manifestation  of  a  profound  intoxication  of  which  there  may  be  other 
and  later  manifestations  according  to  the  susceptibility  of  the  nervous 
system  involved,  the  virulence  of  the  poison  or  the  duration  of  its 
action. 

Etiology. — Some  form  of  profound  intoxication  of  bacterial  origin 
seems  to  be  at  the  bottom  of  Landry's  paralysis.  Neither  the  particu- 
lar toxin  nor  the  micro-organism  has  been  isolated  yet.  The  disease 
seems  most  frequently  to  follow,  or  to  be  associated  with,  the  infectious 


432  THE   NEURONIC   DISEASES 

fevers,  notably  typhus,  typhoid,  pneumonia,  variola,  pleurisy,  diphtheria, 
anthrax,  influenza,  pertussis,  gonorrhoea  (?),  syphilis,  septicaemia  and 
rabies — a  most  suggestive  list!  Other  contributing  causes  have  been 
named  by  various  writers — namely,  exposure  to  cold,  the  puerperium, 
suppressed  menstruation,  coitus  in  the  standing  posture  and  mental 
excitement.  It  is  probable  that  these  were  mere  coincident  circum- 
stances, or  at  most  assisted  only  in  provoking  the  intoxication  or  auto- 
intoxication underlying  the  disease.  Alen  are  more  subject  to  the 
trouble  than  women  are,  the  proportion  being  put  by  some  as  high  as 
twelve  to  four.  The  middle  period  of  life,  twenty  to  forty,  is  when 
the  disease  occurs  most  frequently.  It  will  be  noted,  as  Gowers  well 
remarks,  that  the  remote  etiology  of  acute  ascending  paralysis  re- 
sembles in  general  that  of  acute  myelitis. 

Pathology  and  Pathogenesis. — According  to  the  earlier  obser- 
vations of  Landry,  Westphal  and  others,  a  remarkable  peculiarity  of 
this  disease  was  the  absence  of  all  post-mortem  findings.  Landry 
therefore  concluded  that  the  trouble  was  due  to  some  form  of  poison- 
ing, a  view  which  \'\^estphal  was  the  first  to  establish  upon  a  scientific 
basis.  Even  to-day,  with  our  more  improved  methods  of  investiga- 
tion, there  are  cases  in  which  no  pathological'  changes  can  be  discovered 
at  the  autopsy.  Such  cases,  however,  are  becoming  less  and  less  fre- 
quent every  year.  In  other  words,  the  greater  number  of  the  cases 
nowadays  reveal  changes  of  an  inflammatory  and  degenerative  type 
in  the  nervous  system,  and  more  or  less  the  appearances  of  a  septic 
condition  in  the  other  organs.  These  changes  are  indefinite,  varied 
and  scattered,  just  as  we  would  expect  in  a  general  toxsemia.  Dissem- 
inated foci  of  inflammation  with  exudation  and  capillary  hemorrhages, 
have  been  observed  in  the  medulla,  particularly  the  pyramidal  tracts. 
Similar  changes  and  other  myelitic  processes  have  been  found  in  the 
spinal  cord.  Antero-lateral  tracts  have  been  affected.  In  some  cases 
there  were  findings  of  a  typical  poliomyelitis,  but  of  a  slight  degree. 
Oppenheim  says  that  in  one  case  a  degeneration  of  the  anterior  roots 
was  the  only  alteration ;  in  another  a  small  myelitic  focus  in  addition 
to  a  peripheral  neuritis.  The  lesions  of  the  peripheral  nerves  have  been 
observed  frequently  enough  to  incline  some  authors  to  regard  the  dis- 
ease as  a  peripheral  neuritis.  Outside  of  the  nervous  system  the 
changes  most  commonly  found  included  enlargement  of  the  spleen, 
pleuritic  adhesions,  hemorrhagic  foci  in  the  lungs  and  bowels,  inflam- 
mation of  the  lymph  glands,  especially  in  the  intestines  and  mesenterv', 
and  albuminuria. 

All  of  this  indicates  plainly  the  toxic  origin  of  the  trouble.  The 
bacterial  source  of  the  toxin  is  based  upon  strong  evidence,  though  as 
yet  no  specific  micro-organism  has  been  isolated.  The  researches  of 
Baumgarten,  Eisenlohr,  Centanni,  Curschmann,  Remmlinger,  Oettinger 
and  Marinesco,  Alarie  and  Marinesco,  Bailey  and  Ewing,  Seitz,  Thoi- 
not  and  Maselli,  and  Buzzard  are  almost  conclusive.  By  these  investi- 
gators various  bacteria  have  been  found  in  the  nervous  tissues  of  pa- 
tients dying  of  acute  ascending  paralysis.  By  some  of  them  the  germs 
have  been  cultivated,  injected  into  animals  and  thus  a  set  of  symptoms 
provoked  identical  in  all  respects  with  those  of  the  disease  in  man. 


THE   NEURONIC   DISEASES 


433 


In  the  modern  sense,  Landry's  paralysis  cannot  be  regarded  as  a 
distinct  pathologico-anatomical  entity,  in  spite  of  the  fact  that  clinically 
it  affords  a  fairly  definite  symptom-complex.  It  is  the  expression  of 
an  intoxication  of  bacterial  origin,  some  cases  running  their  course  so 
rapidly  as  to  leave  no  discoverable  lesions,  while  others  of  a  slower  or 
less  virulent  type  exhibit  various,  diffuse,  infectious  lesions.  Why  this 
intoxication  should  seem  to  select  the  peripheral  motor  neurone  in 
most  cases  whereon  to  expend  its  force  primarily  it  is  hard  to  say, 
but  that  it  is  not  limited  solely  in  all  cases  to  that  neurone  is  shown 
by  the  sensory  and  other  symptoms.  This  may  be  explained  when  we 
know  more  about  the  relative  susceptibilities  of  the  different  parts  of 
the  nervous  system,  or  when,  perchance,  we  discover,  if  we  ever  do,  a 
specific  germ  as  the  cause  of  the  intoxication. 

The  diffuse  character  of  this  poison  and  the  irregularly  scattered 
location  of  the  lesions  which  it  provokes  m.ay  well  cause  Landry's 
paralysis  to  closely  simulate  a  diffuse  myelitis,  an  anterior  poliomiyelitis 
or  a  multiple  neuritis.  They  are  not  the  same,  however,  as  will  be 
pointed  out  under  the  head  of  diagnosis. 

The  cases  that  succumb  rapidly  are  apparently  primary,  profound 
intoxications  of  the  neurones.  For  this  reason  I  place  the  disease  pro- 
visionally here.  When  it  is  shown  to  be  always  a  pure  inflammatory 
trouble,  it  will  then  be  removed  from  the  class  of  neuronic  affections  of 
primary  origin. 

Symptoms. — Usually  there  are  premonitory  symiyfovis,  such  as 
a  feeling  of  general  malaise,  numbness  of  the  extremities,  shght  pains 
in  the  back  and  elsewhere,  weakness  of  the  legs  with  tingling  and 
other  symptoms  not  unlike  those  found  in  neurasthenia.  These  prodro- 
maia  may  last  several  days  and  gradually  pass  into  the  typical  symp- 
tomatology. Many  cases,  however,  begin  abruptly  with  a  decided 
weakness  in  one  or  botjj,  legs,  which  in  a  few  hours  become  completely 
paralyzed.  The  paralysis  then  rapidly  travels  up  the  body,  involving 
successively  the  trunk,  the  arms  and  finally  the  muscles  of  respiration 
and  deglutition.  The  patient  cannot  sit  up  on  account  of  the  paralysis 
of  the  back  muscles.  Coughing,  sneezing,  defecation  and  urination  are 
all  difficult  when  the  abdominal  muscles  are  involved.  Swallowing  and 
breathing  become  embarrassed  and  in  the  end  impossible. 

In  a  case  reported  by  Westphal  the  medulla  oblongata  alone  was 
implicated,  the  disease  beginning  and  terminating  with  bulbar  symp- 
toms. 

The  paralysis  is  not  always  paraplegic  in  its  distribution  or  ascend- 
ing in  its  course.  Sometimes  it  skips  about  from  the  arm  to  the  le^ 
or  vice  versa.  Fagge  declares  that  the  great  naturalist  Cuvier  died  of 
a  rapidly  descending  Landry's  paralysis. 

As  a  rule  the  deep  reflexes  are  lost,  but  the  muscles  are  not  atro- 
phied and  the  electrical  irritability  remains  normal.  There  is  no  fever 
except  in  a  very  few  cases,  in  which  there  has  been  observed  a  slight 
temporary  elevation  of  the  temperature.  The  sensations  are  unaffected. 
Trophic  abnormalities  are  absent.  The  rectal  and  bladder  functions 
are  undisturbed.  Finally  the  speecti  grows  heavy  and  indistinct,  swal- 
lowing becomes  impossible,   respiration  grows   rapid   or  assumes  the 


434  THE   NEURONIC   DISEASES 

Cheyne-Stokes  characteristics,  and  death  ensues  in  a  few  days,  usually 
less  than  a  week,  under  asph\-xia.     The  mind  remains  clear  to  the  last. 

Such  is  the  acute  ascending  paralysis  described  by  Landry. 

Even  to-day  many  authors  limit  the  name  Landry's  paralysis  to 
the  above  described  symptom-complex.  The  more  modern  conception 
of  the  disease,  however,  presents  a  broader  clinical  picture.  For  ex- 
ample, with  the  paralysis  in  some  cases  are  associated  a  moderate  de- 
gree of  muscular  atrophy,  sensory  and  trophic  symptoms,  and  involve- 
ment of  the  bladder  and  rectal  sphincters.  Moreover,  the  distribution 
of  the  paralysis  is  less  regular  and  the  progress  of  it  less  rapid  than  as 
Landry  originally  described  it.  And  instead  of  the  disease  being  so 
universally  fatal,  not  a  few  cases  have  gotten  entirely  well  after  several 
w-eeks'  duration.  ^lany  of  these  later  cases  bear  a  close  resemblance 
to  acute  ascending  meningo-myelitis,  disease  of  the  spinal  roots  and 
multiple  neuritis. 

The  sensory  symptoms  when  present  are  very  variable.  At  first 
there  is  numbness,  formication  and  other  parsesthetic  manifestations. 
A  slight  loss  of  sensation  is  common ;  a  complete  anaesthesia  is  rare. 
Hypersesthesia  has  been  observed.  Analgesia  is  sometimes  present, 
and  even  the  muscular  sense  has  been  found  to  be  altered.  Thus  every 
variety  of  sensory  disturbance  may  be  expected.  These  symptoms  are 
doubtless  due  to  a  secondary  involvement  of  the  sensory  apparatus,  as 
Landry's  paralysis  would  seem  to  be  primarily  a  disease  of  the  motor 
apparatus. 

As  a  rule  the  slight  diminution  that  occurs  in  the  muscle-masses, 
when  the  patient  lives  long  enough,  is  not  the  same  as  the  typical 
atrophy  that  is  observed  in  acute  anterior  poliomyelitis.  Even  after 
many  weeks  there  is  still  no  atrophy  nor  any  alterations  of  the  electrical 
reaction.  Exceptionally,  how^ever,  there  is  distinct,  typical  muscular 
atrophy  and  a  characteristic  reaction  of  degeneration.  Remak  errone- 
ously thought  that  this  absence  of  muscular  atrophy  and  normal  elec- 
trical irritability  were  pathognomic  of  Landry's  disease. 

In  exceptional  cases  the  bladder  and  rectal  functions  have  been 
affected.  According  to  Oppenheim,  even  complete  paralysis  of  the 
sphincters  has  been  observed.  In  many  of  the  cases  there  may  be  for  a 
short  time  retention  of  the  urine,  but  as  this  soon  passes  off,  there  is 
seldom  need  for  the  employment  of  the  catheter. 

The  cranial  nerves,  other  than  those  spoken  of  in  connection  with 
the  respiration  and  deglutition,  escape.  In  rare  cases  the  facial  and 
motor-oculi  have  been  implicated. 

As  a  rule  there  is  no  fever,  no  delirium,  no  clouding  of  the  mental 
faculties.  In  a  few  cases  there  have  been  recorded  high  fever,  signs 
of  general  septic  infection  and  more  or  less  obliteration  of  conscious- 
ness. It  may  be  w-ell  questioned  whether  such  manifestations  should 
be  included  under  the  head  of  acute  ascending  paralysis  rather  than 
that  of  a  general  septic  state  of  which  the  paralysis  is  a  concomitant 
symptom.    In  these  cases  hyperidrosis  has  often  been  described. 

Diagnosis. — Multiple  neuritis  of  infectious  origin  has  been  identi- 
fied with  Landry's  disease  (Ross,  Dejerine  and  Goetz.  Nauwerck  and 
Barth,  Putnam,  Klimipke.  Krewer.  Pitres  and  A^aillard.  Mobius,  Kiril- 


THE   NEURONIC   DISEASES  435 

zew  and  Mamurowsky,  Spiller  and  others),  and  yet,  as  Oppenheim 
well  says,  it  is  not  proper  to  regard  them  as  perfectly  identical.  Lan- 
dry's paralysis  of  the  pure  type  differs  from  multiple  neuritis  in  the 
absence  of  distinct  pain  and  other  sensory  disturbances,  in  the  non- 
atrophic  condition  of  the  muscles  and  the  preservation  of  the  normal 
electrical  irritability.  Meningeal  hemorrhage  may  be  distinguished  by 
the  pain  in  the  back  and  the  spasm.  Acuie  anterior  poliomyelitis  does 
not  exhibit  the  peculiarly  rapid,  ascending,  more  or  less  paraplegic 
form  of  paralysis  characteristic  of  Landry's  symptom-complex.  The 
former  is  notable  for  the  distribution  of  the  paralysis  in  particular 
muscles  or  groups  of  muscles,  which  quickly  undergo  atrophy  and 
manifest  well-known  abnormal  electrical  reactions.  Acute  myelitis  or 
me nin go-myelitis  of  the  ascending  type  is  to  be  differentiated  by  the 
presence  of  fever,  sensory  troubles,  bedsores  and  other  trophic  mani- 
festations, and  vesical  and  rectal  phenomena. 

After  all,  however,  it  must  be  admitted  that  there  are  some  cases 
of  Landry's  syndrome  that  cannot  clinically  be  distinguished  from  any 
one  of  these,  especially  from  multiple  neuritis  and  acute  anterior 
poliomyelitis.  And  this  is  not  to  be  wondered  at  when  one  recalls  the 
nature  and  pathogenesis  of  Landry's  group  of  phenomena.  The  same 
observation  will  explain  the  futility  of  arbitrarily  dividing  the  disease 
into  three  distinct  types,  the  bulbar,  spinal  and  peripheral ;  or  of  mak- 
ing such  a  separate  variety  as  the  descending  form,  in  contradistinction 
to  the  ascending. 

Prognosis. — The  course  of  the  disease  is  variable  and  the  prog- 
nosis always  grave.  It  is  not  always  fatal,  however,  as  it  was  at  one 
time  co'nsidered.  Sometimes  death  takes  place  in  a  tew  hours,  or  in 
two  or  three  days,  and  sometimics  it  is  postponed  for  three  or  four 
weeks.  The  rapidity,  duration  or  completeness  of  the  paralysis  does 
not  seem  in  any  way  to  measure  the  gravity  of  the  disease.  The  char- 
acter of  the  bulbar  symptoms  and  the  degree  of  involvement  of  the 
functions  of  respiration,  deglutition,  etc.,  are  the  guides  to  be  closely 
watched  in  forming  a  prognosis.  Steadily  progressing  cases,  even 
though  slow,  are  unfavorable.  Cases  have  recovered,  a  fact  which 
justifies  a  favorable  outlook,  if  there  is  the  slightest  retrocession  in  the 
progress  of  the  malady.  The  fatal  cases  usually  terminate  inside  of 
a  week. 

Treatment. — Recognizing  the  toxic  origin  of  Landry's  paralysis, 
it  is  obvious  that  the  ideal  treatment  would  be  the  use  of  an  antitoxine. 
There  is  none  known,  however,  and  so  we  must  still  resort  to  all  meas- 
ures calculated  to  support  the  patient's  vitality  and  to  eliminate  the 
poison  as  rapidly  as  possible.  Unfortunately  the  rapidity  of  the  dis- 
ease too  often  forestalls  all  such  commendable  efforts.  Nevertheless, 
it  is  wise  to  resort  to  mild  stimulation  with  alcohol,  ammonia  and  other 
diffusible  stimulants,  to  give  an  abundance  of  easily  digested  and  easily 
assimilated  nourishment,  and  to  increase,  as  far  as  possible,  the  func- 
tions of  the  emunctory  organs.  Warm  baths  and  hot  wet  packs  stimu- 
late the  skin  into  'renewed  activity.  Coimter-irritation  over  the  spine, 
and  especially  over  the  region  of  the  kidneys,  should  be  resorted  to. 
The  action  of  the  kidnevs  should  be  favored  bv  the  use  of  diuretics  with 


436  THE   NEURONIC   DISEASES 

the  drinking-  of  an  abundance  of  water.  Free  catharsis  is  advisable 
with  calomel  or  elaterium,  followed  by  salines.  When  swallowing'  be- 
comes difficult  nourishment  and  medicines  should  be  administered  by 
the  rectal  or  nasal  tube. 

As  for  medicines,  there  are  none  known  upon  which  we  can  rely 
with  certainty.  In  one  case  following"  exposure  to  wet  and  cold,  and 
almost  at  the  point  of  death,  ergotin  in  two-grain  doses  every  hour  was 
followed  by  a  speedy  recovery.  Salicylate  and  benzoate  of  sodium  have 
been  recommended.  Iodide  of  potassium  and  mercury  have  had  their 
advocates,  irrespective  of  the  possible  cause  of  syphilis  in  soiiie  cases. 
Belladonna  has  been  tried  with  doubtful  results.  As.  for  the  use  of 
strychnia,  one  would  feel  some  hesitancy  about  employing  so  vigorous 
a  spinal  stimulant  in  a  disease  in  which  there  are  inflammatory  and 
degenerative  changes  going  on. 

In  a  word,  the  nature  of  the  disease,  and  the  results  so  far  ob- 
tained, indicate  a  revulsive  line  of  treatment,  with  the  use  of  anti- 
phlogistic and  diaphoretic  measures.  Perhaps  som.e  day  blood-serum 
therapy  will  make  all  such  crude  measures  unnecessary. 

PERIODICAL  PARALYSIS. 

This  is  perhaps  the  place  to  refer  briefly  to  a  remarkable  form  of 
paralysis  that  comes  and  goes  periodically.  The  phenomenon  has  been 
seen  particularly  in  connection  with  the  movements  of  the  eye  and  of  the 
extremities. 

Periodical  Paralysis  of  the  Extremities.  With  or  without  an  an- 
aesthesia an  intermittent  paraplegia  of  the  arms  and  legs  occurs,  com- 
ing on  with  great  regularity,  without  apparent  cause,  when  the  pa- 
tient is  in  the  full  flush  of  health,  awake  or  asleep.  Weakness  of  the 
limbs,  weariness  and  drowsiness,  and  occasionally  paraesthesiae  precede 
it.  Twenty-four  hours  usually  sees  the  paralysis  complete.  The  arms, 
the  legs,  the  neck  and  occasionally  the  tongue  and  pharynx  are  in- 
volved. The  cranial  nerves  are  unaffected  as  a  rule.  There  is  no  fever, 
but  the  temperature  is  often  subnormal  and  the  pulse  slow. 

The  heredity  in  the  disease  is  quite  marked,  so  much  so  that  it 
assumes  the  form  of  a  "family"  disease.  Goldflam,  for  instance,  saw  a 
family  with  twelve  afflicted  members,  the  heredity  being  through  the 
mother.  Taylor  saw  eleven  cases  in  five  generations  of  a  family.  This 
with  other  features  of  these  periodical  paralyses  makes  one  think  strong- 
ly of  a  hysterical  affection,  but  there  is  a  remarkable  stumbling  block  in 
the  way  of  regarding  it  as  hysterical.  Functional  as  the  disease 
appears  to  be,  there  is  a  reduction,  sometimes  abolition,  of  the  reflexes ; 
and  stranger  yet  than  all,  a  reduction  or  complete  abolition  of  faradic 
excitability  of  both  the  muscles  and  the  nerves.  This  looks  very  much 
like  a  toxic  neurosis  or  temporary  infection  involving  especially  the 
lower  motor  neurones.  Nothing  but  toxaemia  would  produce  such  a 
localized,  short-lived  paralysis.  It  is  not  impossible  that  the  tofxin, 
whatever  it  is,  may  be  periodically  evolved  in  the  patient's  own  body,  as 
the  result  of  his  inherited  neurotic  defect.  This  is  the  only  sort  of  a 
hypothesis  that  would  harmonize  all  the  features  of  these  strange  par- 


THE   XEURONIC   DISEASES 


437 


alyses.  The  evolution  of  the  toxin  results  periodically  from  an  inher- 
ited neurosis.  This  expends  itself  upon  the  lower  motor  neurones  and 
we  have  the  incipiency  of  an  organic  neuronic  disease,  which,  however, 
does  not  last  long  enough  to  provoke  permanent  changes. 

COMBINED  DISEASES  OF  THE  AFFERENT  AND  EFFER- 
ENT SYSTEMS. 

It  is  well  known  that  degeneration  and  sclerosis  in  the  lateral  col- 
umns of  the  cord  occur  late  in  a  few  cases  of  locomotor  ataxia.  This 
is  looked  upon  as  a  mere  complication  or  sequel  and  not  as  an  integral 
part  of  the  disease.  There  are  a  number  of  diseases,  however,  in  which 
the  hardening  of  the  lateral  and  posterior  columns  proceed  simultane- 
ously, seem  to  be  dependent  upon  the  same  causative  influence,  and 
exhibit  a  more  or  less  uniform  clinical  picture.  Heredity  plays  a  sig- 
nificant role  as  a  predisposing  cat:se,  while  infection  and  nutritive  dis- 
turbances are  prominent  among  the  exciting  causes.  The  cord  changes 
observed  in  pernicious  ansemia  afford  a  good  illustration  of  the  domi- 
nance of  an  exciting  cause,  while  Friedreich's  ataxia  shows  well  the 
power  of  a  hereditary  cause. 

When  the  disease  occurs  in  childhood,  as  it  does  in  most  of  the 
hereditary  types,  the  undeveloped  condition  of  the  nervous  system  nat- 
urally causes  a  modification  in  the  clinical  picture  difi"erent  from  that 
which  it  would  have  in  an  adult  after  the  nervous  apparatus  has  ac- 
quired its  full  groAvth  and  has  long  been  subjected  to  disciplined  and 
fixed  habits. 

Again,  a  variation  in  the  clinical  exhibition  would  be  wrought,  as 
Westphal  long  ago  pointed  out,  by  the  relative  intensity  and  extent  of 
the  lesion  in  the  lateral  or  the  posterior  columns.  If  the  disease  process 
in  the  posterior  columns  is  in  advance  of  that  in  the  lateral  columns,  the 
symptoms  bear  a  resemblance  in  some  respects  to  those  of  tabes.  If 
the  disease  is  more  pronounced  in  the  lateral  than  in  the  posterior 
columns,  the  clinical  portraiture  simulates  somewhat  spastic  paraplegia. 

Clinically,  therefore,  we  find  in  these  combined  scleroses  two 
prominent  features  that  justify  their  consideration  as  distinct  and  inde- 
pendent affections.  The  first  is  the  uniformity  of  the  clinical  mani- 
festations due  to  the  combined  posterior  and  lateral  lesion.  The  other 
is  the  particular  modification  of  symptoms  evoked  by  the  age  of  the 
patient  and  the  relative  prominence  of  the  lesion  in  one  or  the  other 
location.  Unless  these  facts  are  kept  V\"ell  in  mind  there  will  be  an  un- 
necessary refinement  of  classification  and  the  elevation  of  mere  symp- 
tom groups  into  distinct  and  separate  diseases. 

From  what  has  already  been  said,  it  is  obvious  that  the  combined 
sclerosis  of  the  two  columns  of  the  cord,  so  different  in  their  general 
functions  as  are  the  lateral  and  posterior  columns,  must  necessarily  pro- 
voke some  marked  differences  between  the  clinical  manifestations  of 
different  cases. 

Theoretically  and  pathologically  there  may  be  no  good  reason  for 
separating  from  one  another  the  spmal  sclerosis  of  pernicious  anaemia, 
ataxic  paraplegia,  hereditary  ataxic  paraplegia,  Friedreich's  disease  any 


438 


THE   NEURONIC   DISEASES 

FIGURES  87,  88  AND 


The  combined  scleros 


es  01  system  diseases.    Fig.  87,  cervical  section.     Fie 


dorsal  section.     Fig.  89.  lumbar  section.     (After  Jakob.) 


THE   XEUROXIC   DISEASES  43Q 

more  than  there  is  for  separating  the  hemiplegias,  diplegias  and  con- 
genital spastic  ■  "paraplegias"  among  the  cerebral  palsies  of  childhood. 
Practically,  however,  it  is  advantageous  to  make  the  distinction,  not 
to  emphasize  them  as  distinct  diseases,  but  to  point  out  the  individual 
etiology  and  minor  symptomatolog}-  in  each  particular  class. 

The  highest  aim  of  science  is  to  generalize  and  not  to  individual- 
ize. The  reduction  of  all  exceptions  and  their  inclusion  under  a  general 
law,  as  rapidly  as  knowledge  in  regard  to  them  will  warrant,  should 
ever  be  the  purpose  of  scientific  endeavor.  Unfortunately  in  this  re- 
spect art  and  science  are  often  in  gentle  conflict,  and  as  a  result  we 
make  for  practical  convenience  distinctions  and  classifications  where 
scientifically  there  are  no  broad  lines  of  difference. 

For  practical  purposes  then  we  will  do  w-ell  to  carry  about  in  our 
memory  the  following  types  of  the  combined  scleroses  enumerated  by 
Dana: 

1.  Combined  scleroses  of  profoundly  ansemic  and  toxic  states 
(Putnam's  type). 

2.  Hereditary  spinal  ataxia  (  Friedreich's  ataxia  and  hereditary 
ataxic  paraplegia). 

3.  Combined  scleroses  complicating  general  paresis. 

4.  Accidental  forms  (Gowers',  ataxic  paraplegia). 

Myelitis,  meningomyelitis,  posterior  leptomeningitis  of  s}"philitic 
and  other  infectious  origin  with  secondary  degeneration  in  particular 
tracts,  will  explain  a  large  number  of  cases  reported  to  belong  to  one  or 
other  of  these  classes.  The  anaemic  and  toxic  scleroses  are  clearly  not 
distinct  disease  entities  and  in  many  cases  they  are  merely  diilnse  condi- 
tions such  as  one  observes  in  all  forms  of  general  constitutional  poison- 
ing. In  pellagra,  in  ergotism,  in  leukemia  and  in  carcinoma  a  combined 
sclerosis  of  the  cord  has  been  observed. 

Hereditary  spinal  ataxia  I  have  discussed  in  the  next  section. 

Under  dementia  paralytica  these  complications  and  sequelse  will 
be  referred  to. 

ATAXIC   PARAPLEGIA. 

This  is  not  a  disease.  It  is  merely  a  characteristic  syndrome  which 
has  many  congeners  and  which  is  the  result  of  a  combination  of  two 
diseases,  or  rather  sets  of  symptoms  dependent  upon  a  lesion  in  both 
the  lateral  and  posterior  columns  of  the  cord.  It  may  beneficially  be 
adopted  as  a  model  for  the  description  of  the  general  s}'mptomatolog}- 
of  these  combined  scleroses  and  for  pointing  out  the  possible  variations 
that  may  occur  in  the  clinical  picture  of  some  other  forms  of  the  com- 
bination. For  the  nonce  then  T  will  discuss  it  as  though  it  were  a 
unique  and  distinct  entity. 

Etiology. — Heredity  of  some  sort  probably  plays  a  role  in  all 
of  these  cases.  In  most  of  them  it  may  amount  to  a  mere  neuropathic 
predisposition,  a  congenital  weakness,  lack  of  resistive  power  to  inju- 
rious influences  in  certain  tracts  or  neurones.  It  may  be  so  decisive, 
as  in  the  six  cases  observed  by  Dana,  as  to  almost  warrant  its  con- 
sideration as  a  separate  disease  under  the  head  of  hereditary  or  familial 
ataxic  paraplegia.     Dana's  cases  were  all  women  and  began  between 


440  THE   NEURONIC   DISEASES 

the  ages  of  twelve  and  sixteen.  Most  cases  begin  between  thirty  and 
forty  years  of  age  and  appear  in  the  male  sex.  Absence  of  a  history 
of  syphilis  or  alcoholism  is  a  striking  feature.  No  exciting  cause  is 
known,  though  it  has  followed  exposure  to  cold,  sleeping  in  clothes 
saturated  with  perspiration,  sexual  excess,  severe  concussion  of  the 
spine  and  certain  cachexias.  I  have  seen  the  symptoms  follow  a  severe 
anaemia  and  a  chronic  diarrhoea  of  twenty  years'  standing.  Whether 
pernicious  anaemia  produces  a  systemic  sclerosis  in  the  lateral  and  pos- 
terior columns  or  merely  a  diffuse  myelitic  condition  is  not  yet  posi- 
tively settled.  Lichtheim,  Nonne,  Minnich,  v.  Noorden,  Taylor,  Water- 
man and  Billings  believe  that  it  is  a  diffuse  process.  Oppenheim  still 
believes  that  it  is  a  true  combined  systemic  neurone  disease.  Taylor 
and  Waterman,  Bastianelli,  Russell,  Batten  and  Collier,  Billings  and 
others  consider  that  the  arteriosclerosis,  the  ansemia,  and  the  other 
concomitant  conditions  observed  in  these  cases  of  combined  degenera- 
tion in  the  cord  are  the  result  of  the  same  general  toxaemia  that  gives 
rise  to  the  spinal  lesion  and  are  not  themselves  the  direct  cause  of  the 
latter. 

Little  as  we  know  about  the  etiology  of  these  combined  degenera- 
tions, be  they  diff'use  or  systemic,  two  factors  seem  to  stand  out  with 
suspicious  prominence,  namely,  an  inherited  predisposition  and  a 
toxcumic  excitation. 

Pathology  and  Pathogenesis. — The  essential  lesion  is  a  degen- 
erative sclerosis  of  the  posterior  and  lateral  cohmms  of  the  cord.  It 
may  extend  throughout  the  entire  length  of  the  cord,  though  the  pro- 
cess is  apt  to  be  more  pronounced  in  the  thoracic  region.  In  some  in- 
stances, as  for  example  Friedreich's  disease,  the  degeneration  is 
sharply  limited  to  certain  tracts,  notably  the  postero-median,  postero- 
lateral and  crossed  pyramidal,  and  the  disease  is  shown  to  be  a  purely 
systemic  one.  In  other  instances,  as  for  example  the  anaemic  cases 
(Bastianelli,  Russell,  Batten  and  Collier,  Spiller  and  others)  the  lesion 
is  less  sharply  defined  and  the  disease  process  may  be  regarded  more 
as  a  diffuse  one.  It  may  be  that  secondary  degenerations  of  a  systemic 
character  follow  and  are  associated  with  the  dift"use  lesions  in  many 
of  the  cases,  thus  accounting  for  their  general  systemic  appearance 
upon  post  mortem  examination. 

Other  tracts  besides  Goll's,  Burdach's  and  the  crossed  pyramidal 
that  sometimes  participate  in  the  degeneration  are  the  direct  cerebellar, 
the  anterior  or  direct  pyramidal  and  the  antero-lateral.  The  gray  mat- 
ter of  the  cord,  the  spinal  roots  and  the  anterior  root  zones  are  not 
implicated.     The  membranes  have  only  rarely  been  diseased. 

The  sclerosis  is  of  the  ordinary  type  though  its  distribution  and 
intensity  are  subject  to  considerable  variation  in  the  respective  columns 
where  it  appears.  In  the  laterial  columns  it  is  always  less  systemic 
in  its  limitations  than  it  is  in  the  posterior  columns ;  and  usually  there 
is  a  narrow  strip  of  healthy  tissue  immediately  adjoining  either  side 
of  the  posterior  horns.  In  the  severe  anaemic  and  toxic  cases  there 
may  be  such  a  rapid  destruction  of  the  neurones  that  a  peculiar  perfor- 
ated appearance  is  given  to  the  cross  section  of  the  cord.    In  such  cases 


THE   NEURONIC   DISEASES  44I 

an  oedematous  condition  with  destruction  of  the  septa  and  the  forma- 
tion of  granule  cells  may  be  observed   (Dana). 

To  sum  up  then,  the  pathology  of  the  combined  scleroses  indicates 
two  great  groups  of  cases,  the  systemic  and  the  diffuse,  with  the  chief 
foci  of  disease  in  the  posterior  and  crossed  pyramidal  tracts.  Outside 
of  Friedreich's  disease  and  the  spinal  sclerosis  of  general  paresis, 
which  are  purely  systemic,  no  sharp  differentiation  can  be  made.  Some 
cases  are  doubtless  systemic  from  the  start,  others  are  diffuse  but  be- 
come later  on  systemic  on  account  of  the  secondary  degenerations. 

Symptoms. — In  analyzing  the  clinical  presentation  of  these  cases 
of  combined  degeneration  as  seen  in  the  cord,  it  must  be  remembered 
that  we  are  dealing  with  two  somewhat  diametrically  opposed  sets  of 
symptoms.  In  the  one  a  spastic  spinal  paralysis  due  to  de generation 
of  the  pyramidal  tracts  is  combined  with  a  true  ataxia,  lancinating 
pains,  pupillary  rigidity,  bladder  trouble  and  other  tabetic  symptoms; 
in  the  other  the  symptom-complex  of  tabes  is  accompanied  from  the 
beginning  by  motor  zveakness. 

Studied  separately  the  clinical  manifestations  of  lateral  degener- 
ation would,  a  priori,  seem  to  neutralize  those  of  posterior  degenera- 
tion. And  yet  such  is  not  strictly  the  case.  There  is  never  a  com- 
plete annihilation  of  one  set  of  symptoms  by  the  other.  One  may  be 
more  prominent  than  the  other  and  thus  determine  the  leaning  of  the 
case  toward  spastic  paralysis  or  locomotor  ataxia.  Whichever  the  dis- 
ease seems  to  tend  toward,  always  search  for  indications  of  the  other. 

Like  the  lesion,  therefore,  the  symptomatology  of  these  cases  is 
always  a  combination.  This,  however,  does  not  express  the  whole 
truth,  for  there  is  more  than  a  mere  combination  of  symptoms,  there 
is  a  more  or  less  characteristic  modification  wrought  in  the  clinical  pic- 
ture by  the  simple  combination.  It  is  the  relative  constancy  of  these 
characteristic  modifications  of  the  symptomatology  in  toto  that  has 
led  to  not  a  little  confusion  in  the  past  and  betrayed  writers  into  estab- 
lishing new  diseases  out  of  the  various  clinical  presentations.  Inter- 
mediate types  are  here  so  numerous,  and  the  gradations  from  one  to 
the  other  are  so  gradual,  that  no  description  will  stand  rigidly  for 
all  types.  The  ataxic  paraplegia  of  Gowers,  while  not  a  fixed  type, 
will  answer  well  enough  as  a  basis  for  a  general  description  of  the 
symptomatology  of  the  combined  sclerosis,  the  description  to  be  ahvays 
modified  to  suit  the  etiology,  age  of  patient  and  prominence  of  the  loca- 
tion of  the  lesion  in  the  particular  case  in  hand. 

Usually  the  symptoms  appear  slowly.  There  is  weakness  in  the 
legs  for  several  months  or  years  and  then  the  walking  becomes  grad- 
ually impaired.  The  weakness  and  incoordination  may  be  confined  to 
the  legs,  though  it  is  not  infrequent  that  they  extend  to  the  arms.  Ex- 
ertion, turning,  walking  in  the  dark  become  arduous.  Examination 
reveals  even  at  this  time  a  real  condition  of  paresis  in  the  muscles.  One 
leg,  one  set  of  muscles  may  be  implicated  more  than  another.  The 
gait  resembles  that  of  tabes  but  the  high  elevation  of  the  leg  and  the 
stamping  of  the  heel  on  the  floor  are  not  so  marked  as  in  the  latter 
disease.     The  ataxia  is  both  static  and  motor. 

In  the  great  majority  of  cases  the  knee-jerk  is  markedly  exagger- 


442  'IHE   NEURONIC   DISEASES 

ated  and  a  distinct  rectus  clonus  can  be  elicited.  Foot  clonus  is  also 
generally  present.  This  exaggeration  of  the  patella  reflex  contrasts 
these  cases  strongly  from  locomotor  ataxia.  It  continues  mostly 
throughout  the  entire  course  of  the  disease.  In  the  cases  in  which  the 
knee-jerk  is  at  first  increased,  and  later  annulled,  the  degeneration  in 
the  posterior  columns  fias  descended  into  the  lumbar  region.  The  case 
then  resembles  more  nearly  tabes  but  differs  from  it  in  manifesting  a 
true  progressive  motor  weakness  or  paresis. 

The  marked  absence  of  sensory  symptoms  also  distinguishes  these 
cases  from  tabes.  Lightning  pains  are  scarcely  ever  observed.  Some- 
times dull  pains  occur  in  the  legs,  in  the  spine  and  around  the  body. 
As  a  rule  cutaneous  sensation  is  unaffected.  Hypersesthesia  has  been 
rarely  noted.  I  have  seen  the  cutaneous  reflex  of  the  sole  of  the  foot 
highly  exaggerated,  especially  in  the  aneemic  cases.  The  tickling  was 
not  distressing  to  the  patient  though  the  limb  was  violently  drawn 
up.  The  cremasteric  and  abdominal  cutaneous  reflexes  may  be  lost  at 
times.  In  exceptional  instances  the  sensory  phenomena  may  be  as 
positive  as  they  are  in  tabes.  These  are  the  cases  in  which  the  knee- 
jerks  are  lost  and  the  tabetic  resemblance  is  marked.  According  to 
Gowers  these  intermediate  cases  between  ataxic  paraplegia  and  true 
tabes  do  not  constitute  more  than  five  per  cent,  of  all  the  cases  with 
ataxia  and  motor  weakness. 

The  muscles  are  not  wasted  to  any  extent  and  the  electrical  re- 
sponses are  normal. 

Sexual  vigor  may  be  lost  early.  The  sphincters  are  usually  im- 
paired but  only  moderately. 

The  eye  symptoms  when  present  are  the  same  as  those  met  with 
in  tabes.  They  are  less  frequent,  however,  than  they  are  in  the  lat- 
ter disease.  Nystagmus  does  not  occur  generally ;  though  with  other 
bulbar  symptoms  it  is  a  positive  feature  in  Friedreich's  hereditary  type 
of  combined  sclerosis. 

Articulation  is  slightly  impaired  in  some  cases.  Gowers  says  it 
is  not  uncommon.  A  slight  amnesia  as  a  rule  is  all  that  character- 
izes the  mental  state  in  the  way  of  deterioration. 

As  the  disease  continues  to  advance  the  paresis  becomes  more  and 
more  marked  until  it  quite  overwhelms  the  incoordination.  Finally 
after  a  period  of  going-  about  on  crutches,  the  patient  takes  to  his  bed 
never  to  leave  it.  Stiffness  and  rigidity  in  the  muscles  increase  and 
even  before  becoming  bedridden  the  case  develops  into  one  of  spastic 
paraplegia.  The  arms  are  now  involved,  if  they  have  been  fortunate 
in  escaping  so  far.  At  length  complete  paralysis  comes  on  and  the 
case  terminates  as  spinal  spastic  paralysis  usually  does.  To  the  end 
sensation  usually  remains  unimpaired,  crises  are  absent,  and  the  re- 
flex action  of  the  iris,  unless  lost  early,  remains  normal. 

Among  the  complications  are  dementia  paralytica  with  its  array  of 
mental  symptoms,  occasional  slight  muscular  atrophy  and  arthritis. 

Such  in  th€  main  is  the  clinical  picture  of  ataxic  paraplegia,  or 
combined  sclerosis  of  the  posterior  and  lateral  columns  of  the  cord. 
The  differences  to  be  observed  in  the  symptomatology  of,  and  the  prob- 
able reasons  for  those  differences  in,  the  combined  sclerosis  of  Fried- 


THE   NEURONIC   DISEASES  443 

reich's  ataxia  and  dementia  paralytica  will  be  pointed  out  when  these 
diseases  are  discussed. 

Some  other -modifications,  not  sufficient  to  constitute  the  basis  for 
the  establishment  of  new  diseases,  may  perhaps  be  profitably  referred 
to  here. 

In  hereditary  ataxic  paraplegia  there  is  stiffness  and  weakness  in 
the  legs  and  the  ataxia  is  more  cerebellar  in  type  than  spinal.  Re- 
flexes are  exaggerated.  There  is  some  parzesthesia.  The  arms  are 
only  slightly  involved.  Optic  neuritis  was  present'  in  one  case.  The 
sphincters  are  intact,  the  mind  is  clear  and  the  prognosis  is  more  fav- 
orable than  in  Friedreich's  disease.  Xo  autopsy  having  been  made 
the  true  nature  of  these  cases  is  not  determined.  They  may  be  re- 
lated to  Friedreich's  ataxia  or  to  Alarie's  hereditary  cerebellar  ataxia. 

In  the  ancemic  and  toxic  cases  of  combined  sclerosis  there  are  apt 
to  be  early  sensory  symptoms  chiefl}-  of  a  parsesthetic  character. 
Numbness,  pain  and  anaesthesia  may  appear  in  ail  four  extremities. 
Gradually  the  motor  weakness  comes  on  and  finally  the  paraplegia. 
These  are  associated  with  the  ataxia.  Spasticity,  exaggerated  knee- 
jerks,  ankle-clonus  are  all  present.  The  mind  is  weakened  toward  the 
end.  Severe  anemia,  diarrhcea,  emaciation  are  all  concomitant  mani- 
festations suggestive  of  a  profound  tox^emic  condition. 

Diagnosis. — Enough  has  been  said  under  the  head  of  symptoms 
to  indicate  the  dififerential  diagnosis  of  a  combined  sclerosis  from  sim- 
ulated diseases.  Locomotor  ataxia  on  the  one  hand,  and  spinal  spas- 
tic paralysis  on  the  other,  are  the  affections  most  likeh'  to  cause  con- 
fusion. In  tabes  the  patella  refiex  is  always  and  early  lost ;  it  is  usu- 
ally exaggerated  in  the  combined  disease.  The  sensory  and  pupillary 
phenomena  are  as  a  rule  sufficiently  different  in  the  two  diseases  to  go 
a  long  way  in  establishing  the  dififerential  diagnosis.  In  primary  spas- 
tic paraplegia  there  is  no  ataxia.  As  Gowers  says  epigrammatically, 
ataxic  paraplegia  is  spastic  paraplegia  plus  incoordination.  The  hered- 
itary and  familial  types  of  combined  sclerosis  are  distinguished  by 
their  history,  the  age  of  the  patient  and  the  repetition  of  the  disease  in 
the  same  family.  Myelitis  is  sometimes  hard  to  distinguish,  and  in  fact 
Oppenheim  declares  that  the  toxeemic  cases,  while  symtomatically  allied 
to  the  combined  scleroses,  are  pathologically  related  to  myelitis.  ]\Iye- 
litis,  however,  is  regressive,  though  of  course  it  may  set  up  a  sec- 
ondary progressive  degeneration  in  the  lateral  and  posterior  tracts. 
Such  cases  cannot  be  differentiated.  Cerebellar  tumor  may  cause  symp- 
toms resembling  ataxic  paraplegia,  but  the  headache,  vertigo,  optic 
neuritis  and  other  well  known  signs  of  an  intra-cranial  neoplasm  are 
present  to  aid  in  the  diagnosis. 

Prognosis. — These  degenerations  are  incurable.  They  are  chronic 
and  progressive  in  their  course.  Sometimes  they  remit  symptomatically 
for  a  time  but  the  onw^ard  course  of  the  disease  is  again  resumed.  The 
danger  to  life  is  not  great.  Kidney  disease  and  bedsores  are  the  ac- 
cidents most  to  be  dreaded  as  these,  or  general  exhaustion,  usually 
close  the  scene.  Improvement  has  occurred  and  life  been  prolonged  in 
a  few^  cases.  Very  exceptionally  a  cure  has  been  observed.  The  prog- 
nosis therefore  as  to  life  is  fair :  as  to  recovery  bad. 


444  '^HE   NEURONIC   DISEASES 

Treatment. — The  treatment  is  the  same  as  that  for  tabes  and 
spastic  paraplegia,  the  two  diseases  out  of  which,  as  it  were,  ataxic 
paraplegia  is  framed.  It  is  no  less  and  no  more  satisfactory  than  it 
is  in  them.  The  etiology,  especially  in  the  anaemic  and  toxic  cases^ 
and  the  symptoms,  are  the  chief  points  of  attack  in  the  therapeutic  man- 
agement of  ataxic  paraplegia. 

HEREDITARY  ATAXIA. 

Under  the  broad  term  hereditary  ataxia  are  included  several  forms- 
of  degenerative  disease  of  the  central  nervous  system,  particularly  of 
the  cerebellum  and  spinal  cord,  in  which  etiologically  heredity  plays  a 
dominant  role  and  symptomatically  ataxia  stands  forth  as  a  leading 
phenomenon. 

Three  types  of  hereditary  ataxia  are  recognized,  namely,  Fried- 
reich's ataxia,  hereditary  ataxic  paraplegia  and  hereditary  cerebellar 
ataxia. 

There  will  doubtless  come  others. 

The  exact  relationship  of  these  troubles  to  one  another  is  not 
clear,  though  there  is  such,  since  they  overlap,  to  a  certain  extent,  both 
symptomatically  and  pathologically.  The  last  is  primarily  an  atrophic 
disease  of  the  cerebellum,  with  certain  secondary  changes  in  the  cord.. 
I  will  refer  to  it  more  in  detail  elsewhere.  The  other  two  are  often 
regarded  as  diseases  of  the  spinal  cord.  Their  principal  lesion  seems 
to  be  spinal  though  there  are  frequent  intra-cranial  manifestations- 
which  link  them  together  and  give  them  both  a  sort  of  connection 
with  the  cerebellar  type  of  hereditaiy  ataxia. 

In  one  thing  they  all  agree,  namely,  in  being  dependent  primarily 
upon  an  inherited  developmental  defect,  on  account  of  which  the  sys- 
temic degeneration  occurs  in  certain  encephalo-spinal  tracts. 

Before  a  more  accurate  classification  of  these  various  types  of 
hereditary  ataxia  can  be  made,  more  definite  data  will  have  to  be  forth- 
coming in  regard  to  their  pathogenesis. 

For  the  further  description  of  hereditary  cerebellar  ataxia  the 
reader  is  referred  to  the  section  on  diseases  of  the  cerebellum. 

FRIEDREICH'S  DISEASE. 

It  was  in  1861  that  Friedreich  first  described  the  disease  that  now 
bears  his  name.  It  is  a  rare  affection,  though  upwards  of  two  hun- 
dred cases  have  been  so  far  reported.  Our  knowledge  of  it  has  been 
increased  by  the  labors  of  Fere,  Mobius,  Cuche,  Ormerod.  Bury,  Sep- 
pilli,  Vizioli,  Ladame,  Griffith,  Burr  and  others. 

Heredity  and  ataxia  are  the  cardinal  features  of  the  malady,, 
though  there  are  many  other  characteristics  that  serve  to  identifv  the 
particular  form  of  hereditary  ataxia  which  Friedreich  described.  Of 
the  various  names  that  have  been  given  to  the  disease  from  time  to- 
time  all  have  proved  to  be  defective  and  misleading;  hence,  objection- 
able as  it  is  to  name  an  affection  after  a  man,  in  this  particular  in- 


THE   NEURONIC   DISEASES  445 

Stance,  it  is  almost  necessary  to  do  so  until  the  pathology  and  noso- 
logical position  of  the  trouble  is  more  definitely  established. 

Etiology. — Heredity  is  the  predominant  factor  in  the  etiology 
-of  this  disease.  It  is  both  direct  and  i)idirect.  In  the  broadest  sense, 
therefore,  Friedreich's  disease  is  a  family  disease,  a  characteristic 
which  stamps  it  at  once.  In  a  goodly  number  of  cases  one  or  more 
ancestors  of  the  patient  have  been  afflicted  with  the  same  malady. 
Sometimes  it  can  be  traced  through  four  generations,  increasing  in 
•extent  and  intensity  as  it  passes  on  down  through  the  family.  Often 
several  members  of  the  same  family  and  generation  are  attacked.  The 
heredity  is  not  always  direct.  In  the  remaining  cases  it  is  indirect  and 
seems  to  follow  some  neurosis  or  profound  ner^-ous  strain  in  the  fore- 
bears. This  indirect  heredity  is  much  more  frequently  traceable  than 
is  the  direct.  The  disease  therefore  is  in  all  likelihood  the  result  of 
-an  inherited  defect  of  a  developmental  and  neuropathic  character.  In 
the  parents  we  find  the  following  influences  at  work :  neuropathies, 
such  as  epilepsy,  psychoses,  great  nervous  irritability;  alcoholism;  tu- 
berculosis ;  syphilis ;  consanguinity,  and  other  imclassified  cachexije 
-and  constitutional  abnormalities.  The  hereditary  influence  need  not 
necessarily  be  obvious  in  the  parents,  for  in  some  cases  they  have  been 
Tiealthy  and  sound.  In  such  instances  somewhere  among  the  blood 
relations  will  the  taint  be  found  lurking.  In  some  cases  the  disease 
Tias  been  precipitated  by  an  infectious  fever,  notably  typhoid,  pertussis, 
variola,  meningitis,  periostitis,  njeasles,  scarlatina,  rheumatism  and 
probably  diphtheria.  This  form  of  ataxia  never  follows  tabes  dorsalis 
either  in  the  parent  or  in  the  patient  himself.  If  it  does  it  must  be 
exceedingly  rare. 

Though  the  affection  is  hereditary  and  familial,  it  is  rarely  seen 
before  the  seventh  or  after  the  forty-fifth  year  of  age.  A  large  number 
of  cases  develop  about  the  age  of  puberty.  After  twenty  it  rapidly 
becomes  more  and  more  rare.  The  majority  of  the  cases  make  their 
appearance  between  the  ages  of  six  and  ten.  In  fact,  roughly  speaking 
the  age  of  ten  is  the  time  to  expect  its  onset.  It  has  been  seen  in  a 
number  of  instances  as  early  as  two  years  of  age.  Most  authors  de- 
clare that  it  manifests  no  marked  preference  for  either  sex  and  yet 
in  Griffith's  143  collected  cases  the  percentage  of  males  was  almost 
double  that  of  females.  Dana  says  that  in  America,  where  more  cases 
"have  been  observed  than  in  any  other  country,  the  females  outnumber 
the  males  in  the  ratio  of  three  to  two.  The  laboring  and  agricultural 
•classes,  rather  than  the  denizens  of  the  crowded  cities,  include  chiefly 
the  parents  of  these  children.  In  some  instances  the  outbreak  of  the 
disease  has  been  attributed  to  falls  and  other  traumata,  child-bearing^ 
lactation  and  similar  depressing  factors. 

Pathology  and  Pathogenesis. — ]\Iuch  discussion  has  been  ex- 
pended upon  the  pathology  of  the  disease  and  this  is  not  to  be  won- 
dered at.  It  is  the  most  interesting  feature  about  it  and  necessarih 
underlies  its  correct  nomenclature  and  nosological  position.  Clinicalh 
the  disease  seems  to  be  intermediate  between  tabes  dorsalis  and  dis- 
seminated sclerosis,  having  several  of  the  leading  symptoms  of  both. 
Pathologically,  however,  it  is  related  to  Gowers'  ataxic  paraplegia  or 


446  THE   XEUROMC   DISEASES 

the  combined  scleroses  of  the  lateral  and  posterior  columns  of  the  cord. 
Seppilli,  Brousse,  Charcot  and  others  regard  it  entirely  as  a  distinct 
and  independent  malady. 

Constant  lesions  are  found  only  in  the  spinal  cord  and  medulla. 
The  brain  and  nerves  remain  intact  or  are  so  very  rarelv  implicated 
as  to  be  excluded  from  consideration. 

The  cord  is  generally  smaller  than  normal  throughout,  and  some- 
what flattened  laterally  and  posteriorly.  Along  the  posterior  surface 
there  are  indications  of  a  chronic  leptomeningitis.  The  characteristic 
and  constant  finding  in  the  cord  is  a  systemic  degeneration,  involving 
the  posterior  columns,  the  postero-lateral  cerebellar  tracts  and,  to  a 
lesser  degree  perhaps,  the  crossed  pyramidal  tracts.  Gowers'  tract  is 
sometimes  included.  The  change  extends  the  entire  length  of  the 
cord,  though  it  is  as  a  rule  most  pronounced  in  the  lumbar  region. 
Goll's  columns  are  completely  hardened  :  Burdach's  almost  entirelv  so. 

FIGURE  90. 


Cross-section  of  the  spinal  cord  in  Friedreich's  disease,    Pai's  stain.      (After 
Marinesco  and  Oppenheim.) 

A  trace  of  healthy  tissue  sometimes  lies  between  Burdach's  column 
and  the  posterior  horn.  The  crossed  pyramidal  tracts  are  always,  and 
quite  completely,  sclerosed.  The  process  seems  to  be  more  diffuse  in 
the  lateral  columns,  leaving  a  slip  of  healthy  tissue  alongside  of  the 
posterior  horn,  and  rarel}^  or  never  extending  in  front  of  a  line  drawn 
transversely  through  the  middle  of  the  cord.  In  a  large  number  of 
cases  the  disease  implicates  the  direct  cerebellar  tract,  and  the  ascend- 
ing antero-lateral  tract.  Rarely  are  the  anterior  median  columns  in- 
volved. The  anterior  root-zones  and  the  gray  matter  are  normal.  All 
the  nerve-roots  may  be  hardened,  the  anterior  much  less  frequently 
than  the  posterior.     The  peripheral  nerves  are  not  regularly  involved. 

The  central  canal  of  the  cord  has  been  seen  to  be  inflamed  in 
some  instances  and  there  have  been  present  distinct  but  small  cavities. 
The  cells  of  Clarke's  columns  are  often  shrunken  and  without  pro- 
cesses.   Degeneration  of  the  posterior  horns  has  been  observed. 

In  the  medulla  are  found  traces  of  the  upward  extension  of  this 
sclerosis,  the  hypoglossal  nucleus  portraying  the  most  significant 
change. 

The  interpretation  that  is  to  be  given  all  these  findings  is  still 
largely  hypothetical.     If  we  exclude  rigidly  those  cases  in  which  some 


THE   NEURONIC   DISEASES  447 

change  in  the  cerebelhuii  has  been  observed  we  find  ourselves  confronted 
by  a  spinal  cord  disease  apparently.  In  a  sense  it  is  a  systemic  affec- 
tion but  the  lesion  does  not  confine  itself,  especially  in  the  lateral  col- 
umns, within  sharp  outlines  in  any  one  tract.  There  is  a  certain  de- 
gree of  diffuseness  that  nullifies  all  idea  of  the  degeneration  being  sec- 
ondary to  some  brain  lesion  in  the  larger  number  of  cases  at  least, 
and  the  view  is  strengthened  that  Friedreich's  disease  is  a  primary 
sclerosis  of  the  xord  tracts.  The  similarity  of  hereditary  syphilis  and 
Friedreich's  ataxia  lends  support  to  this  conception.  When  we  attempt 
to  follow  the  many  explanations  ofi^ered  by  various  investigators  at 
different  times  to  determine  the  real  pathogenesis  of  the  disease,  the 
original  focus  of  the  disease  process,  and  the  connection  of  the  many 
pathological  findings  with  one  another,  we  find  ourselves  tossed  about 
on  a  sea  of  theories  and  hypotheses. 

The  only  theory  worth  considering  is  the  one  which  refers  the 
whole  trouble  to  an  inherited  defect  in  the  cerebellum.  This  theory 
promulgated  by  Hammond  has  been  lately  revived  and  vigorously  sup- 
ported by  Menzel,  Nonne,  Auscher,  Senator  and  others.  The  post  mor- 
tem findings,  however,  in  the  cerebellar  tissues  are  far  from  being  con- 
clusive. 

Marie's  hereditary  cerebellar  ataxia  is  probably  an  entirely  differ- 
ent trouble  and  is  not  to  be  confused  with  the  cerebellar  theory  of 
Friedreich's  ataxia  just  referred  to.  The  insignificance  of  the  changes 
in  the  cerebellar  cortex,  their  great  rarity,  as  well  as  the  constancy 
and  character  of  the  spinal  cord  changes,  all  incline  me  to  believe  that 
in  Friedreich's  disease  we  have  a  combined  degenerative  sclerosis  of 
the  posterior  and  lateral  columns,  with  their  related  structures.  It  is 
probably  developmental  in  origin  in  most  cases,  certain  congenitally 
weak  neurones  succumbing  under  various  exciting  influences.  In 
other  words  the  disease  in  my  judgment  approaches  very  closely  to 
being  a  congenital  or  hereditary  ataxic  paraplegia. 

The  pathological  process  being  in  advance  in  the  posterior  col- 
umns, the  symptoms  are  largely  ataxic  in  character,  to  such  an  extent 
even  as  to  cause  the  disease  to  closely  resemble  locomotor  ataxia. 

To  put  it  in  another  way,  Friedreich's  disease,  in  its  present  form, 
is  the  hereditary  or  congenital  analogue  of  those  cases  of  ataxic 
paraplegia  or  combined  sclerosis  in  which  the  ataxia,  absent  knee-jerks 
and  other  manifestations,  ally  it,  symptomatically  at  least,  with  tabes 
dorsalis. 

The  cases  which  have  been  reported  as  cases  of  hereditary  ataxia 
and  connected  with  Friedreich's  disease,  such  as  those  of  Sanger 
Brown,  Dana  and  others,  in  which  the  reflexes  have  been  exagger- 
ated, and  which  have  been  called  hereditary  ataxic  paraplegia,  are 
also  inherited  or  congenital  types  of  combined  sclerosis  of  the  lateral 
and  posterior  columns  in  which  the  disease  process  in  the  lateral  col- 
umns is  far  in  advance  of  that  in  the  posterior. 

If  this  conception  of  Friedreich's  disease  and  of  hereditary  ataxic 
paraplegia  should  ultimately  prove  to  be  the  correct  one,  both  diseases 
will  fall  under  the  general  classification  of  ataxic  paraplegia  or  com- 
bined sclerosis  of  the  lateral  and  posterior  columns.     The  difiference 


448  THE  NEURONIC  DISEASES 

between  these  and  the  ordinary  form  of  the  trouble  is  dependent 
upon  the  hereditary  origin  of  the  former,  while  the  difference  between 
each  other  is  the  result  of  the  relatively  greater  severity  of  the  dis- 
ease process  in  the  lateral  or  the  posterior  tracts. 

Symptoms. — Ataxia  is  not  only  the  earliest,  but  it  is  the  domi- 
nant symptom  throughout  the  entire  course  of  the  disease.  It  usually 
attacks  the  lower  limbs  first  and  the  upper  limbs  later.  The  reverse 
occasionally  takes  place.  Before  the  ataxia  is  fully  established  there 
are  generally  preceding  symptoms,  such  as  weakness,  unsteadiness, 
oscillation  and  staggering  in  the  gait,  even  frequent  falling.  The 
ataxia  is  not  exactly  like  that  of  tabes,  jerky,  irregular,  with  stamping 
of  the  heel  first.  It  more  nearly  resembles  a  disturbance  of  equilibrium, 
a  cerebellar  ataxia,  for  which  reason  Charcot  used  to  speak  of  it  as  a 
demarche  tabeto-cerebellense.  It  is  marked  even  when  the  patient  is 
standing  still.  It  is  not  increased,  however,  by  closing  the  eyes,  prob- 
ably because  the  earh-age  of  the  patient  is  such  that  he  has  not  ac- 
quired the  habit  of  using  his  eyes  yet  in  maintaining  his  equilibrium. 

As  I  have  intimated  the  characteristic  differences  between  the 
symptoms  of  this  disease  and  tabes  are  due  to  the  associated  degenera- 
tion in  the  lateral  columns  and  the  occurrence  of  the  disease  in  young, 
undeveloped  individuals. 

Eclampsia  and  hysterical  attacks  have  preceded  and  accompanied 
the  ataxia  in  a  few  cases.  In  many  there  are  painful,  cramp-like 
spasms  in  some  of  the  muscles.  The  face,  neck,  hands  and  feet  have 
thus  been  involuntarily  contracted.  Tremor,  not  of  the  intentional 
type,  but  rather  simple  oscillations,  is  not  infrequent  in  various  parts 
of  the  body.  Choreiform  movements  are  almost  constant  in  accom- 
panying the  ataxia  and  may  appear  in  any  group  of  muscles.  In  ad- 
vanced cases  decided  weakness  and  more  or  less  paralysis  are  com- 
mon features.  The  gait,  which  has  been  difficult  from  the  first  on 
account  of  the  incoordination,  later  on  becomes  so  afifected  that  walk- 
ing is  an  absolute  impossibility,  and  the  patient  keeps  to  his  bed.  The 
paralysis  and  subsequent  contractures  add  to  this  unfortunate  condi- 
tion. In  many  cases  curvature  of  the  spine  takes  place  and  marked  dor- 
sal flexion  of  the  toes.  Talipes,  chiefly  of  the  equino-varus  type  is 
frequent.  The  knee-jerks  are  lost  in  pure  cases  of  Friedreich's  ataxia, 
which  is  a  most  important  indication  of  the  disease.  In  the  few  cases 
in  which  they  have  been  exaggerated,  the  trouble  was  probably  of 
cerebellar  origin.  Exceptionally  ankle-clonus  has  been  observed.  The 
cutaneous  reflexes  are  all  intact  or  only  very  rareh'  altered.  As  there 
are  scarcely  any  sensory  manifestations  the  ataxia  and  the  altered  ten- 
don reflexes  cannot  be  attributed  to  them.  The  muscles  are  not  typ- 
ically atrophied,  though  there  ma}-  be  some  slight  wasting  late  in  the 
disease.  Their  electrical  contractibility  is  not  in  the  least  modified. 
Coldness  of  the  surface  of  the  body,  cyanosis,  oedema,  chilblains,  thick- 
ening of  the  skin,  development  of  adipose  tissue  and  even  bedsores 
have  been  reported  as  among  the  rare  vasomotor  and  trophic  symptoms, 
and  as  particularly  late  in  the  disease. 

Sensory  symptoms  are  not  entirely  wanting  though  they  are  so 
rare  as  to  I'ustifv  the  general  statement  that  sensation  is  normal   in 


THE  NEURONIC  DISEASES 


449 


Friedreich's  disease.  The  absence  of  the  characteristic  pains  of  tabes 
distinguishes  it.  And  yet  headache  has  preceded  and  accompanied  the 
ataxia.  When  the  disease  is  well  established,  occasional  dull  pains  are 
noticed  elsewhere.  There  may  be  tenderness  over  the  spine.  The 
muscles  may  be  subjected  to  painful  cramps.  Pains  in  the  articulations 
have  been  complained  of.  The  cutaneous  sensibility  is  not  generally 
involved.  Formication,  tingling  and  numbness  may  be  present  and 
even  anaesthesia.     The  muscle-sense  is  usually  intact. 

Disturbance  of  the  speech  is  a  frequent  trait  and  is  one  of  the  most 
prominent  of  the  bulbar  symptoms.  It  is  generally  a  late  symptom 
and  appears  about  the  same  time  as  nystagmus,  another  most  impor- 
tant symptom.  It  is  a  true  dysarthria.  The  speech  is  slow  and  labor- 
ed, irregular  and  mangled.  Sometimes  it  is  rapid  and  slurring,  typic- 
ally scanning,  jerky,  or  confluent.     The  trouble  may  at  times  be  very 

FIGURE  91. 


Position  of  the  great  toe  and  condition 
of  the  foot  in  Friedreich's  disease.  (After 
Brissaud.) 

marked.  At  other  times  it  is  scarcely  noticeable.  On  account  of  the 
rushing,  tumbling  character  of  it  Seeligmuller  spoke  of  it  in  one  of 
his  cases  as  an  "ataxia  of  thought,"  as  the  patient  seemed  to  begin  a 
new  sentence  before  finishing  the  old  one.  The  tongue  frequently  ex- 
hibits a  tremor,  an  oscillatory  movement  and  a  peculiar  curling  and 
uncurling.     Mastication  and  deglutition  are  not  generally  affected. 

The  chief  eye  symptom  is  nystagmus.  Though  this  is  a  late  symp- 
tom it  is  a  most  significant  one.  It  is  less  common  than  the  speech 
disorders,  though  the  two  usually  appear  together.  Static  nystagmus 
has  been  observed  in  a  few  cases.  Strabismus  has  been  mentioned  and 
also  a  slight  degree  of  ptosis.  The  pupillary  reactions  and  the  vision 
are  undisturbed  in  the  vast  majority  of  cases,  which  again  distinguishes 
Friedreich's  ataxia  from  tabes  dorsalis.  The  changes  in  the  color 
fields  and  the  blindness  that  have  been  noted  have  been  so  rare  that 
they  probably  represented  some  complication. 

The  mental  faculties  are  but  little  affected,  a  feature  of  Fried- 
reich's disease  which  helps  to  differentiate  it  from  disseminated  sclero- 
sis.    There  may  be  some  amnesia  and  in  rare  instances  an  arrest  of 


450  THE  NEURONIC  DISEASES 

mental  development.  Vertigo  is  rather  a  frequent  symptom,  occurring 
both  early  and  late  in  the  disorder.  It  may  be  associated  with  mere 
giddiness,  fainting  or  actual  loss  of  consciousness.  It  may  come  on 
while  the  patient  is  standing  or  reclining. 

Visceral,  secretory  and  sexual  disorders  are  rare  and  are  probably 
mere  accidents. 

Diagnosis. — The  essential  points  to  be  noted  in  the  diagnosis  of 
Friedreich's  form  of  hereditary  ataxia  are  the  hereditary  and  fa»iilial 
character  of  the  disease,  the  early  age  at  which  the  symptoms  first 
appear,  the  peculiar  ataxia  starting  in  the  legs  and  extending  to  the 
arms,  the  speech  disturbances,  nystagmus,  curvature  of  the  spine, 
talipes  and  late  paralysis.  With  these  symptoms  it  is  also  to  be  noted 
that  usually  the  patella  reflexes  are  lost,  sensory  symptoms  are  absent 
or  very  slight,  trophic  phenomena  are  not  marked,  vision  and  the  eyes 
generally  are  intact,  the  intellect  is  clear,  and  the  visceral  and  circu- 
latory systems  show  no  disorder. 

The  two  diseases  with  which  Friedreich's  ataxia  is  liable  to  be 
confused  are  tabes  dorsalis  and  disseminated  sclerosis.  Locomotor 
ataxia  follows  a  history  of  syphilitic  infection  and  appears  later  in  life. 
It  does  not  reveal  any  direct  heredity  and  only  slightly  an  indirect.  It 
is  very  exceptional  for  the  offspring  of  tabetic  parents  to  suffer  from 
Friedreich's  disease.  Tabes  is  to  be  distinguished  by  the  more  char- 
acteristic ataxic  gait,  the  increase  of  Romberg's  phenomenon  when 
the  eyes  are  shut,  the  marked  pains  and  other  sensory  symptoms,  the 
crises,  the  constant  loss  of  the  knee-jerk,  the  Argyll-Robertson  pupil, 
optic  atrophy  and  the  more  prominent  late  arthritic  and  other  trophic 
symptoms. 

Ataxic  paraplegia  is  an  adult  disease,  occurring  usually  between 
the  ages  of  thirty  and  forty.  It  does  not  appear  like  Friedreich's  dis- 
ease in  several  members  of  the  same  family.  The  patella  reflexes  are 
exaggerated,  nystagmus  is  w^anting  and  there  is  no  marked  speech 
trouble.  It  is  to  be  remembered,  however,  that  Friedreich's  malady  is, 
like  ataxic  paraplegia,  a  mere  combined  sclerosis  of  the  posterior  and 
lateral  columns.  The  differences  between  the  two  are  the  result  of 
the  differences  in  the  ages  between  the  two  sets  of  patients,  the  heredi- 
tary influence,  and  the  greater  intensity  of  the  disease  process  in  the 
one  or  the  other  column  of  the  cord. 

Some  cases  of  Friedreich's  disease  reveal  cerebral  and  cerebellar 
symptoms.  Indeed  it  has  been  thought  by  some,  that  the  primary  trou- 
ble originates  in  the  cerebellum.  They  are  not  typical  cases,  however, 
though  at  times  it  is  extremely  difficult  to  differentiate  them. 

Simple  developmental  inhibition  of  the  cerebellum,  an  agenesis, 
such  as  Marie  has  described,  can  but  rarely  be  separated.  And  yet  in 
these  rare  cases  the  reflexes  may  be  exaggerated,  the  ocular  muscles 
may  be  paralyzed,  the  pupils  may  be  rigid,  the  vision  affected  and  the 
deglutition  markedly  disturbed. 

Tumor  of  the  cerebellum  produces  headache,  optic  neuritis,  ver- 
tigo, vomiting  and  epileptiform  attacks.  The  gait  is  "drunken"  and  is 
distinctly  cerebellar.  There  is  no  spinal  sclerosis  and  other  deformities 
such  as  are  observed  in  Friedreich's  trouble. 


THE   NEURONIC   DISEASES  45 1 

Disseminated  sclerosis  sometimes  can  scarcely  be  differentiated, 
especially  when  the  nystagmus,  tremor  and  speech  disorders  are  pres- 
ent. Multiple  sclerosis  is  an  adult's  disease,  however,  developing  usu- 
ally after  twenty,  it  is  not  under  hereditary  influence,  and  it  progresses 
remittently.  The  nystagmus  is  marked  and  the  speech  is  more  scan- 
ning in  character  than  it  is  in  hereditary  ataxia.  Other  distinguishing 
symptoms  of  multiple  sclerosis  that  aid  in  the  differential  diagnosis  are 
exaggeration  of  the  knee-jerks,  the  ankle-clonus,  the  intentional  tre- 
mor, the  rhythmic  oscillations,  the  rigidity  and  spasticity  of  the  limbs, 
the  disturbances  of  the  mtellect,  and  the  epileptiform  and  apoplecti- 
form attacks. 

Prognosis  and  Course.^ — Friedreich's  disease  is  a  chronic  and 
progressive  affection.  It  may  last  twenty,  thirty  or  forty  years.  It 
never  remits,  though  at  times  it  seems  to  cease  progressing  for  a  while. 
The  symptoms  may  abate  and  thus  raise  false  hopes  of  a  cure.  The 
patient,  as  a  rule,  ultimately  becomes  bedridden  and  dies  of  nephritis, 
decubitus  or  some  intercurrent  malady.  In  regard  to  the  duration  of 
life  the  prognosis  is  favorable ;  m  regard  to  cure  it  is  absolutely  bad. 

Treatment. — There  is  no  direct  treatment  known  that  will  mod- 
ify the  progress  of  the  malady.  Tonics  are  always  in  order,  of  course, 
as  well  as  good  regimen  and  proper  hygiene.  Nitrate  of  silver,  arsenic, 
phosphorus,  iodine,  zinc,  have  all  been  tried  and  found  wanting.  In 
one  case  the  constant  current  applied  to  the  spine  produced  some  bene- 
fit. It  is  a  measure  to  be  used,  however,  very  guardedly.  Sympto- 
matic treatment  includes  electricity  and  massage  for  the  weakening 
muscles,  a  jacket  for  the  curvature  of  the  spine,  and  the  closest  atterL- 
tion  to  all  the  functions  of  the  viscera. 

AMAUROTIC   FAMILY  IDIOCY. 

In  1896  Sachs  gave  this  name  to  a  hereditary  disease  in  which 
idiocy,  spastic  paralysis  and  blindness  constitute  the  cardinal  symp- 
toms. On  account  of  the  eye  trouble,  Tay,  in  i88i,  first  called  atten- 
tion to  the  cases.  The  first  autopsy  on  a  case  was  made  by  Sachs,  in- 
1887,  who  at  that  time  attributed  the  manifestations  to  a  simple  agen- 
esis corticalis.  Later  on  Kingdon  reported  an  autopsy  upon  a  case 
and  was  the  first  to  attract  attention  to  the  similarity  between  the  cases 
noted  early  by  the  ophthalmologists  and  those  reported  by  Sachs. 
Cases  and  studies  of  the  disease  have  since  been  reported  by  Claiborne, 
Patrick,  Kuh,  Jacobi,  Hirsch,  Peterson,  Koplik,  Cotton,  Hirschberg 
and  others.    About  thirty  or  more  cases  have  now  been  put  upon  record. 

Etiology. — The  affection  seems  to  be  distinctly  hereditary  and 
of  the  familial  type  of  troubles.  Peterson  reported  three  members  of 
one  family  afflicted  with  it.  This  would  seem  to  declare  most  posi- 
tively for  an  inherited,  rather  than  a  mere  congenital,  cause,  as  would 
also  the  absence  of  all  birth  difflculties  and  the  presence  of  a  progres- 
sive degeneration  of  the  cellular  elements  of  the  entire  nervous  sys- 
tem. The  children  are  of  the  Jewish  race  generally,  though  not  ex- 
clusively so.  They  are  born  normally,  and  at  birth,  and  for  the  first 
few  months  thereafter,  seem  in  every  way  to  be  healtlw.     The  dis- 


452  THE   NEURONIC   DISEASES 

order  makes  its  appearance,  however,  in  the  first  six  months  of  Hfe  as 
a  rule. 

Pathology  and  Pathogenesis. — The  autopsies  have  not  been  nu- 
merous enough  to  enable  us  to  form  a  definite  pathology.  In  some 
cases  the  findings  have  suggested  a  simple  arrest  of  development;  in 
others  an  infective  process,  possibly  of  a  meningo-encephalitic  type ; 
and  in  still  others  a  meningitis.  No  vascular  or  inflam.matory  changes 
have  actually  been  discovered  and  if  they  were  at  all  present  before 
birth  they  must  have  completely  disappeared.  There  are  no  signs  of 
inherited  syphilis  or  other  diathesis.  Hydrocephalus  of  a  pronounced 
character  has  been  noted.  The  entire  nervous  system  reveals  a  con- 
dition of  progressive  degeneracy.  In  this  connection  it  is  suggestive  that 
many  of  these  children  exhibit  external  degenerative  stigmata. 

A  dispute  wages  around  the  question  as  to  the  primary  or  sec- 
ondary nature  of  the  neuronic  degeneration.  Many  pathologists  feel 
that  simple  agenesis  will  not  wholly  account  for  it.  There  is,  as  Kuh 
puts  it,  "a  distinctly  retrogressive  and  destructive  change."  Hirsch 
and  Jacobi  suspect  that  an  infection,  possibly  derived  from  the  moth- 
er's milk,  is  to  be  blamed  for  the  trouble.  Sachs  reported  two  cases, 
in  opposition  to  this  theory,  that  were  not  breast  fed.  All  such  ex- 
planations have  to  combat  the  apparently  hereditary  and  frequently 
familial  features  of  the  disease.  In  Cotton's  case,  the  father's  cousin's 
only  child  died  in  convulsions  at  twenty  months,  blind  and  idiotic.  I 
have  mentioned  Peterson's  three  cases  in  one  family. 

Symptoms. — Three  great  symptoms  stand  out  with  special  prom- 
inence in  amaurotic  idiocy,  namely,  the  mental  deterioration,  the  spastic 
paralysis  of  all  four  limbs  and  the  blindness  from  optic  atrophy,  with  a 
peculiar  appearance  of  the    macula  lutea. 

During  the  first  five  or  six  months  of  life  the  child  seems  normal 
in  every  respect.  Then  it  is  noticed  that  it  gradually  begins  to  fail 
in  strength,  to  be  disinclined  to  move,  and  to  show  a  falling  off  of  the 
intelligence.  It  grows  apathetic,  is  at  times  restless  and  silly.  In  some 
cases  convulsions  and  epileptiform  seizures  have  occurred.  Gradually 
it  becomes  stupid  wnth  such  a  hyperacuity  of  the  reflexes  that  a  sudden 
noise  or  a  gentle  slap  will  cause  a  great  start,  even  a  convulsion. 

During  these  mental  changes  there  is  an  increasing  spastic  paraly- 
sis creeping  over  the  muscles  of  the  body.  The  head  and  trunk  can- 
not be  held  erect,  and  the  voluntary  movements  are  distinctly  athetoid 
in  character.  The  associated  movements  and  the  reiiexes  are  all  mark- 
edly exaggerated.  Tonic  contractions  occur  in  the  whole  musculature 
upon  the  slightest  stimulation.  The  general  spasticity  and  reflex  ex- 
aggerations point  to  profound  degenerative  changes  in  the  upper  mo- 
tor segment.     Towards  the  end  there  is  complete  paralysis. 

The  paralvtic  svmptoms  involve  the  eyes  also.  Nystagmus,  strab- 
ismus and  unequal  pupils  may  all  be  expected.  Amblyopia  is  thus 
present  at  first  but  as  the  optic  atrophy  proceeds  it  disappears  before 
the  growing  amaurosis.  The  appearance  of  the  optic  disc  is  pathog- 
nomonic in  this  disease  and  has  been  graphically  described  by  Tay, 
Wadsworth,  Carter.  Beard,  Wescott  and  others.  It  is  so  characteris- 
tic that,  as  a  symptom  of  a  general  disorder,  it  stands  alone,  "grand, 


PLATE    II. 

Fundus  ocuU  in  amaurotic  family  idiocy.     Drawn 
from  life.      (iVfter  Beard.) 


THE  NEURONIC  DISEASES  '     453 

gloomy  and  peculiar."  The  atrophy  of  the  optic  nerve  and  retina  does 
not  appear  to  be  as  pronounced  as  one  would  expect.  The  change  in 
and  around  the  macula  lutea  is  the  absolutely  diagnostic  manifesta- 
tion. Beard  describes  it  thus :  Surrounding  the  fovea  centralis,  con- 
centric with  it,  and  two  or  three  times  its  size,  is  a  liver-colored  disc. 
This  disc  is  the  center  of  a  zone  of  grayish-white  which  gradually  fades 
away  into  the  normal  red-orange  of  the  eye  ground.  As  clear  cut  as 
a  coin  is  this  livid  disc.  It  is  not  irregular  in  outline  as  is  the  case 
in  acute  inflammatory  conditions,  where  the  surrounding"  retina  is  infil- 
trated, nor  is  it  cherry-red  or  carmine,  as  in  those  cases,  but  is  dis- 
tinctly brownish.  It  is  larger  than  the  fovea ;  that  is  to  say,  instead 
of  marking  the  area  which  is  occupied  by  the  cones  alone,  it  marks 
that  which  is  devoid  of  the  ganglion  cells.  The  whitish  zone  that  sur- 
rounds the  center  is  also  highly  characteristic.  It  is  nebulous  rather 
than  cloudy.  It  is  almost  white  at  the  circumference  of  the  liver- 
colored  disc,  thence  gradually  thins  away  to  nothing,  but  is  translucent 
and  exhibits  some  color  throughout.  It  does  not  obscure  the  retinal 
vessels  which  enter  it.  It  only  serves  to  make  them  more  distinct  by 
contrast,  so  that  one  is  able  to  trace  the  tiniest  of  them  right  up  to  the 
central  spot. 

In  addition  to  those  that  have  just  been  described,  other  symp- 
toms that  have  occasionally  been  noted  in  the  disease  are  muscular 
flaccidity,  tremor,  normal  and  even  subnormal  reflexes,  dysphagia, 
vomiting,  hyperacusis  and  hyperaesthesia.  Some  of  the  children  have 
been  badly  nourished  and  rachitic.  The  head  has  been  enlarged  and 
the  fontanelles  still  open.  In  some  cases  atrophy  of  the  muscles  has 
been  observed  in  one  part  of  the  body  while  marked  rigidity  was  noted 
in  another  part.  Occasionally  the  tendency  toward  a  localization  of  the 
symptoms,  such  as  in  a  hemiplegic  condition,  has  been  strongly  sug- 
gestive of  a  gross,  focal  lesion.  The  pulse  rate  is  often  rapid ;  the 
temperature  is  practically  normal. 

Diagnosis. — Given  a  case  of  idiocy  with  a  general  spastic  J>araly- 
sis  and  the  typical  appearance  of  the  fundus  oculi,  the  diagnosis  is  posi- 
tive and  easy.  Unless  an  ophthalmoscopic  examination  be  made,  the 
condition  might  well  be  mistaken  lor  a  diplegic  one  due  to  some  form 
of  prerfatal  gross  vascular  lesion  or  Striimpell's  type  of  meningo- 
encephalitis or  polioencephalitis. 

In  dealing  with  all  of  these  various  forms  of  infantile  neuronic 
degenerations  we  are  on  the  borderline  between  those  that  are  due  to 
mere  developmental  incapacity  and  those  that  owe  their  deterioration 
to  some  more  gross,  external  influence,  like  hemorrhage,  inflammation 
or  vascular  obstructions.  Hence  the  difficulty  in  always  determining 
the  pathogenesis  of  these  cases  and  the  still  more  discouraging  diffi- 
culty of  knowing  how  always  to  make  an  accurate  diagnosis. 

On  account  of  the  heredity,  and  above  all,  on  account  of  the 
unique  ocular  presentation,  I  am  inclined  to  lean  towards  the  view 
that  this  disease  is  a  fundamental  developmental  defect,  one  in  which 
the  newly-coined  word  of  Gowers,  abiotrophy,  could  be  applied. 

All  cases  diagnosed  as  amaurotic  family  idiocy  in  which  the 
typical   eye   grounds    were   not   present,    and   especially   all    cases   in 


454  THE   NEURONIC   DISEASES 

which  focal  symptoms  were  pronounced  and  not  typical  e}-e  grounds 
present,  would  be  open  to  very  great  criticism.  Infantile  hemiplegia 
and  diplegia  would  be  more  of  a  probability  for  such  cases.  Without 
the  typical  eye  ground,  amaurotic  family  idiocy  may  be  mistaken  for 
rachitic  pseudo-paralysis,  cerebellar  tumor,  tubercular  marasmus  and 
congenital  blindness  in  an  idiot. 

Prognosis. — This  is  decidedly  bad.  The  children  all  die  sooner 
or  later,  usually  in  a  few  months  or  a  year  or  two,  from  convulsions 
and  general  marasmus.  Herein  this  disease  differs  from  the  diplegic 
cases.  The  early  death  has  even  been  spoken  of  as  its  fourth  car- 
dinal symptom,  so  uniformly  certain  is  it.  This  again  suggests  to  my 
mind  the  profound  biological  origin  of  the  degeneration  here,  as  dis- 
tinguished from  the  secondary  degeneration  that  accompanies  encepha- 
litic  and  vascular  processes.  It  is  in  harmony  with  what  I  have  several' 
times  pointed  out  before,  namely,  that  the  prognosis  of  the  primary 
neuronic  degenerations  are  almost  uniformly  bad ;  whereas  the  prog- 
nosis of  the  vascular  troubles  is,  comparatively  speaking,  good. 

Treatment.- — There  is  no  treatment  for  this,  any  more  than  there 
is  for  any  of  the  other  forms  of  primary,  progressive  neuronic  degen- 
eration. 

MULTIPLE  XEURITIS  AXD  NEUROMYELITIS. 

In  this  place  would  naturally  fall  some  of  the  cases  of  toxic  and 
infectious  polyneuritis  and  ascending  neuromyelitis.  The  latter  are 
exceedingly  rare  and  their  existence  doubted  by  some  pathologists.  It 
is  believed  that  a  toxic  poliomyelitic  primary  degeneration,  rather  than 
an  ascending  degeneration,  is  the  pathological  basis.  In  many  of  the 
cases  of  peripheral  neuritis,  the  lesion  is  believed  to  be  a  primary  de- 
generation, without  any  interstitial  inflammation,  the  result  of  the  pro- 
found toxamia.  Lesions  are  found  of  a  degenerative  sort  in  the  cord 
and  even  in  the  brain  in  these  cases,  so  that  the  view  is  fast  gaining 
ground  that  these  cases  represent  a  diffuse  and  chronic  constitutional 
or  general  intoxication  with  a  wide  neuronic  degenerative  process  tak- 
ing place  throughout  the  entire  nervous  apparatus.  The  special  changes 
in  the  peripheral  nerve  filaments  are  believed  to  be  due  to  the  dis- 
turbed nutrition  in  the  anterior  horn  cells  and  posterior  ganglia,  just 
as  we  believe  is  the  case  in  other  forms  of  infectious  trouble.  We  are 
not  ready,  however,  to  relinquish  the  idea  entirely  that  the  toxin  may 
act  also  directly  upon  the  nerve  terminals  and  so  provoke  a  local  de- 
generation there.  All  of  this  of  course  does  not  preclude  the  idea  that 
some  of  the  polyneuritides  are  toxic  interstitial  inflammations  with 
secondary  neuronic  degeneration.  This  will  be  referred  to  again  un- 
der the  head  of  multiple  neuritis  discussed  in  the  section  devoted  to 
diseases  of  the  peripheral  nen^es. 

PROGRESSIVE  INTERSTITIAL  HYPERTROPHIC  NEURITIS 

OF  INFANTS. 

This  •  is  an  interesting  and  rare  aft"ection,  described  recently  by 
Dejerine  and  Sottas,  which  lies  between  the  progressive  muscular 
atrophies  on  the  one  hand  and  the  frank,  interstitial  neuritides  on  the 


THE   NEURONIC   DISEASES  455 

other.  It  seems  to  be  a  family  disease  and  it  always  begins  in  child- 
hood. The  clinical  picture  resembles  a  combination  of  locomotor 
ataxia  with  progressive  muscular  atrophy,  so  much  so  that  Striimpell 
believed  the  cases  were  nothing  more  than  combinations  of  Fried- 
reich's disease  with  the  hereditary  peroneal  type  of  progressive  muscu- 
lar atrophy.  The  name  indicates  Dejerine's  own  idea,  however,  that  it 
is  a  form  of  interstitial  neuritis.  The  post  mortem  findings  were  a 
chronic  interstitial  neuritis  decreasing  in  severity  from  the  periphery 
to  the  center,  and  involving  the  posterior  roots.  There  was  also  a 
sclerosis  of  both  Goll's  and  Burdach's  columns.  Nerves  were  hyper- 
trophied  and  indurated. 

Symptomatically  there  were  lightning  pains,  various  sensory  dis- 
turbances, an  ataxic  gait,  sluggish  pupils,  myosis,  nystagmus,  static 
ataxia  and  a  kypho-scoliosis.  There  were  no  electrical  reactions  of 
degeneration  though  there  was  a  quantitative  decrease  in  the  electrical 
excitability. 


SECTION   C. 


THE   NON-NEURONIC   DISEASES. 


Interstitial,  Inflammatory  Troubles  with  Secondary  Neu- 


ronic Degenerations. 


THE  NATURE  OF  THE  NON-NEURONIC  DISEASES. 

In  our  earlier  studies  upon  the  histology  of  the  Nervous  System, 
we  found  that  its  wonderful  network  of  neurones,  making 
up  the  innumerable  pathways  along  which  the  afferent  and 
efferent  impulses  travel,  was  supported  by  a  scaffolding,  so  to  speak, 
of  connective  tissue,  neuroglia,  bloodvessels,  lymphatics  and  epithe- 
lium. The  neuroglia  we  remarked  was  a  peculiar  epiblastic  tissue  that 
belonged  solely  to  the  nervous  system.  Its  function  is  purely  susten- 
tacular  and  it  is  capable  of  undergoing  hyperplasia  and  degeneration. 
An  illustration  of  the  former  is  the  gliomata  that  are  seen  in  the 
gray  and  white  substance  of  the  brain,  the  cranial  nerves  and  the 
retina.  These  unique  neurotic  growths  break  down  easily  sometimes 
and  leave  huge  cavities.  Gliosis  therefore  is  a  degenerative  process, 
affecting  a  special  variety  of  extra-neuronic  elements  and  causing 
them  to  press  upon  and  infiltrate  among  the  nerve-cells  to  their  great 
detriment. 

Excluding  the  neuroglia,  the  extra-neuronic  tissue  of  the  nervous 
system  is  exactly  the  same  as  it  is  in  every  other  part  of  the  body. 
The  connective-tissue  elements  and  the  changes  they  undergo,  the 
bloodvessels  and  the  disturbances  which  they  are  subjected  to,  differ 
in  no  respect  here  from  what  they  do  elsewhere.  The  inflammations, 
hemorrhages,  neoplastic  over-growths  and  infective  processes  are  in 
themselves  the  same  in  the  brain  as  they  are  in  the  lungs.  A  neuritis, 
as  an  inflammatory  process,  differs  in  no  respect  from  an  interstitial 
nephritis.  An  intra-cranial  sarcoma  is  the  same  sort  of  a  sarcoma  that 
appears  in  the  foot.  The  only  thing,  therefore,  that  makes  these  dis- 
eases, of  the  extra-neuronic  type,  especially  interesting  to  the  neurolo- 
gist is,  that  when  they  occur  in  the  nervous  system,  they  necessarily 
damage  the  neighboring  neurones.  The  damage  is  usually  of  a  me- 
chanical sort  and  represents  compression,  laceration  and  distortion. 
This  is  seen  in  the  inflammatory  and  hemorrhagic  conditions.  Some- 
times, however,  they  shut  off  the  nourishment  of  the  neurones.  This 
is  observed  in  the  embolic  and  thrombotic  conditions.     Sometimes  they 


458  THE  XOX-NEURONIC  DISEASES 

even  twist,  stretch  and  displace  the  neurones  in  such  a  way  that  they 
cannot  functionate  properly.  This  is  illustrated  in  the  infiltrations  of 
the  gliomata  and  other  neoplasms. 

Whatever  the  nature  of  the  trouble  may  be  in  these  extra-neu- 
ronic  structures,  the  damage  of  the  neurones  themselves  is  strictly  a 
secondarx  affair.  The  degeneration  is  therefore  often  spoken  of  as 
secondary.  The  disease  which  primarily  starts  it,  and  which  is  a  dis- 
ease entirely  outside  of  the  neurones,  is  very  properly  therefore  spoken 
of  as  a  non-nenronic  disease. 

As  inflammation  is  really  a  regressive  process,  an  effort  of  nature 
to  rid  and  protect  herself  from  some  noxious  influence,  it  tends  always 
to  disappear  as  soon  as  the  harmful  agent  has  been  banished.  It  is 
thus  more  or  less  of  an  acute  and  temporary  process  and  when  prop- 
erly assisted  it  tends  always  toward  recovery.  In  this  way  the  prog- 
nosis of  the  inflammatory  diseases  of  the  nervous  system  is  favorable. 

It  must  not  be  confused  with  the  very  unfavorable  prognosis  of 
the  neuronic  degenerations,  whether  these  be  primary  or  secondary. 

Hemorrhages,  neoplasms,  etc.,  each  have  their  own  special  prog- 
nosis, which  may  be  good,  bad,  or  indift'erent,  but  which  should  be  care- 
fully distinguished  from  the  prognosis  of  the  mere  resulting  degenera- 
tion in  the  damaged  neurones. 

In  a  broad  sense  then,  we  may  say  that  the  prognosis  and  treat- 
ment of  the  non-neuronic  diseases  are  most  favorable.  The  outlook  in 
regard  to  the  secondary  neuronic  changes  which  these  diseases  pro- 
duce, will  depend  entirely  upon  how  severe  and  destructive  the  pri- 
mary disease  was  in  its  action  upon  the  neurones. 

There  are  all  grades  of  disturbance  that  may  be  produced  in  the 
neuronic  elements ;  and  unless  one  keeps  this  fact  well  in  mind,  he  will 
find  himself  treating  hopeless  and  hopeful  cases  all  alike  with  the  ob- 
vious consequences.  If  an  arterio-sclerosis,  for  instance,  is  amenable 
to  treatment  at  all.  the  neurasthenic  manifestations  that  often  accom- 
pany it  may  be  made  to  disappear  by  the  treatm.ent.  A  neurasthenia 
that  is  due  to  a  defective  heredity,  however,  and  which  really  repre- 
sents an  actual  nervous  incapacity  from  birth,  cannot  be  expected  to 
be  removed  by  any  sort  of  treatment.  The  trouble  in  the  former  case 
was  a  mere  secondary  result  of  mild  degree  from  a  non-neuronic  dis- 
ease. Its  prognosis,  therefore,  was  good,  and  its  treatment  satisfac- 
tor3^  In  the  latter  case  the  trouble  in  the  neurones  is  essential  and 
primary ;  it  is  a  positive  neuronic  defect  or  degenerative  condition ;  and 
hence  it  is  irremediable  by  any  human  agency.  It  is  too  common  an 
error,  and  one  that  oft  leads  to  pessimistic  views  in  regard  to  neurol- 
ogy, to  say  nothing  of  treatment,  to  confound  the  prognosis  of  these 
non-neuronic  diseases  with  the  prognosis  of  their  secondary  results,  the 
neuronic  secondary  degenerations. 

For  the  sake  of  convenience,  the  non-neuronic  diseases  are  usu- 
ally divided  into  those  of  the  Spinal  Cord,  the  Peripheral  Nerves  and 
the  Brain.  That  this  is  an  artificial  division  is  shown  by  the  fact  that 
many  of  these  diseases  imiplicate  the  whole  cerebrospinal  axis  at  the 
same  time,  as,  for  instance,  leptomeningitis  and  disseminated  sclerosis. 
As  the  lesion,  however,  is  more  or  less  focal,  and  as  the  brain  and 


THE    NON-NEUROXIC    DISEASES  459 

spinal  cord  have  each  their  own  localization  symptoms,  it  is  conve- 
nient to  divide  these  diseases  in  accordance  with  these  gross  anatomical 
■divisions. 

The  order  that  will  be  followed  in  discussing  them  will  begin  with 
the  bony  encasement,  taking  up  next  the  membranes,  and  finally  the 
■connective  tissues  and  bloodvessels.  At  this  point  the  neurones  them- 
selves will  have  been  reached  and  there  will  be  nothing  left  but  the 
neuronic  degenerative  troubles  which  were  treated  of  first  in  the  book, 
because  they  constitute,  in  their  last  analysis,  the  only  true  specific 
nervous  diseases. 


PART 


Non-Neuronic  Diseases  of  the  Spinal  Cord. 


ANATOMY  AND  PHYSIOLOGY  OF  THE  SPINAL  CORD. 
SPINAL  LOCALIZATION  AND  TOPOGRAPHY.  SYMP- 
TOMS OF  DISEASE  OF  THE  SPINAL  CORD.  LUMBAR 
PUNCTURE. 

Anatomy  and  Physiology. — It  is  unfortunate,  from  the  neurolog- 
ical point  of  view,  that  the  artificial  division  of  the  nervous  system  into 
Brain,  Spinal  Cord  and  Nerves  is  so  firmly  engrafted  upon  the  minds 
of  the  profession.  These  divisions  are  not  made  upon  a  neurological 
basis,  but  upon  the  bony  encasements  and  other  gross  factors.  Essen- 
tially, neither  in  anatomy  nor  in  physiology,  does  the  brain  differ  from 
the  spinal  cord.  The  cells  and  their  inter-connections  are  arranged 
and  functionate  in  practically  the  same  way.  Their  processes  inter- 
lace and  run  back  and  forth  in  such  a  manner  between  the  brain  and 
cord  that  the  cerebrospinal  axis  is  practically  a  unit.  The  nerves  are 
merely  the  processes  that  connect  this  unit  with  the  outlying  parts  of 
the  body.  They  are  not  separate  structures  but  merely  extensions  from 
and  into  the  cerebrospinal  organ.  This  cerebrospinal  organ  is  made 
up  of  a  series  of  bunches  of  neurone  bodies  and  in  this  way  carry  out 
the  dictum  of  Owen  when  he  declares  that  a  vertebrate  animal,  such 
as  man  is,  is  nothing  but  a  clothed  sum  of  segments. 

The  segmental  character  of  the  bony  spine  is  obvious  enough  and 
indicates  an  evolution  out  of  a  lower  or  articulate  form  of  life.  '  The 
collections  of  neurone  bodies,  the  ganglionic  masses,  that  lie  side  by 
side  serially  all  along  the  cerebrospinal  axis,  and  which  make  up  the 
so-called  gray  matter  of  the  brain  and  cord,  indicate  also  the  seg- 
mental character  of  the  central  nervous  system.  In  the  cord  this  is 
almost  as  obvious  as  it  is  in  the  bony  spine.  It  is  suggested  in  the 
longitudinal  series  of  spinal  nerve-roots  which  have  their  origin  from 
a  series  of  super-imposed  discs.  In  the  brain  the  same  serial  disc-like 
arrangement  obtains,  but  there  it  has  been  elaborately  broken  up  and 


460  THE  NON-NEURONIC  DISEASES 

the  ganglionic  masses  have  been,  in  the  course  of  evolutionary  devel- 
opment, scattered  about  in  order  to  accommodate  the  enormously  devel- 
oped condition  of  these  frontal  ganglia  within  the  confined  space  ta 
which  they  are  limited  by  the  more  slowly  developing  skull. 

In  its  essential  architecture  the  brain  is  only  .an  enormous  develop- 
ment of  the  frontal  portion  of  the  spinal  cord,  and  the  spinal  cord  is 
but  a  series  of  little,  primitive  brains  lying  side  by  side  all  the  way 
along  the  spinal  canal. 

To  bring  about  harmony  of  action  in  this  series  of  ganglionic  de- 
posits of  neurone-cell  bodies,  the  latter  must  necessarily  be  joined,  at 
least  physiologically,  together.  They  are.  The  processes  from  one 
ganglionic  set  of  cells  run  up  and  down  and  here  and  there  to  arborize 
around  the  neurone  cell-bodies  in  the  neighboring  and  distant  gangli- 
onic deposits.  Some  of  these  processes  run  through  the  nearby 
ganglia  to  reach  the  more  distant  ones,  and  in  this  way  constitute  the 
so-called  gray  commissures.  Some  of  them  run  along  just  outside  of 
the  neighboring  ganglia,  and  thus  constitute  the  ivhite  associating,, 
commissural  and  projection  tracts.  The  serial  deposits  of  cell-bodies,, 
so-called  gray  ganglia,  gray  matter,  gray  columns,  and  the  long  and 
short  processes  or  branches  from  these  cell-bodies  that  run  here  and 
there  to  connect  them  with  one  another,  the  ganglionic  deposits  with 
one  another,  and  the  ganglionic  centers  with  the  outlying  parts  of  the 
body,  all  making  up  the  so-called  white  matter  of  the  commissures  and 
columns,  is  the  essential  completed  structure  of  the  central  nervous, 
system. 

When  we  employ  the  gross  divisions  of  the  anatomists  in  our 
terminology,  we  merely  mean  to  say  that  the  hrain  is  that  part  of  the 
series  of  gray  deposits,  and  that  part  of  the  white  processes,  that  hap- 
pen to  lie  within  the  skull  above  the  foramen  magnum ;  the  cord  is 
that  part  which  happens  to  be  found  within  the  bony  vertebral  column ; 
and  the  nerves  are  that  part  of  the  processes  that  lie  between  the 
cerebro-spinal  axis  and  the  outlying  organs  and  tissues  of  the  body. 

This  is  a  most  important  conception  of  the  nervous  system  to 
grasp  in  order  to  understand  the  symptomatology  of  its  diseases.  For 
purposes  of  rough  localization  we  may  conveniently  speak  of  brain, 
cord  and  nerve  diseases,  but  as  a  matter  of  fact  there  are  no  dis- 
tinctive brain,  cord  and  nerve  diseases.  There  are  no  distinctive  brain^ 
cord  or  nerve  functions.  All  the  functions,  all  the  abnon-nal  symptoms 
of  the  nervous  system,  are  neuronic  functions  and  neuronic  symptoms. 
If  they  happen  to  be  the  functions  and  the  symptoms  of  those  particu- 
lar neurones  that  lie  within  the  skull  we  call  them  encephalic :  if  of 
those  within  the  cord,  spinal;  if  of  those  in  the  outlying  nerves,  neu- 
ritic.  Remember,  however,  that  there  is  no  sharp  line  of  demarkation 
between  these.  Encephalic  diseases  produce  spinal  lesions  and  symp- 
toms and  vice  versa;  spinal  diseases  produce  neuritic  lesions  and  symp- 
toms and  vice  versa.  The  greatest  convenience  of  this  artificial  di- 
vision of  the  nervous  system  into  brain,  cord  and  nerves  is  in  localizing 
the  extra-neuronic  lesions  that  constitute  the  inflammations,  the  vascu- 
lar abnormalities,  the  neoplasms,  etc. 


THE    NON-NEURONIC    DISEASES 


461 


I  will  now  discuss  that  part  of  the  nervous  system  commonly 
■called  the  spinal  cord. 

The  spinal  cord,  spinal  marrozv,  medulla  spinalis,  is  that  part  of 
the  cerebro-spinal  organ  that  extends  from  the  edge  of  the  foramen 
magnum  in  the  occipital  bone  to  the  lower  part  of  the  body  of  the  first 
lumbar   A^ertebra.      The    section    just   above   it   is   called    the   medulla 

FIGURE  93- 


. — Cervical  por-  —Dorsal  por-  . — Inferior  por- 

tion of  the  spinal  cord       tion   of   the    spinal       tion  of  the  spinal  cord, 
(Hirschfeld).  cord  (Hirschfeld),  and      cauda     equina 

(Hirschfeld). 
1,  antero-inferior  wall  of  the  fourth  ventricle  ;  2,  superior  peduncle  of  the 
cerebellum  ;  3,  middle  peduncle  of  the  cerebellum  :  4,  inferior  peduncle 
of  the  cerebellum  ;  5,  inferior  portion  of  the  posterior  median  columns 
of  the  cord ;  6,  glosso-pharynpeal  nerve  ;  7,  pneumogastric  ;  8,  spinal 
accessory  nerve  ;  9,  9,  9,  9,  dentated  ligament ;  10,  10,  10,  10,  posterior 
roots  of  the  spinal  nerves  ;  11,  11,  11,  11,  posterior  lateral  groove  ;  12,  12, 
12,  12,  ganglia  of  the  posterior  roots  of  the  nerves  ;  13,  13,  anterior  roots 
of  the  nerves  ;  14,  division  of  the  nerves  into  two  branches  ;  15,  lower  ex- 
tremity of  the  cord  :  16,  16,  coccygeal  ligament ;  17,  17,  cauda  equina ; 
I- VIII,  cervical  nerves  ;  I,  II,  III,  IV-XII,  dorsal  nerves  ;  I,  II-V,  lumbar 
nerves  ;  I-V,  sacral  nerves. 


■oblongata.  At  the  other  end  it  terminates  in  a  slender  filament,  the 
■filum  terminale  or  central  ligament.  It  is  about  eighteen  inches  long 
and  does  not  quite  extend  to  the  full  length  of  the  bony  canal.  Its 
relation  to  this  canal  varies  slightly  in  accordance  with  the  flexions  of 
the  body. 

It  is  inclosed  in  a  theca,  which  is  longer  and  larger  than  itself 
and  which  constitutes  the  dura  mater.     Two  other  membranes  encase 


462 


THE  NOX-NEUROXIC  DISEASES 


the  cord  also  within  the  dura  mater  and  are  known  as  the  arachnoid 
and  the  pia  inafcr.  Between  the  dura  mater  and  the  bony  canal  is  a 
space  containing  much  fat  and  loose  areolar  tissue,  and  large  venous 
plexuses.  The  arachnoid  is  a  double  membrane,  the  outer  layer  of 
which  hugs  closely  the  under  surface  of  the  dura,  while  the  inner 
layer  unites  somewhat  with  the  pia.  Many  delicate  fibres  pass  from 
one  laver  to  the  other.     The  dural  laver  is  regarded  bv  manv  histolo- 


— Horizontal  section  of  the  cord  and  its  envelopes,  at  the  middle  of  a  vertebral  body 
(Schematic).  1,  Spinal  cord  -nith  a,  its  anterior  median  fissure:  3.  its  posterior  median  fissure; 
4,  anterior  roots;  5,  posterior  roots;  6.  pia  mater  7,  ligamentum  denratum;  8,  connect- 

ing fibres  passing  from  the  pia  to  dura  mater;  9,  visceral  layer  and  9',  parietal  layer  of  the 
arachnoid  10,  subarachnoid  space:  11,  arachnoid  cavity;  12,  dura  mater  13, 

periosteum;  13',  external  periosteum;  ]4,  cellular  tissue  situated  between  the  dura  mater  and  the 
wall  of  the  vertebral  canal;  15,  common  posterior  vertebral  ligament:  16,  intra-spinal  veins:  17. 
vertebra  in  section.    (Testui.)  o  •     .  t-  >      > 

gists  as  the  arachnoid.  The  space  beneath  it  then  becomes  the  sub- 
arachnoid space  and  contains  the  cerebro-spinal  fluid  and  is  in  direct 
connection  with  the  lymph  paths  of  the  peripheral  nerves  and  with  the 
subarachnoid  space  of  the  brain.  The  pia  mater  is  a  highly  vascular, 
lace-like  membrane  which  closely  invests  the  spinal  cord  and  sends  a 
thick,  fibrous  septa  into  the  anterior  fissure.  It  is  important  to  note 
this,  as  certain  dififerences  between  the  diseases  of  the  anterior  and  of 
the  posterior  parts  of  the  cord  are  probably  due  in  part  to  this  arrange- 
ment of  the  pia  and  the  corresponding  difference  of  blood  supply. 
With  its  investing  pia  mater,  the  cord  swings  within  the  subarachnoid 
space  and  cerebro-spinal  fluid,  being  suspended  from  above  and  kept 
in   position   by   the   tooth-like   ligamentum  dentatum   that  fixes   it   at 


THE   NON-NEURONIC   DISEASES  463 

various  points  to  its  sheath  and  by  the  spinal  nerve-roots  that  cross 
to  reach  the  various  intervertebral  foramina. 

The  cord  is  not  of  the  same  thickness  throughout.  In  the  upper 
part  is  the  cervical  enlargement  where  the  great  nerves  of  the  arms 
come  off,  extending  from  the  upper  limit  of  the  cord  to  about  the 
first  or  second  dorsal  vertebra,  while  in  the  lower  part  is  the  lesser 
lumbar  enlargement^  where  the  nerves  of  the  lower  extremities  orig- 
inate and  extending  from  the  tenth  dorsal  vertebra  down  to  its  greatest 
width  opposite  the  twelfth  dorsal  vertebra  on  to  its  final  tapering  into 
the  thin  conns  nieduUaris. 

Above  the  nerve  roots  pass  almost  horizontally  across  the  sub- 
arachnoid space ;  in  the  mid-dorsal  region  they  incline  strongly  down- 
ward and  thus  run  for  a  short  distance  obliquely  across  the  space; 
in  the  lumbar  and  lower  regions  they  become  almost  vertical  and 
run  quite  a  long  distance  beside  the  cord  before  they  pass  out  through 
their  respective  foramina.  This  is  to  be  carefully  noted  as  having  a 
most  important  bearing  upon  clinical  localization  of  the  lesions  within 
the  cord.  This  mass  of  almost  vertical  nerve-roots  hanging  round 
about  and  concealing  the-  terminal,  central  ligament  of  the  cord  con- 
stitutes the  Cauda  equina,  or  horsetail.  The  Hhun  terminate  is  a  pro- 
longation of  the  pia  mater,  inclosing  for  about  a  half  of  its  length 
the  lower  end  of  the  central  canal  of  the  cord.  In  the  portion  below  the 
canal  there  are  connective  tissue,  blood  vessels  and  three  or  four 
minute  bundles  of  medullated  nerve  fibres,  some  of  which  have  a 
few  ganglion  cells  attached.  According  to  Rauber  these  represent 
rudimentary  coccygeal  nerve-roots,  but  they  have  no  real  connection 
with  the  proper  coccygeal  nerves. 

Superficially  the  cord  is  seen  to  be  longitudinally  divided  by 
fissure-like  depressions,  along  which  emerge  the  nerve-roots.  As  the 
nerve-roots  form  themselves  on  each  side  into  an  anterior  and  a 
posterior  set,  the  cord  is  thus  grandly  divided  into  anterior,  lateral  and 
posterior  columns.  The  anterior  column  is  again  divided  into  two  by 
the  anterior  median  ilssnre  into  which  dips  the  pia  mater.  The  pos- 
terior column  is  also  divided  into  two  by  a  so-called  posterior  median 
fissure,  which  is  not  a  true  fissure,  but  merely  a  septum  of  connective 
tissue  and  blood  vessels  projected  down  into  the  cord  from  the  pia 
mater  on  its  surface.  Thus  each  half  of  the  cord  has  an  anterior 
column  in  front  of  the  anterior  nerve  roots,  a  later  column  between 
the  anterior  and  posterior  nerve-roots  and  a  posterior  column  behind 
the  posterior  nerve-roots.  We  now  begin  to  see  that  the  cord  is  a 
bilateral  organ  or  represents  two  sides  of  the  nervous  system,  identical 
in  all  respects.  This  is  further  demonstrated  most  beautifully  when 
a  transverse  section  of  the  cord  is  made  and  the  ends  of  the  section 
are  examined.  If  we  were  to  unite  the  anterior  and  posterior  median 
fissures  with  one  cut  of  the  knife  longitudinally  we  would  have  the 
two  halves  of  the  cord  separated,  but  presenting  exactly  the  same 
picture. 

Before  taking  up  the  description  of  the  inner  appearance  of  the 
cord,  it  may  be  well  to  devote  a  paragraph  to  its  blood  supply.  The 
upper  part  of  the  cord  is  nourished  by  branches  from  the  vertebral, 


464 


THE  NON-NEURONIC  DISEASES 


ascending  cervical  and  superior  intercostal  arteries.  The  lower  part 
receives  its  supply  of  blood  from  the  dorsal  intercostal,  lumbar  and 
sacral  arteries.  These  all  send  off  branches  which  penetrate  the  inter- 
vertebral foramina  and  are  finally  spread  out  on  the  pia  mater  and  the 
cord.     The  anterior  and  posterior  spinal  arteries  run  along  the  cor- 


FIGURE  95    (A). 


Tor  mat  retrcult 


First  Cervical. 

J'nterme.ei.   Ce//s 


Second  Cemcal 


Clork'^    Col, 
Su6st.  ge/at>/t. 

^uhst^  gelatfn   »  ^''^-^ 
col  post. 


'ttertred.  CeXts 


Cent.  Caned 
Cominls.  cb//s 
J^ed.  motor  cells 

Lat.  motor  cells 
Sixth  Cervical. 


Ca/nmiss.  ce//sj 

-J^otor  ce/is 

Latej-a/  horn 

First  Dorsal. 


—Showing  Arrangement  op  Gray  and  White  Matter  at  Different  Letels 
OF  the  Cord  (After  Merkel). 

responding  surfaces  of  the  cord  and  send  off  everywhere  small 
branches.  The  branches  from  the  intercostal,  lumbar  and  sacral 
arteries  communicate  laterally  with  the  branches  from  the  anterior 
and  posterior  medians.  Thus  are  effected  the  arterial  chains.  From 
the  anterior  spinal  artery  at  the  bottom  of  the  anterior  fissure  minute 


THE    NOX-NEUROXIC    DISEASES 


465 


branches  enter  and  supply  the  greater  part  of  the  central  gray  matter  of 
the  cord.  They  do  not  supply  the  posterior  horns.  From  the  periphery 
of  the  cord  other  branches  from  the  arterial  chains  dip  into  the  ^yhite 
matter  and  the  posterior  horns.  The  artcricE  sulci  come  from  the  an- 
terior tract,  pass  into  the  cord  and  reach  the  anterior  commissure. 
Here  as  arterias  sulco-commissurales  they  enter  the  anterior  horns 
and  supplv  them  and   a  small   area   of   surrounding     white     matter. 


FIGURE  95    (B). 


C/ar/cs  col. 
Post,  column- 


JInt.CoL 

Eighth  DorsaL 


C/arK's   col. 


Ant. root 
First  Lumbar. 


Clark's  col. 


CoajwJss.  cells 


Ant.  root 
lareral  ceii« 

Third  Sacral. 
Median    cells. 

First  SacraL 
-Showing  Arraxgesient  of  Gray  axd  White  Matter  at  Different  Levels 
OF  THE  Cord  (After  Merkel). 


Clarke's  column  is  supplied  by  branches  from  these  anterior  arteries. 
Most  of  the  white  matter  and  the  posterior  horns  are  supplied  by  the 
vasocorona  or  minute  arteries  which  dip  directly  into  the  cord  from  the 
pia  mater. 

The  practical  points  about  all  these  arteries  of  the  cord  are  that 
the  anterior  and  peripheral  set  do  not  anastomose,  that  they  are  ter- 
minal arteries,  that  the  anterior  are  larger  than  the  peripheral  and  are 
so  much  larger  than  the  corresponding  venous  system  that  their  blood 
pressure  is  probably  very  high. 


466 


THE  XOX-XEUROXIC  DISEASES 


The  first  sight  to  catch  the  eye,  after  making  a  transverse  section 
of  the  cord,  is  the  arrangement  of  the  gray  and  white  matter.  The 
gray  matter  is  in  the  center  and  by  means  of  the  cross  bar  of  the 
H-shape  connects  the  two  halves  of  the  cord.  Outside  of  the  gray 
matter  and  constituting  the  edge  of  the  cord  spreads  the  zvhite  matter. 
As  the  ends  of  the  H-hke  gray  matter  correspond  with  the  anterior 


FIGURE  96. 

Traxsversk 

SECTtON  OF  HALF  THK 
SPINAL  MARROW  IN  THE 
LUMBAR    'ENLARGEMENT 

(Allen  Thomson),     f 

This  is  a  semidiagram- 
matic  representation  taken 
from  a  specimen,  and 
founded  in  part  on  the 
statements  of  Lockhart 
Clarke  and  of  KoUiker. 

1,  anterior  median  fis- 
sure 5  2,  posterior  median 
fissure ;  3,  central  canal 
lined  with  epithelium  ;  4, 
posterior  commissure  ;  5, 
anterior  commissure  ;  6, 
posterior  column  ;  7,  la- 
teral column  ;  8,  anterior 
column  ;  9,  fasciculus  of 
posterior  nerve-root  enter- 
ing in  one  bundle,  a  part 
of  which  passes  into  the 
posterior  comu,  and  a  part 
into  the  posterior  column  ; 
10,  fasciculi  of  anterior 
roots ;  a,  a,  caput  comu 
posterioris  with  the  gelati- 
nous substance  of  Rolando ; 
b,  the  cervix  comu ;  c,  pos- 
terior vesicular  column  of 
Clarke  ;  te  the  right  of  d, 
the  group  of  cells  in  the 
intetmedio  -  lateral  tract ; 
<,  c,  fibres  oE  the  anterior  roots,  entering  the  anterior  comu,  and  passing  through  among 
the  cells  ;  e,  fibres  from  the  anterior  roots  which  decussate  in  the  anterior  commissure  ; 
■e",  extemal  fibres  from  the  roots  running  round  the  outside  of  the  a/iterior  grey  comu 
towards  the  lateral  columns  ;  /,  fibres  from  the  posterior  commissure  and  from  the  pos- 
terior comu  muring  towards  the  anterior.  Three  groups  of  cells  are  seen  in  the  anterior 
comu  in  this  region  of  the  cord  ;  and  from  thpir  position  may  be  described  as  external, 
internal,  and  posterior. 

(From  Quain's  Anatomy.) 

and  posterior  nerve-roots  respectively,  we  see  that  the  white  matter 
is  naturally  divided,  as  the  nerve-roots  cross  it  and  enter  the  gray 
matter,  into  the  anterior,  lateral  and  posterior  columns  that  made  up 
the  superficial  arrangement  of  the  cord.  If  we  make  other  sections 
of  the  cord  we  find  that  the  general  appearance  remains  the  same,  but 
that  the  relative  amounts  of  gray  and  white  matter  differ  at  different 
levels.     In  the  cervical  and  lumbar  enlargements  we  note  especially 


THE    NON-NEURONIC    DISEASES 


467 


the  relative  increase  of  gray  matter  ;  and  high  up  in  the  cervical  region 
it  is  beginning  to  lose  its  regular  H-like  outline. 

Beyond  a  cellular-like  appearance  in  some  parts  of  the  gray  matter 
and  perhaps  the  greater  vascular  supply  of  this  over  the  neighboring 
white  matter,  the  appearance  of  the  central  canal  in  the  middle  and 
some  other  unimportant  features,  we  cannot  learn  much  more  about 
the  cord  from  a  mere  macroscopical  examination. 

The  moment  we  turn  the  microscope  upon  the  picture,  however, 
and  especially  if  we  avail  ourselves  of  the  marvelous  staining  methods 

FIGURE  97. 


Part  of  the  gray  matter  of  the  anterior  horn,  with  the  neighboring  portion  of  the  lateral  tract, 
showing  the  fine  medullated  fibres  which  pass  from  the  lateral  tract  into  the  gray  matter,  sur- 
rounded by  (pigmented)  nerve-cells.     (Stained  by  Weigert-Pal's  method.)     (After  KoUiker.) 

of  modern  histological  research,  we  are  confronted  with  a  most  beauti- 
ful and  suggestive  view.  The  ~  gray  matter  is  at  once  seen  to  be  made 
up  of  a  great  mass  of  neuronic  cells  with  their  interlacing  processes, 
all  supported  by  a  matrix  of  rich  neuroglia,  connective-tissue  and  vas- 
cular elements.  The  cells  are  variable  in  size,  seem  to  be  specially 
grouped  together  here  and  there  and  send  their  processes  into  almost 
every  imaginable  direction.  The  processes  that  run  horizontally  across 
the  cord  will,  of  course,  be  seen  in  their  full  length  like  fine  hairs. 
Those  that  run  up  and  down  in  the  cord  will,  being  cut  across,  appear 
as  minute  spots  with  a  delicate  ring  of  white  matter  around  them. 
Those  that  pass  here  and  there  obliquely  will,  of  course,  present  a 
more  or  less  oval  appearance  with  the  spot  in  the  middle. 


468 


THE  NOX-XEURONIC  DISEASES 


It  is  clear  then  that  we  have  in  the  gray  matter  of  the  cord  a  repre- 
sentative ganghon  or  bunch  of  nenrone-cell  bodies. 

A  full  description  of  a  neurone  will  be  found  in  an  earlier  part  of 
the  book  in  a  section  headed  the  Neurone  and  the  Neurone  Doctrine. 

FIGURE  98. 


Diagram  of  the  Relaxjons  of  the  Cells  and  Fibers  op  the   Spinal, 
Cord.     (Baker„  after  Lenhossek.) 

The  right  side  shows  the  cells  of  different  classes  found  in  the  cord,  and  their  processes.  The 
left  side  gives  the  processes  of  cells  whose  bodies  are  either  beyond  the  cord  or  at  other  levels, 
•with  the  distribution  of  their  collaterals. 

a,  a.  Motor  cells  of  the  anterior  horn. 

c.  Commissural  cells. 

d.  Golgi  commissural  cell. 

e.  e.   Columnar  cells  of  antero-lateral  column. 

f.  f.    Columnar  celft  of  posterior  column. 

g.  Golgi  cell  of  posterior  horn. 

1.  Fibers  of  posterior  root  forming  the  ant«ro-posterior  redes,  tract. 

2.  Fibers  passing  to  the  column  of,  Clarke. 

3.  Commissural  fibers  of  posterior  root. 

4.  Fibers  that  enter  the  posterior  horn, 
■fc,  k.   Collaterals  of  antero-posterior  column. 

1,  I.     Collaterals  from  the  pyramidal  tracts. 


The  cells  in  the  anterior  part  of  the  gray  matter  are  larger  and 
more  angular  than  they  are  in  the  middle  or  posterior  part.  Moreover, 
they  arrange  themselves  in  little  groups  that  can  almost  be  observed 
v/ith  the  naked  eye.  These  groups  are  seen  to  lie  anteriorly  and 
antero-laterally  and  from  them  run  processes  that  finally  pass  out 
through   the  anterior  nerve-roots.     Another  group   is    seen   near  the 


THE    NON-NEURONIC    DISEASES  469 

outer  and  mid-lateral  part  of  the  gray  matter.  The  course  of  their 
processes  is  not  quite  so  distinct.  In  the  middle  of  the  gray  matter 
just  a  little  back  of  the  end  of  the  cross-bar  of  the  H  is  another  group 
of  small  cells  which  make  up  the  column  of  Clarke.  And  finally,  in 
the  posterior  parts  are-  scattered  groups  of  quite  small  and  roundish 
cells,  intermingled  with  processes  that  come  in  from  the  posterior 
nerve-roots. 

On  account  of  the  gross  and  minute  differences  thus  observable 
in  the  gray  matter  of  each  half  of  the  spinal  cord,  it  will  be  convenient 
for  us  to  use  the  names  of  the  old  anatomists  and  speak  of  the  anterior 
part  as  the  anterior  horn,  the  middle-lateral  part  as  the  middle  horn, 
and  the  posterior  part  as  the  posterior  horn.  If  we  look  upon  the 
various  groups  of  cells,  just  described,  in  their  longitudinal  distribu- 
tion up  and  down  the  whole  cord,  we  may  justly  speak  of  them  as 
vesicular  columns.  In  the  anterior  horns,  therefore,  are  two  vesicular 
columns,  an  anterior  and  a  mesial.  In  the  lumbar  region  there  is  a 
third  or  posterior  vesicular  column  of  the  anterior  cornu.  Laterally 
between  the  two  horns  is  the  inter-medio-lateral  vesicular  column,  and 
at  the  base  of  the  posterior  horn,  internally,  is  the  posterior  or  vesicular 
column  of  Clarke.  In  the  posterior  horns  the  cells  are  not  so  well 
grouped  as  to  be  contemplated  in  the  light  of  vesicular  columns. 

When  we  turn  the  microscope  upon  the  zvhite  matter  of  the  cord 
we  note  a  marked  change  in  the  appearance  of  the  field.  There  is  a 
complete  absence  of  ganglionic  cells  and  instead  a  well-packed  mass  of 
transversely  cut  fibres.  They  appear  as  little  rings  with  a  stained 
dot,  the  axis  cylinder,  in  the  middle  of  them.  The  position  of  the  dot 
in  the  ring  and  the  shape  of  the  ring  will  depend,  of  course,  upon 
whether  the  fibre  happened  to  be  cut  transversely  or  obliquely  across. 
These  fibres  vary  in  size,  the  largest  of  them  appearing  in  the  posterior 
part  of  the  lateral  columns,  and  the  smallest  in  the  neighborhood  of  the 
processus  reticularis.  It  is  clear  that  they  are  the  medullated  processes 
from  some  neurone  bodies  embedded  somewhere  in  the  ganglionic  sub- 
stance of  the  cerebro-spinal  axis. 

Around  the  outer  edge  of  the  sectional  field  of  the  cord  we 
notice  a  layer  of  neurogliar  tissue.  It  sends  septa  transversely  into 
the  cord  and  thus  subdivides  the  white  columns  into  a  number  of 
smaller  columns,  which  have  a  relatively  fixed  position.  The  neuroglia 
is  relatively  abundant  in  a  ring  that  surrounds  the  central  canal. 
Along  the  line  of  the  posterior  roots  the  peripheral  neuroglia  enters 
into  the  posterior  horns  and  there  expands  to  form  the  substantia 
gelatinosa  of  Rolando. 

The  minute  description  of  the  histological  elements  that  we  have 
just  been  observing,  including  the  neurones,  the  neuroglia  and  the 
rest  of  the  substentacular  tissue,  will  be  found  in  the  chapter  headed 
the  Neurone  and  the  Neuronic  Architecture. 

We  have  now  to  analyze  further,  if  possible,  these  columns  and 
vesicular  masses  of  gray  matter.  The  methods  that  enable  us  to  do 
this  are  experimental  and  pathological.  The  degeneration,  regenera- 
tion and  development  of  the  neurone,  together  with  the  happy  dis- 
covery that  certain  parts  of  the  neurone  stain  differently  with  different 


470 


THE  NOX-XEUROXJC  DISEASES 


clinical  reagents,  enable  us  to  trace  out  with  an  exquisite  beauty  of 
detail  the  paths  of  the  various  impulses  through  the  cord.  This  has 
been  referred  to  partly  elsewhere. 

The  neurone  body  being  the  center  of  nutrition  for  the  entire 
neurone,  if  it  is  destroyed  the  neuraxone  immediately  begins  to  break 
dovvu  and  in  a  short  time  is  entirely  gone.     Sometimes  we  can  accom- 

FIGURE  99- 


—Transverse  section  through  half  the  spinal  cord,  showing  the  ganglia  : 
A,  anterior  cornual  cells ;  B,  axis-cylinder  process  of  iDne  of  these  going  to  posterior 
root;  c,  anterior  (motor)  root ;  I),,*posterior  (sensory)  root;  E.  spinal  t;anglion  on 
posterior  root ;  F,  sympathetic  ganglion  ;  G,  ramus  communicans ;  H,  posterior 
branch  of  spinal  nerve  ;  J,  anterior  branch  of  spinal  nerve  ;  a,  long  collaterals  from 
posterior  root-fibers  reaching  to  anterior  horn  ;  h.  short  collaterals  passing  toClarke's 
column  ;  c.  cell  in  Clarke's  column  sending  an  axis-cylinder  (d)  process  to  the  direct 
cerebellar  tract :  e.  fiber  of  the  anterior  root ;  /,  axis-cylinder  from  sympathetic 
ganglion  cell,  dividing  into  two  branches,  one  to  the  peripherj-,  the  other  toward 
the  cord  ;  g.  fiber  of  the  anterior  root  terminating  by  an  arborization  in  the  sympa- 
thetic ganglion  :  li,  sympathetic  fiber  passing  to  periphery  'Ramon  y  Cajal). 


plish  this  result  by  direct  experiment.  Alore  often  and  better,  dis- 
ease accomplishes  it  for  us.  It  is  easy  to  be  seen  that  if  by  an  ex- 
perimental or  pathological  insult,  a  minute  focal  lesion  is  established 
in  a  mass  of  neuronic  gray  matter,  the  processes  from  the  damaged 
neurones  can  be  traced  throughout  their  long  course  by  the  degenera- 
tion they  undergo.  Both  primary  and  secondary  neuronic  diseases  have 
been  most  invaluable  aids  to  histology  and  physiology-  in  this  way. 

When  a  neuraxone  is  cut  across  artificially  or  severed  from  its 
cell-body  by  a  pathological  process,  that  part  of  the  neuraxone  that 
has  been   cut  off  undergoes  complete  and   rapid   degeneration.     The 


THE    NON-NEURON IC    DISEASES 


471 


proximal  part  undergoes  a  much  slower  and  partial  degenerative 
process.  If  a  great  bundle  of  neuraxones  be  thus  treated,  the  appear- 
ance in  the  variously  lengthened  severed  ends  will  be  that  of  a  de- 
generation that  seems  to  begin  at  the  place  of  damage  and  travel 
towards  the  periphery.  This  is  known  as  secondary,  or  Wallerian, 
degeneration,  after  the  man  who  first  called  attention  to  it.  The 
degeneration,  it  is  to  be  again  repeated,  is  always  in  the  direction 
away  from  the  related  cell  body  or  center  of  nutrition.  When  the 
white  matter  of  the  cord  is  cut  across  it  is  noticed  that  in  some  parts 
of  the  columns  the  degeneration  travels  upward,  in  other  parts  down- 

FIGURE  100. 


A  SMALt   PORTION   OF   A   TRANSVERSE   8K0TION   OF   THE   HUMAN    SPINAL   CORD. 
HlGHLT    MAGNIFIED.       (E.  A.   S.  ) 

a,  a,  superficial  neuroglia  ;  b,  b,  ti-ansverse  section  of  part  of  the  lateral  column  of  the 
cord  in  which  the  dark  points  are  the  axis-cyKnders,  and  the  clear  areas  the  medullary 
substance  of  the  nerve-fibres  :  the  superficial  neuroglia  is  seen  to  exhibit  the  iippearance 
of  a  fine  network  in  which  numerous  nuclei  and  one  or  two  corpora  amylacea  (c.  a)  are 
embedded,  and  to  extend  inwards  among  the  nerve-fibres. 

(From  Quain's  Anatomy.) 

ward.  Obviously,  then,  we  have  to  look  for  the  cell-bodies  of  the 
former  below  the  cut  and  of  the  latter  above  the  cut.  In  this  way  the 
afi'erent  and  efferent  tracts  of  the  cord  have  been  most  accurately 
traced  out  and  their  cellular  origin  definitely  located. 

After  a  large  number  of  these  tracts  were  thus  mapped  out  and 
demonstrated  by  experimentation  upon  the  lower  animals,  and  by 
disease  m  man,  it  was  discovered  that  they  did  not  all  develop  simul- 
taneously and  to  the  same  degree  in  the  embryo.  Some  appeared  and 
reached  maturity  earlier  than  others.  The  acquisition  of  the  myelin 
sheath  was  taken  as  a  fair  evidence  of  the  full  development  of  a 
neiu-one  and  its  neuraxone.  This  process  of  myelination  then  not 
occurring  at  the  same  time  in  all  tracts  of  the  embryo,  it  was  only 
necessary  to  get  a  sufficiently  large  series  of  embryos  representing  dif- 
ferent ages  and  stages  of  development,  and  to  study  them,  in  order 
to  follow^  out  the  lines  of  location  of  these  particular  tracts.  This  was 
the  embryonic  method  of  Flechsig  to  which  we  are  indebted  for  much 


472  THE  NOX-NEUROXIC  DISEASES 

of  our  knowledge  of  the  minute  pathways  in  the  nervous  system,  es- 
pecially in  the  brain. 

Comparative  zoology  and  embryology,  coupled  with  the  observa- 
tions of  evolution  and  biology,  have  lent  their  aid  and  given  much 
valuable  information. 

Finally,  the  marvelous  staining  methods,  for  which  we  are  iu 
debt  to  Golgi,  Ramon  y  Cajal,  Xissl,  Marchi,  Van  Gehuchten  and  a 
host  of  enthusiastic  and  untiring  investigators,  have  laid  bare  for  us 
the  architecture  of  the  very  citadel  of  thought  and  life.  Certain 
reagents,  as  bichromate  of  potash,  osmic  acid  and  nitrate  of  silver, 
methylene  blue,  haematoxylin,  when  properly  used,  cause  changes  of 
coloration  in  certain  parts  of  the  neurones.  It  would  be  out  of  place 
to  consider  in  detail  here  these  various  methods,  but  their  great  im- 
portance in  giving  us  a  proper  conception  of  the  structure  of  the 
nervous  system  must  be  acknowledged.  It  was  out  of  the  results  of 
the  employment  of  these  methods  that  the  neurone  doctrine  was 
formulated,  one  of  the  grandest  and  most  useful  scientific  generaliza- 
tions ever  made  in  the  realm  of  medicine. 

As  a  lesult  of  all  these  methods  of  investigation  we  have  learned 
that  the  white  matter  of  the  cord  consists  of  three  kinds  of  tracts, 
projeciicn  tracts,  commissural  and  associating. 

The  anterior  commissure,  just  at  the  bottom  of  the  anterior  fis- 
sure, transmits  neuraxones  that  run  from  one  side  of  the  cord  to  the 
other. 

The  association  or  short  tracts  make  up  all  of  the  anterior,  lateral 
and  posterior  columns  that  are  not  included  in  the  projection  tracts. 
They  connect  one  level  of  gray  matter  with  another  and  thus,  like  long 
and  short  stitches,  sew,  as  it  were,  the  various  ganglionic  segments  of 
the  cord  together.  The  parts  of  the  columns  where  these  association 
fibres  exist  reveal,  when  cut  across,  both  upward  and  downward  de- 
generation. 

The  projectioji  tracts  are  several  in  number  and  need  special  de- 
scription. Those  that  connect  the  brain  with  the  cord  are  motor  in 
function  and  degenerate  downwards.  Those  that  connect  the 
peripheral  nerves  of  sense  with  the  cord,  and  certain  parts  of  the  cord 
with  the  brain,  are  sensory  and  degenerate  upwards.  These  tracts 
consist  of  the  following: 

1.  Direct  or  Uncrossed  Pyramidal  Tract.  Turck's  Column.  This 
is  a  small  tract  that  lies  immediately  on  either  side  of  the  median  fis- 
sure. It  only  extends  as  far  as  the  middle  of  the  dorsal  region.  Its 
fibres  are  the  processes  of  the  cells  in  the  Rolandic  area  of  the  cerebral 
cortex.  They  do  not  change  their  direction  until  just  before  they 
terminate,  when  they  bend  somewhat  at  a  right  angle  possibly,  cross 
to  the  other  side  of  the  cord  through  the  anterior  commissure,  and 
finally  arborize  at  various  levels  around  the  cells  in  the  anterior  horns 
of  the  upper  part  of  the  cord. 

2.  Indirect  or  Crossed  Pyramidal  Tract.  This  is  rather  a  large 
tract,  found  in  the  posterior  part  of  the  lateral  columns.  It  nowhere 
approaches  the  edge  of  the  cord  and,  except  at  its  postero-internal 
edge,  it  is  separated  by  the  lateral  limiting  zone   from  the  posterior 


THE    XOX-NEURONIC    DISEASES 


473 


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m    r^ 

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^^ 

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474 


THE  NON-NEURON IC  DISEASES 


horn.  It  represents  the  neuraxones  of  the  cells  of  the  Rolandic  cerebral 
cortex.  These  processes  all  cross  at  the  decussation  of  the  pyramids, 
pass  down  the  opposite  side  of  the  cord  and  then  arborize  around  the 
cells  of  the  anterior  horn  at  various  levels  all  alono-  the  cord. 


FIGURE  103. 


Atxt. 


Huct 


Diagram  of  the  tracts  of  the  cord. 

The  crossed  and  uncrossed  pyramidal  tracts  represent  respectively 
ninety  and  ten  per  cent,  of  the  entire  cerebro-spinal  motor  paths.  In 
spite  of  the  misleading  name  of  the  latter,  they  both  carry  inhibitory, 
controlling  and  volitional  impulses  from  one  side  of  the  brain  respective- 
ly to  the  opposite  vesicular  columns  of  the  anterior  horn  of  the  cord. 
Speaking  from  the  neuronic  standpoint,  they  constitute     the     upper 


THE    NON-NEURONIC    DISEASES  475 

motor  segment.    There  are  no  other  projection  motor  paths  in  the  cord 
that  we  know  of. 

3.  Post  era -median  Tract.  Goll's  Column.  Funiculus  gracilis. 
This  is  a  narrow,  wedge-shaped  tract  that  Hes  immediately  next  to  the 
median  septum  in  the  posterior  cohimn.  The  point  of  the  wedge  does 
not  quite  reach  to  the  gray  matter  anteriorly.  The  column  itself  does 
not  extend  much  below  the  mid-dorsal  region.  It  degenerates  upwards 
and  is  thus  an  afferent  or  sensory  tract.  It  represents  the  sensory 
iieuraxones  that  come  into  the  cord  by  way  of  the  posterior  roots  of 
the  same  side  and  that  pass  up  to  arborize  around  the  cells  of  the 
Tiucieus  gracilis  found  at  the  top  of  the  column  in  the  medulla.  It 
carries  special  forms  of  sensation  from  the  muscles,  the  articulations 
and  the  tendinous  sheaths  of  the  same  side. 

4.  Postero-lateral  Tract.  Burdach's  Column.  Funiculus  cune- 
<itus.  This  tract  constitutes  all  of  the  posterior  columns,  except  the 
postero-median  columns.  It  is  a  very  complicated  tract  and  contains 
iibres  that  degenerate  both  ways.  All  afferent  neuraxones  that  enter 
the  cord  by  way  of  the  posterior  roots  pass  sometime  through  the 
column  of  Burdach.  Some  of  these  fibres  have  collaterals  that  bend 
and  run  downward  a  short  distance  in  the  column,  thus  simulating 
a  downward  degeneration.  Other  fibres  of  the  tract  are  purely  asso- 
ciating, and  hence  exhibit  both  an  upward  and  a  downward  degenera- 
tion. All  forms  of  sensation,  tactile,  thermic,  pain  and  muscular  sense, 
are  transmitted  by  Burdach's  column.  Some  of  the  posterior  root 
fibres  that  enter  it  turn  around  and  arborize  directly  about  the  cells 
lying  in  the  adjoining  posterior  horn.  Others  enter  the  gray  matter 
at  the  same  level,  cross  through  the  posterior  gray  commissure  to  the 
opposite  side  of  the  cord,  where  they  arborize  around  the  cells  in  the 
opposite  posterior  horn.  Some  pass  forward  into  the  gray  matter  and 
arborize  around  the  cells  in  the  anterior  horn  of  the  same  side.  Oth- 
ers again  enter  the  gray  matter  and  spread  their  terminal  branches 
around  the  cells  of  the  vesicular  column  of  Clarke.  Still  others  are 
known  to  bend  upward  at  a  right  angle  and  after  giving  off  a  rather 
long  descending  branch  {descending  comma  tract),  continue  on  their 
way  upwards  through  both  Burdach's  and  Goll's  columns,  giving  off 
collaterals  and  finally  arborizing  around  the  cells  that  constitute  the 
nuclei  of  the  posterior  columns   (gracilis  and  cuneatus). 

The  column  of  Burdach  is  sometimes  subdivided  into  the  anterior 
radicular  zone,  or  that  part  of  it  which  lies  next  to  the  posterior  horn 
(many  association  fibres  connecting  dift'erent  levels  of  the  posterior 
horn  with  each  other  run  along  in  this  zone)  ;  the  postero-internal  radic- 
ular zone;  and  the  lesser  radicular  zone  with  its  two  kinds  of  fibres. 
That  part  of  the  posterior  column  that  is  just  behind  the  gray  com- 
missure is  sometimes  spoken  of  as  the  ventricidar  zone. 

5.  Direct  Cerebellar  Tract.  This  narrow  tract  lies  along  the 
outer  edge  of  the  lateral  column  and  extends  from  the  edge  of  the 
posterior  horn  around  forward  to  about  midway  of  the  column.  It 
is  a  long  tract  and  represents  the  neuraxones  from  the  cells  making  up 
the  vesicular  column  of  Clarke.  The  fibres  enter  the  cerebellum  on 
the  same  side  and  arborize  around  other  cells  in  the  cerebellar  cortex. 


4/6  THE  NON-NEURONIC  DISEASES 

The  tract  degenerates  upward  and  is  therefore  sensory  in  function. 
It  carries  impulses  from  the  muscles,  joints  and  viscera  and  belongs  to 
the  indirect  sensory  system. 

6.  Antero-lateral  Ascending  and  Descending  Tract.  Gozvers' 
Tract.  Ventral  Cerebrospinal  Fasciculus.  This  tract  also  lies  on  the 
edge  of  the  lateral  column  and  extends  from  the  middle  of  the  edge, 
where  the  direct  cerebellar  tract  ends,  on  around  forward  as  far  as, 
and  even  somewhat  to  the  other  side  of,  the  anterior  roots.  It  reaches 
down  the  side  of  the  lateral  column  as  far  as  the  hunbar  region.  It 
is  supposed  to  represent  the  neuraxones  of  the  cells  found  in  the  pos- 
terior horns  of  the  opposite  side  of  the  cord.  These  neuraxones  pass 
upward  and  arborize  around  other  cell  bodies  nesting  in  the  optic 
thalamus.  The  tract  is  sensory,  as  it  degenerates  upwards.  Pain  and 
temperature  sensations  are  supposed  to  be  transmitted  by  it.  We  are 
in  need  of  further  information,  however,  about  the  tract. 

Goirs,  Burdach's,  direct  cerebellar  and  Gowers'  tracts  are  all  of 
the  projection  sensory  paths  that  we  know  of.  Through  them  pass 
all  of  the  various  sensory  impulses  that  have  entered  by  way  of  the 
posterior  roots  and  are  on  their  way  to  the  sensory  cortex  of  the  brain. 

The  remaining  parts  of  the  columns  of  the  cord  are  the  anterior 
fiuidaniental  root  zone,  embracing  the  anterior  root  fibres  and  including 
the  lateral  part  of  the  anterior,  and  anterior  part  of  the  lateral  col- 
umns ;  the  lateral  limiting  layer*,  or  mixed  lateral  zone,  along  the  lat- 
eral edge  of  the  gray  matter  in  the  lateral  column  ;  and  the  zone  of 
Lissauer  just  at  the  edge  of  the  posterior  horn.  We  know  very  little 
about  these  except  that  they  degenerate  both  ways  and  thus  contain, 
in  all  probability,  short  association  tracts.  Whether  any  other  sort  of 
tracts  run  through  them  we  do  not  know. 

In  describing  the  minute  anatomy  of  the  spinal  cord  I  referred 
somewhat  to  some  of  its  more  important  physiological  functions.  As 
there  are  other  special  functions,  it  may  be  well  to  present  here  a  brief 
resume  of  all  of  the  activities  of  this  part  of  the  nervous  system.  I 
shall  thus  refer  to  (a)  Conduction,  (b)  Reflex  Action,  (c)  Automatic 
Reflex  Action,  .{d)  Vasomotor  Action,  (e)  Trophic  Influence,  (f) 
Tonic  Influence. 

The  segmental  character  of  the  ganglionic  gray  matter,  as  shown 
in  the  serial  arrangement  of  the  spinal  nerve  roots,  is  an  evidence  of  its 
primitive  structure.  Somewhat  alter  tlie  manner  of  a  low  articulate, 
such  as  a  worm  with  its  various  metameres  attached  end  to  end  as  it 
were  and  each  presided  over  by  a  central  gray  mass  with  outlying- 
afferent  and  efferent  processes,  various  levels  of  the  human  body  are 
presided  over  by  the  particular  segments  of  the  cord.  This  is  so  true 
that  we  make  use  of  this  segmental  arrangement  and  its  peripheraf 
representation  to  base  many  of  our  spinal  localization  diagnoses  upon. 
In  spite  of  the  fact  that  the  segmental  ganglionic  spinal  centers  are 
welded  tightly  together  by  innumerable  association  tracts,  and  are 
powerfully  dominated  by  the  highly  developed  anterior  segments  that 
enter  into  the  morphological  structure  of  the  brain,  their  primitive 
segmental  functions  are  still  in  marked  evidence  in  the  reflex  and 
automatic  functions  of  the  cord. 


THE    NON-NEURONIC    DISEASES  47? 

Both  in  its  anatoni}'  and  in  its  physiology  we  behold  in  the  cord 
the  most  elementary  part  and  condition  of  the  nervous  system.  There 
are  animals  that  are  devoid  of  a  brain,  but  there  are  no  animals  that 
are  without  a  more  or  less  primitive  spinal  cord.  The  functions,  the 
essential  functions,  of  the  cord,  therefore,  are  of  a  crude,  simplified, 
automatic  nature.  In  a  general  way  they  represent  a  mere  form  of 
reflex  irritability.  The  central  gray  deposits  constitute  the  mere  center 
through  which  plays  the  reflex  sensory-motor  impulse. 

Whether  this  sensory-motor  impulse  has  to  do  with  the  somatic 
musculature,  the  blood  vessels,  the  viscera  or  the  genital  apparatus, 
it  is,  after  all,  but  a  low-grade  automatic  function.  The  trophic  and 
tonic  control  of  these  outlying  tissues  by  the  spinal  gray  matter  is 
largely  of  a  reflex  and  low  order. 

Such  are  the  essential  functions  of  the  spinal  cord  and  such  is 
the  organ  in  its  independently  working  mass  of  gray  matter  with  its 
projecting  motor  processes  (anterior  root  fibres)  and  receiving  sensory 
processes  (particular  short  posterior  root  fibres).  Were  we  creatures 
endowed  with  nothing  but  a  spinal  cord,  we  would  lead  a  low,  auto- 
matic sort  of  a  life.  Our  vegetative  organs  would  go  on  functionating, 
but  our  muscles  would  be  in  a  state  of  constant  tension  from  the  cease- 
less inpouring  sensory  stimuli.  We  would  be  the  victims  of  every 
form  of  mere  reflex  stimulation,  moving  hither  and  thither,  without 
purpose,  without  reason,  merely  as  a  feather  blown  by  the  winds  of 
our  ever-changing  reflexes.  Alas !  in  disease,  it  is  too  often  seen  that 
human  beings  reach  this  sad  state  almost.  In  certain  forms  of  idiocy 
and  cerebral  agenesis  it  is  approached.  In  extensive  lesions  of  the 
cerebrum  and  of  the  upper  motor  segment  whereby  the  control  of  the 
brain  over  the  cord  is  greatly  withdrawn,  how  the  muscles  stiffen 
and  contract,  and  how  the  reflexes  become  exaggerated !  What  are 
associated  movements  and  the  waxy,  athetoid  phenomena  but  the  ex- 
pression of  liberated  spinal  cord?  Nay,  more,  who  does  not  recognize 
in  those  of  weakened  brain  power  the  yielding  to  every  gratif}^- 
ing  or  alarming  form  of  sensation,  even  to  such  a  degree  as  to  suffer 
a  reflex  over-action  of  the  bowels,  the  kidneys,  the  sexual  apparatus, 
even  the  muscles? 

We  must  keep  closely  in  mind,  then,  that  reflex  action,  of  a  very 
simple  primitive  order,  is  the  essential  function  of  the  spinal  cord.  In 
the  direct  exhibition  of  reflex  action,  the  projection  tracts  of  the  cord 
take  no  part.  It  is  prohable,  more  than  probable,  that  the  association 
tracts  take  only  a  secondary  part. 

•  For  a  pure  reflex  action  there  is  needed  only  an  afferent  fibre,  a 
central  relay  station  and  an  efferent  fibre.  This  completes  the  arc.  It 
is  but  a  little  more  complicated  and  highly  developed  exhibition  of 
the  primitive  irritability  that  constitutes  the  inherent  functional  prop- 
erty of  all  nervous  matter.  This  simple  type  of  reflex  arc  is  so 
primitive  that  it  limits  itself  in  its  essential  manifestation  to  a  single 
level  or  segment  of  the  cord.  The  impulse,  say  from  the  skin,  passes 
up  a  particular  fibre  in  the  sensory  nerve,  through  the  posterior 
ganglion,  on  through  the  posterior  root  of  the  column  of  Burdach, 
the  posterior  horn,  to  the  anterior  horn  of  the  same  side,  where  it  is 


478  THE  NON-NEURONIC  DISEASES 

transferred  to  a  motor  cell  and  sent  on  out  over  its  process,  through 
the  anterior  root,  along  the  motor  nerve,  to  stimulate  the  correspond- 
ing muscle  into  action.  Such  is  the  essential  story  of  every  form  of 
reflex  action.  Corresponding  sensory  and  motor  areas,  as,  for  instance^ 
the  skin  and  muscles  of  the  same  leg,  are  always  the  subject  of  it. 
There  are  reflexes  a  little  more  complicated  than  these,  however,  and 
illustrate  the  old  physiological  laws  of  Pfliiger  in  regard  to  the  spread- 
ing of  the  reflex  action.  If  the  sensory  excitation  is  a  strong  one  ia 
one  limb,  the  opposite  limb  will  respond.  If  a  still  stronger  stimulus 
be  used,  the  upper  limbs  will  manifest  the  action.  This,  of  course,  is 
due  to  the  close  association  between  the  special  segments  in  the  higher 
classes  of  animals. 

I  have  already  hinted  at  the  fact  that  the  reflex  arc,  in  a  normal 
individual,  is  not  a  liberated  circuit.  Just  exactly  how  it  is  under  the 
control  of  the  brain  we  do  not  know,  but  we  believe  that  certain, 
reflex-inhibitory  processes  pass  from  the  cerebral  cortex,  or  rather  its 
cells,  down  through  the  pyramidal  tracts  to  arborize  around  the  reflex- 
motor  cefls  in  the  anterior  horns.  In  this  way  every  reflex  arc  is 
inhibited  from  above.  We  are  thus  saved  from  being  the  victims  of 
every  stimulus  that  attacks  us  and  that  otherwise  would  keep  us  in  a 
state  of  everlasting  movement  and  muscular  rigidity. 

It  is  obvious,  therefore,  that  a  reflex  may  be  modified  by  a  con- 
siderable number  of,  and  variously  localized,  lesions.  In  the  first  place,, 
any  injury  to  the  arc  itself,  upon  the  motor  or  sensory  side  (neuritis)^ 
or  at  the  center  (poliomyelitis),  will  diminish  or  abolish  it.  In  deep 
coma  it  is  lost.  Any  disease  that  increases  the  inhibitory  force  from 
above  may  diminish  it,  as  is  seen  in  some  cases  of  hysteria.  On  the 
other  hand,  how  easy  it  is  to  comprehend  that  it  may  be  exaggerated 
by  any  disease  that  suppresses  the  inhibitory  force  from  the  brain. 
Hemiplegia  and  pyramidal  degenerations  generally  are  characterized 
by  exaggeration  of  the  reflexes.  Slight  irritation  of  the  posterior  roots^ 
when  the  arc  is  not  broken,  also  increases  it,  so  does  strychnine  and 
tetanus  and  the  neuroses,  and  certain  diflruse  diseases  above  the  arc 
which  exalt  the  excitability  of  its  center. 

There  are  many  forms  of  reflex  that  we  could  probably  trace 
out,  but  in  clinical  practice  the  skin,  or  superficial,  and  the  tendon,  or 
deep,  reflexes  are  those  we  are  most  interested  in.  In  the  former  the 
skin  is  irritated ;  in  the  latter  some  muscle  tendon  is  tapped.  The 
termination  of  the  reflex  may  be  in  a  gland,  a  blood  vessel  or  a  muscle. 

I  have  elsewhere  described  the  more  common  forms  of  reflex  and 
the  methods  employed  in  eliciting  them. 

Closely  related  to  the  reflex  is  the  automatic  function  of  the  cord. 
In  fact,  this  function  is  a  form  of  reflex  in  which  the  sympathetic  sys- 
tem relieves  the  brain  and  makes  the  management  of  the  reflex  appear 
all  the  more  independent  and  automatic.  In  the  cord  are  found  here 
and  there  deposits  of  cells  in  the  gray  matter  that  clearly  preside  over 
certain  actions  of  the  pupil,  micturition,  defecation,  erection  in  the 
genital  apparatus  and  parturition. 

In  the  lower  cervical  and  upper  dorsal  region  of  the  cord,  near  the 


THE    XOX-XEUKOXIC    DISEASES 


479 


origin  of  the  first  dorsal  root,  is  the  ciliospinal  center,  or  group  of  cells 
which  regulate  automatically  the  muscle  that  dilates  the  pupil  and  the 


FIGURE  104. 


^JLml^C/ 


Diagram  to  illustrate  the  mechanism  of  a  spinal  reflex  and  its  inhibition  from 
above. 

unstriated  muscle  by  whose  contraction  the  palpebral  fissure  is   en- 
larged.    Stimulation  of  this  center,  or  of  its  path  in  the  anterior  root 


480  THE  NON-NEURONIC  DISEASES 

of  the  first  dorsal  nerve,  causes  the  pupil  and  the  palpebral  fissure  both 
to  dilate. 

The  genital  center,  for  the  erection  of  the  penis  and  ejaculation  of 
semen,  is  in  the  gray  matter  from  the  first  to  the  third  sacral  segment 
inclusive.  It  is  not  close  to  the  ano-vesical  center.  From  the  first, 
second  and  third  sacral  nerves  arise  the  nervi  erigentes ;  from  the  third 
and  fourth  spring  the  ischio-cavernous,  transverse  perineal  and  bulbo- 
cavernous. The  vasomotor  phenomena  of  the  penis  are  under  the  con- 
trol of  the  sympathetic.  In  the  fourth  and  fifth  sacral  segments  are  the 
centers  for  the  bladder  and  rectum,  the  former  being  a  little  the  lower 
of  the  two. 

The  mechanism  of  micturition,  like  that  of  defecation,  is  explained 
partly  upon  a  hypothetical  basis.  We  know  that  it  is  a  reflex,  but  in 
regard  to  the  antagonistic  action  of  the  various  sets  of  muscles  we  have 
little  information  that  is  at  all  positive.  In  micturition  a  sensory  im- 
pulse is  first  started  from  the  mucous  membrane  of  the  bladder ;  this 
travels  along  the  second,  third  and  fourth  sacral  nerves  to  the  spinal 
center  and  also  to  the  brain.  From  the  spinal  center  a  motor  impulse 
passes  out  through  the  anterior  roots  of  the  third  and  fourth  sacral 
nerves  to  the  common  pudendal  nerve,  or  to  the  hemorrhoidalis  medius, 
and  so  on  through  the  sympathetic  to  the  muscles  of  the  bladder.  The 
detrusor  muscle  and  the  sphincter  vesicae  are  presumed  to  act  an- 
tagonistically, so  that  a  stimulation  of  one  causes  an  inhibition  of  the 
other.  When  there  is  a  desire  to  void  the  urine,  the  will  relaxes  the 
sphincter  and  checks  its  reflex  contraction,  while  the  detrusor,  stimu- 
lated from  the  cord,  contracts  the  walls  of  the  bladder.  The  act  is 
also  assisted  by  the  will  through  the  associated  contraction  of  the 
abdominal  muscles.  The  impulses  from  the  brain  to  the  vesical  cord 
center  are  believed  by  some  to  travel  by  way  of  the  antero-lateral  tracts. 
It  is  obvious  how  disease  can  disturb  the  function.  Disease  of  the 
cord  above  the  sacral  segment  may  result  in  both  sensory  and  motor 
paralysis  of  a  volitional  character.  The  motor  reflex,  however,  may 
not  be  disturbed ;  in  fact,  may  be  highly  exaggerated.  Under  such 
conditions  there  is  no  desire  felt  by  the  patient  to  void  his  urine, 
but  as  soon  as  the  bladder  is  distended  there  is  a  reflex  evacuation. 
This  is  intermittent  incontinence  of  urine.  In  disease  of  the  spinal 
centers  themselves,  both  sphincter  and  detrusor  are  paralyzed  and 
there  is  constant  dribbling.  The  simple  elasticity  of  the  mouth  of 
the  bladder  may  check  this  somewhat,  by  keeping  it  closed.  A  total 
section  of  the  cord  at  any  height  seems  to  result  in  the  paralysis  of 
the  function  of  vesical  and  rectal  evacuation.  This  may  be  but  another 
phase  of  Bastian's  phenomenon  observed  in  connection  with  other 
forms  of  reflex  action.  According  to  Bastian,  complete  transverse 
lesions  of  the  cord  produce  loss  of  all  the  reflexes  below  the  lesion ; 
where  there  is  exaggeration  of  the  reflex  from  a  transverse  lesion,  the 
latter  is  not  a  complete  one.  Ischuria,  or  retention  of  the  urine,  results 
from  detrusor  paralysis.  The  same  result  may  occur  from  spasm 
of  the  sphincter.  Ischuria  paradoxa  is  where  there  is  an  enormous 
distention  of  the  bladder  from  paralysis  of  the  detrusor  and  the  urine 
merely  drips  away  mechanically. 


THE   NON-NEURONIC    DISEASES  481 

The  same  sort  of  mechanism  is  supposed  to  regulate  the  evacua- 
tion of  the  rectum.  Disease  above  the  center  may,  as  in  the  case  of 
the  bladder,  shut  off  the  transmission  of  both  the  sensory  and  volitional 
impulses-.  In  such  cases  the  finger  inserted  into  the  rectum  will  detect 
the  vigorous,  reflex  contraction  of  the  sphnicters.  The  reflex  may  be 
destroyed  in  accordance  with  Bastian's  hypothesis. 

Other  automatic  reflex  centers  that  exist  in  the  cord,  though  we 
know  very  little  about  them,  are  a  respiratory  center,  subsidiary  and 
minor  to  the  respiratory  center  in  the  medulla,  cardio-accelerator  cen- 
ter, vasomotor  and  sudorific  centers. 

We  can  hardly  speak  of  a  muscnlo-tonic  center,  for  though  it  is 
one  of  the  functions  of  the  cord  to  keep  all  the  muscles  of  the  body 
in  a  state  of  slight  tonic  contraction,  it  is  a  function  that  probably 
belongs  to  all  of  the  cells  that  send  out  motor  impulses.  The  same 
may  be  said  of  the  trophic  function  of  the  cells  in  the  anterior  horns. 
It  is  easy  to  understand  how  the  muscles  directly  under  the  control  of 
these  cells,  where  the  nutritive  center  for  the  related  neurones  has  its 
seat,  may  have  their  nutrition  maintained  from  the  same  source.  It  is 
impossible  to  say,  however,  how  or  from  what  particular  cells  the  in- 
fluence originates  that  supports  the  nutrition  of  the  joints,  bones  and 
skin. 

Thus  far  I  have  described  briefly  all  of  the  essential  functions  of 
the  spinal  cord,  and  in  their  final  analysis  they  were  all  seen  to  be 
nothing  but  a  simple,  low  form  of  sensory  motor  reflex.  Were  we 
possessed  of  nothing  but  a  spinal  cord,  we  would  be  nothing  but  auto- 
matic reflex  creatures,  living  and  moving  in  accordance  with  every 
stimulus  that  happened  to  come  down  upon  us.  Such  is  the  way  that 
such  creatures  as  the  amphioxus  lanceolatus,  with  practically  only  a 
spinal  cord,  lives  in  the  mud  at  the  bottom  of  the  streams. 

From  time  immemorial  authors  have  spoken  of  conduction  as  one 
of  the  functions  of  the  cord,  meaning  by  this  that  through  the  cord 
passed  the  impulses,  motor  and  sensory,  between  the  braii:  ctnd  the 
body.  Such  a  conception  is  erroneous  and  misleading.  Moreover, 
it  stands  in  the  way  of  understanding  many  of  the  phenomena  of 
■disease.  The  cord  is  not  a  direct  transmitter  of  impulses,  as  physiology 
clearly  teaches  every  day.  It  is  singular  how  the  statement  is  con- 
stantly repeated  in  the  modern  books  upon  the  functions  of  the  nervous 
system,  that  the  spinal  cord  transmits  impulses  between  the  brain  and 
the  skin  and  muscles ;  and  yet  on  the  very  next  page  it  is  demonstrated 
that  all  impulses,  whether  afferent  or  efferent,  are  first  lodged  in  the 
gray  matter  of  the  cord,  undergo  certain  modifications  there,  and  are 
then  sent  out  as  distinct  original  cord  impulses.  This  is  a  most  im- 
portant distinction.  It  gives  the  cord  the  dignity  it  should  hold  and 
it  explains  many  of  the  motor,  sensory,  reflex  and  trophic  phenomena 
of  disease  states  in  a  way  that  cannot  even  be  conceived  of  upon  the 
basis  of  the  cord  being  a  mere  conduit  through  which  rush  the  stimuli 
between  the  brain  and  the  outlying  organism.  Strictly  speaking, 
therefore,  conduction  is  not  a  spinal  cord  function,  as  the  function 
has  heretofore  been  usually  thought  of,  and  for  that  reason  I  have 
postponed  its  consideration  until  the  last. 


482  THE  XOX-NEUROXIC  DISEASES 

Let  it  be  clearly  understood  then  that  no  impulse  of  au^^  sort, 
between  the  brain  and  the  periphery,  passes  without  being"  broken  and 
modified  more  or  less  in  the  ganglionic  gray  matter  of  the  cord. 

The  white  conducting  tracts,  which  we  studied  a  few  paragraphs 
back,  are,  strictly  speaking,  not  a  part  of  the  cord.  They  are  processes 
reaching  down  from  the  brain  cells  above  and  from  the  peripheral 
ganglionic  sensory  neurones  from  below,  to  carry  the  impulses  from 
either  hand  into  the  gray  ganglionic  masses  of  the  cord.  This  was 
clearly  pointed  out  in  our  discussion  of  the  neuronic  architecture  of 
the  nervous  system  and  in  the  consideration  of  the  minute  anatomy  of 
the  part  of  the  nervous  system  called  by  the  anatomists  the  spinal  cord. 

The  motor  pyramidal  tracts  are  cerebral  structures  and  are  loosely 
spoken  of  as  being  parts  of  the  spinal  cord  merely  because  they  lie 
close  to  it.  The  same  is  to  be  said  of  the  long,  projection  sensory 
tracts.  To  emphasize  this,  which  I  regard  as  a  most  important  neu- 
rological fact,  let  me  mal<:e  use  of  a  homely  illustration  by  saying  that 
if  a  boy  in  search  of  jam  has  his  whole  arm  thrust  down  deep  into 
a  long,  narrow  jar,  his  arm  does  not  thereby  become  a  part  of  the  jar 
or  be  regarded  as  entering  into  the  general  functions  of  the  jar.  In 
the  same  way  the  cortical  neurone  cells,  thrust  their  long  arms  down 
along  side  of  the  true  spinal  cord,  consisting  of  its  various  segments  of 
gray  deposit  bound  together  by  short,  associative  tracts  of  white  mat- 
ter, and  with  their  arborization  fingers,  so  to  speak,  stimulate,  inhibit 
and  control  the  cells  in  the  cord  that  stimulate  the  muscles  and  sub- 
serve the  movements  of  the  body.  Here  again  we  observe  the  beau- 
tiful uniformity  and  consistency  of  nature.  Such  a  phenomenon  is 
again  nothing  but  a  reflex,  but  the  stimulus  comes  from  the  brain  this 
time  and  not  from  the  skin  or  tendon.  The  movement  that  is  pro- 
vdced  by  it  is  said  to  be  a  volitional,  a  sort  of  intellectual  movement, 
because  the  afferent  stimulus  to  the  cord  comes  from  a  finer  and  more 
complicated  source,  the  cerebral  mechanism  and  cells  that  underlie 
psychic  acts,  but  the  movements  of  the  muscles  themselves  are  imme- 
diately due  to  the  cord  stimulation  and  are  the  result  of  the  old, 
primitive  reflex  function  of  the  spinal  cord. 

The  whole  phenomenon  then  of  a  volitional  impulse  is  of  the 
nature  of  a  higher  form  of  reflex,  so  far  as  the  spinal  cord  is  con- 
cerned. 

It  would  probably  take  us  wide  of  the  mark  to  discuss  here 
whether  the  impulse  that  starts  from  the  cerebral  cortex,  and  which 
eventuates  in  a  so-called  volitional  movement,  originates  there  or  is 
itself  a  reflex  acting  under  the  stimulus  of  an  impulse  sent  up  from  the 
skin  by  way  of  the  spinal  cord.  The  question  is  a  philosophical  one 
and  belongs  to  psychology.  Nevertheless  it  must  be  noted  here  that 
very  often  such  so-called  volitional  impulses  are  the  direct  result  of 
fresh  afiferent  stimuli.  This  is  a  matter  of  daily  common  observation. 
These  afferent  stimuli  do  not  reach  the  brain  cortex  in  the  original 
state  in  which  they  started  from  the  periphery.  Our  anatomy  shows, 
and  physiology  and  pathology  amply  prove,  that  they  are  first  received 
from  the  peripheral  sensory  neurones  into  the  gray  ganglionic  deposits 


THE    XON-XEUROXIC    DISEASES  483 

of  the  cord,  are  there  switched  off  and  m  all  probability  moditied,  and 
then  sent  on  up  as  cord  impulses  to  the  brain.  In  other  words,  our 
cortex,  our  consciousness,  does  not  anywhere  directly  perceive  the 
original  stimulus  that  aft'ects  the  outermost  organ  of  sense;  it  only 
perceives  the  related  stimulus  from  the  cord.  It  is  a  startling  fact, 
but  one  none  the  less  true,  that  our  real  sensations  are  from  the  cord. 
We  have  no  conception  of  what  the  skin  feels,  except  as  the  cord  in- 
terprets it  to  us.  How  obvious  this  is  sometimes.  Take  the  following 
illustration :  A  man  touches  a  red  hot  plate.  Two  phenomena  take 
place  from  the  one  instantaneous  stimulation.  The  first  is  the  simple 
cord  reflex  without  the  sense  of  pain.  The  hand  is  jerked  away  before 
the  man  realizes  it.  The  second  is  the  feeling  of  pain  which  comes  a 
second  or  two  after.  Was  the  stimulus  changed?  No,  but  the  cord 
perceived  the  stimulus  and  acted  accordingly  (reflex)  ;  the  brain  ex- 
perienced the  cord's  commotion  and  in  the  language  of  the  brain  called 
it  pain.  The  significance  of  this  from  the  clinical  standpoint  is  of 
tremendous  importance.  It  clarifies  the  discussion  in  regard  to  the 
nature  of  pain.  It  shows  how  it  is  really  a  cerebral  (mental)  phenome- 
non, though  dependent  upon  the  physical  basis  of  the  cord  and  its 
condition.  It  will  lead  to  the  avoidance  of  such  childish  conceptions  as 
that  pain  is  located  in  the  skin  somehow,  or  in  the  peripheral  ends  of 
the  nerves,  and  that  there  is  no  such  thing  as  pain  without  some  gross 
lesion  that  you  can  cut  away  with  the  knife.  It  opens  the  way  for 
the  clearer  conception  of  psychalgia  and  mental  pain,  such  as  are  some 
of  the  pains  of  hysteria.  Moreover,  it  accounts  in  part  for  our  greater 
ignorance  of  the  spinal  pathways  for  the  various  forms  of  sensation, 
as  compared  with  our  knowledge  of  the  motor  pathways.  An  efferent 
impulse  alw^ays  terminates  in  the  same  sort  of  an  element,  which  in 
its  last  analysis,  whether  it  be  muscular,  glandular  or  vasomotor,  is 
largely  a  contractile  or  muscle-like  element.  Afferent  impulses  may 
terminate  in  a  number  of  dift'erent  sorts  of  cellular  combinations  and 
elements  in  the  cord.  These  travel  up  in  various  ways  toward  the 
brain,  w^hich  puts  its  own  interpretation  upon  them,  calling  some  touch, 
some  heat  and  some  pain.  Of  course,  the  nature  of  the  end  apparatus 
which  first  receives  the  stimulus  determines  the  pathway  along  which 
it  shall  travel,  and  thus  the  brain  interprets  it.  This  is  glaringly  dem- 
onstrated in  connection  with  the  special  senses.  Vibrations  doubtless 
hit  all  organs  and  parts  of  the  body  alike,  but  the  eye  directs  the  one 
set  along  the  optic  nerve  and  the  brain  calls  the  vibratory  movement 
light,  the  ear  directs  another  set  along  the  auditory  nerve  and  the  brain 
calls  it  sound.  Both  sets  of  vibrations,  however,  are  interrupted  and 
doubtless  prepared  for  the  brain  by  the  optic  centers  in  the  corpora 
quadrigemina,  etc..  and  by  the  auditory  nucleus  in  the  medulla.  It  is 
not  the  eye  or  the  ear  that  the  brain  itself  perceives,  but  the  commo- 
tion in  the  primary  optic  and  auditory  nuclei. 

The  functions  of  the  motor  and  sensory  projection  tracts  may  be 
recapitulated  as  follows : 

Crossed  and  Uncrossed  Motor  Tracts.  These  bear  impulses^ 
chiefly  of  an  inhibitory  and  controlling  character,   from  the  cerebral 


484  THE  NON-NEURONIC  DISEASES 

cortex  to  the  motor  cells  of  the  anterior  horns  of  the  cord.  If  they  are 
diseased  so  that  they  excite  the  cord  cells,  spasmodic  movements  may 
occur  in  the  limbs  and  body,  involving  groups  of  muscles  that  sub- 
serve volitional,  purposive,  intellectual  physiological  acts.  Individual 
muscles  are  not  thrown  into  a  state  of  spasm.  In  the  higher  cerebral 
and  psycho-neurotic  disorders,  like  hysteria,  permanent  spasms  and 
contractures  may  be  produced.  Note  always,  however,  that  the  whole 
limb,  or  part  of  the  body,  is  affected  in  an  attitudinizing  manner,  and 
not  distinct  muscles.  The  reflexes  and  even  the  normal  automatic 
functions  of  the  cord  may  be  thus  stimulated  and  exaggerated.  When 
the  disease  of  these  motor  tracts  is  such  as  to  suppress  their  control 
over  the  anterior  horn  cells,  paralysis  of  a  spastic  character  occurs  in 
the  limbs.  The  reflexes  are  exaggerated.  Here  again  physiologically 
associated  muscles  and  groups  of  muscles  are  affected,  not  individual 
muscles.  There  is  no  atrophy  and  the  electrical  reactions  are  un- 
changed. Spastic  paraplegia  and  exaggeration  of  the  reflexes  are  the 
principal  manifestations  of  disease  in  these  tracts.  These  are  usually 
bilateral.  Other  symptoms  as  well  as  these  will  be  considered  under 
the  head  of  diseases  of  the  brain. 

Postero-median  Tract.  GoU's  Cohiinn.  This  tract  carries  special 
sensations  from  the  muscles,  articulations  and  tendon  sheaths  of  the 
same  side  to  the  cells  of  the  nucleus  gracilis  in  the  medulla.  When 
it  is  diseased  the  muscular  sense,  including  the  position  of  the  limbs 
and  the  power  of  estimating  weights,  is  lost.  Incoordination  of  move- 
ment, or  ataxia,  occurs,  and  probably  some  astereognosis. 

Poster o-lateral  Tract.  Burdach's  Column.  All  forms  of  sensation 
pass  through  this  compound  and  complex  bundle  of  afferent  processes. 
When  it  is  diseased,  all  forms  of  sensation  are  disturbed ;  ataxia  oc- 
curs; astereognosis,  loss  of  the  reflexes  and  every  physiological  act 
that  involves  sensation,  directly  or  reflexly,  are  diminished  or  abol- 
ished. 

Direct  Cerebellar  Tracts.  As  these  carry  sensations  to  the  cere- 
bellum, their  disease  results  in  a  loss  of  equilibrium. 

Antero-latcral  Tracts.  Cowers  Tracts.  Through  these  pass  the 
pain  and  temperature  sensations  that  originate  on  the  opposite  side. 

It  is  to  be  understood,  as  I  have  tried  to  show,  that,  like  the  optic 
and  auditory  tracts,  these  tracts  that  seem  to  carry  special  cutaneous 
sensations,  do  so  merely  by  reason  of  the  adaptability  of  their  end 
organs  to  receive  particular  sorts  of  vibrations.  Just  as  the  cortex  does 
not  directly  see  and  hear  the  outer  world,  but  merely  interprets  into 
the  psychic  terms  of  light  and  sound,  the  commotion  produced  in  the 
primary  optic  and  auditory  nuclei,  so  it  does  not  feel  the  outer  world 
directly  pressing  against  the  skin,  but  merely  interprets  into  the 
psychic  terms  of  touch  and  heat  and  pain  the  commotion  produced 
in  the  spinal  and  other  nuclei  where  the  processes  of  these  so-called 
spinal  sensory  columns  terminate  and  arborize,  or  possibly  in  some 
higher  ganglionic  center  like  the  optic  thalamus  where  the  next  set 
of  afferent  neurones  terminate.  Our  knowledge  of  the  sensory  func- 
tions is  not  as  well  defined  as  could  be  desired. 


THE    XOX-XEUROXIC    DISEASES  485 

SPIXAL  LOCALIZATIOX  AXD  TOPOGRAPHY. 

The  topography  and  locahzation  of  lesions  within  the  spinal  cord 
are  important  from  the  standpoint  of  surgery.  The  segmental  charac- 
ter of  the  cord  arrangement  here  serves  us  well.  At  regular  intervals 
emerge  from  the  cord  the  anterior  and  posterior  roots  which  unite 
together  to  form  mixed  nerves  that  issue  from  the  spinal  canal  by  way 
of  the  intervertebral  foramina.  High  up  in  the  cord  the  foramina  are 
nearly  opposite  the  place  of  emergence  of  the  spinal  roots.  As  the 
cord  is  shorter  than  the  vertebral  column,  it  necessarily  follo^^.s  tnat 
the  lower  we  go  down  the  cord  the  lower  the  foramina  will  be  in  rela- 
tion to  the  points  of  emergence  of  the  roots.  The  lattev  are  thus 
oblique  and  are  obliged  to  run  a  more  and  more  descending  course, 
after  they  leave  the  cord,  to  reach  the  vertebral  outlet.  It  becomes  a 
matter  of  the  first  importance,  therefore,  to  comprehend  the  topo- 
graphical relationship  of  the  vertebrtz  to  the  underlying  segments  of 
the  cord.  The  spinous  process  of  each  vertebra  is  selected  as  the 
point  beneath  which  it  is  desired  to  know  what  particular  segment  of 
the  cord  may  be  lying.  This  has  been  carefully  worked  out  and  the 
accompanying  diagram  of  Gowers"  reveals  the  facts  in  a  most  graphic 
way.  It  will  be  noted  that  except  in  the  cervical  region,  and  even 
here  to  some  extent,  the  segments  of  the  cord  are  to  be  respectively 
found  two  and  three  spines  higher  than  the  spine  of  the  same  number. 
For  instance,  the  seventh  spinal  segment  is  directly  beneath  the  fifth 
vertebral  spine.  In  the  cervical  region  the  segment  is  only  one  remove 
above  the  corresponding  vertebra.  According  to  Reid  and  Starr,  there 
are  marked  individual  diflrerences  in  regard  to  the  topographical  rela- 
tionship between  the  vertebrae  and  spinal  segments. 

The  determination  of  the  segmental  localizations  involves  a  knowl- 
edge of  the  functions  of  the  nerve  roots.  It  is  needless  to  say  that 
the  anterior  root  is  efferent  and  carries  motor  and  trophic  impulses 
from  the  cells  of  the  anterior  horns  to  the  muscles  of  the  body.  Xor 
need  it  be  repeated  that  the  posterior  root  is  afferent  and  brings  in 
sensory  impulses  from  the  skin  and  other  sensory  organs.  If,  there- 
fore, we  can  work  out  the  correspondence  between  the  segmental 
origin  of  these  nerve-roots  and  the  particular  muscles  and 
cutaneous  areas  that  their  composite  nerves  innervate,  we 
will  have  a  definite  guide  in  the  distribution  of  the  atrophic 
paralysis  and  the  anaesthesia  to  the  exact  segmental  seat  of 
the  lesion.  Allowance  must  be  made  somewhat  for  the  fact  that  no 
segment  is  absolutely  alone  in  its  action,  for  it  is  associated  in  func- 
tion with  the  neighboring  segments,  and  that  no  motor  or  sensory  root 
is  limited  absolutely  to  one  segment  for  its  internal  origin. 

A  segmental  lesion  does  not  produce  a  complete  muscular  atrophy, 
for  instance,  because  the  adjoining  unafi'ected  segments  assist  to 
maintain  the  muscle's  nutrition.  The  same  is  true  in  regard  to  the 
sensation.  A  lesion  of  a  single  pair  of  posterior  nerve  roots  may  not 
even  be  noticed  on  account  of  sensory  disturbance ;  and  a  small  lesion 
in  a  particular  segment  may  not  cause  any  anaesthesia  in  the  area  of 
distribution  of  the  corresponding  nerve. 


486 


THE  NOxNi-NEURONIC  DISEASES 


FIGURE  105. 

MOTOR. 


SENSORY. 

f   Neck  and  scalp 
J   Neck  and  shoulder 

Shoulder 
r  Arm 
Hand 


Abdominal 
Muscles 


Front  of  thorax 


Ensiform  area 


Abdomen 
(Umbilicus  lOlh) 


REFLEX. 


■  Scapular 


'  Epigastric 


Buiiock,  upper 

)      ^'"' 
I  Groin  and  scrotum 
S       front 

f  outer  side 

Flexors,  hip 
■    Extensors,  knee         f  Thigh     -i    front 


-hip 


"  Abdominal 


Adductois 


Abductors  ~i  I 

'  It  (^  inner  side 

Leg,  inner  side 
C  Buttock,  lower 


■  2 

-3 

■1 

a 
■Co 


"    I    Exiensors(?)J 
Flexors,  knee  (?) 


(   Muscles      of     leg 
moving  foot 


(  Perineal     and     Anal   f   p^ 
)       Muscles  ^ 


Back  of  Thigh 

Leg 

and 


Cremasteric 
J    Xnce  reflex 


f  Gluteal 


Foot  clonus 
Plantar 


rineEum  and  Anus 


Skin  from  coccyx  to 
Anus 


A  D:.CH.M   D-tONEO  TO  S^«ow  ™^R---^  o.^^  - 

Spinal  Segments,  and  of  the  spinal  :nerve.  tu  im«i  ' 
Functions  of  the  Spinal  Cord.     (Gowkrs.) 


THE 
EPLEX 


THE    NON-NEURONIC    DISEASES 


487 


For  our  knowledge  of  these  segmental  and  peripheral  correspond- 
ences we  are  indebted  to  Starr,  Alills,  Ross,  Thorburn,  Sherrington, 
Bruns,  Sachs  and  others.  Following  their  teachings,  I  will  give  the 
muscles,  areas   of  sensation  and  the  reflexes,  and  the  corresponding 


Sensibilitt. 


FIGURE  106. 
LOCATION  OF  THE  SEGMENT 

FOR 


Motility. 


'  Thalajrh   Muscles 


a 


Sight  • 

Head  . 

Eyes  . 
Face 


Tongue 
Hearing 


Pharynx 

Larynx 

CEsophagus 

Viscera  of 

Chest  and  Abdomen 

Occiput. 


Shoulder 
W  f  Musculo-spirai  nerve 

^1  Median  nerve 

^  (.Ulnar  nerve 


I  <■•  PuU 


IT , 


^Sphincter  of  the  iris 

ciliary 
-loternal  rectus,  levator  palpebrn.- 

rectus,  inferior  and  superior 
"Inferior  oblique 
^Superior  oblique 
.  Masseter,  temporal, 

pterygoids  [("pper  facial) 

External  rectus,  frontalis,  orbicularis  of 


-^ 


EpigaHtrlum    •«..• 


Gluteal  regiou 
Inguinal  region 


I  Hip 
anterior 
external 
posterior 

internal    

anterior  .— -. 

Foot  — • 

Scrotum,  Penis,  etc.  '•-- ' 

Rectum,  Bladder  „.„, 


...,..^^ 


..,1 


Anus  ••' 


Laryngeal  muscles 
Tongue  muscles 
Sterno-cleido  mastoid 
Deep  neck  muscles 


Trapezius,  Serratus  anticus 

Diaphragm 

Deltoid,  biceps,  pectoralia  (clavicular  part) 

Brachialis  anticua,  supinator  longua 

Triceps,  latissimus  dorsi,  pectoralis  (costal  por- 

Extensorsof  the  fingers  and  phalanges  I     tion) 

Flexors  of  the  fingers  and  phalanges     ("  g.^^" 
Interossei  and  luinbricales  , 

Thenar,  hypothenar  ) 


Intercostal  muscles 
Back  muscles 
Abdominal  muscles 


........  Iliopsoas 

...   Sartorius 
....  Adductors 

,...   Abductors 
....  Quadriceps 


Thigh 


Leg 


....Peronei 

Flexors,  extensors  of  foot  and  toes 
Oluteal  ^    ,       ,     • 
--■    --Perineal  j 

■     Bladder    [-Musculature 
--     ...      Rectum    j 


(After  Jakob.) 


segments  from  which  they  are  innervated.  The  accompanying  ex- 
quisite diagrams  of  Head  will  assist  in  showing  the  segmental  sensory 
innervations.  It  is  to  be  remembered,  however,  that  there  are  no 
sharp  lines  in  nature  between  the  various  areas  as  the  picture  indicates. 
One   area  blends   into  its   neisrhbors,  hence  the  sensory   localizations 


488  THE  NON-NEURONIC  DISEASES 

must  be  made  guardedly.  The  reflex  and  muscular  localization  mani- 
festations are  somewhat  more  distinctly  defined. 

Second  and  Third  Cervical  Segments.  The  sterno-mastoid, 
trapezius,  scaleni  and  deep  neck  muscles,  together  with  the  diaphragm, 
are  innervated  from  these  segments.  Sensation  is  perceived  through 
them  in  the  back  of  the  head  up  to  the  vertex,  and  in  the  neck.  The 
sensory  nerves  involved  are  the  occipitalis  major  and  minor,  auricularis 
magnus,  superficialis  colli  and  the  supraclavicular.  The  so-called 
hypochrondrium  reflex  is  possibly  dependent  upon  them.  This  con- 
sists of  a  sudden  inspiration  produced  by  a  quick  pressure  beneath  the 
lower  border  of  the  ribs.  This  is  not  an  important  reflex.  It  is  prob- 
ably due  to  diaphragmatic  excitability. 

Fourth  Cervical  Segment.  The  diaphragm,  deltoid,  biceps,  coraco- 
brachialis,  supinator  longus,  rhomboid,  supra-  and  infra-spinatus  are 
all  partially  innervated  from  this  area.  The  sensory  distribution  in- 
cludes the  neck,  anterior  surface  of  the  shoulder  and  outer  surface  of 
the  arm ;  and  the  following  nerves,  supra-clavicular,  circumflex  and 
musculo-cutaneous  externally.  An  important  reflex  is  the  pupillary, 
involving  the  fourth  cervical  to  the  second  dorsal  segments,  and  re- 
vealed in  a  dilatation  by  irritation  of  the  neck. 

Fifth  Cervical  Segment.  This  takes  part  in  the  innervation  of 
many  muscles,  especially  those  of  the  arm.  They  are  the  deltoid, 
biceps,  coraco-brachialis,  brachialis  anticus,  supinator  longus,  supinator 
brevis,  deep  muscles  of  the  shoulder  blade,  rhomboid,  teres  minor, 
clavicular  portion  of  the  pectoralis  and  the  serratus  magnus.  The 
sensory  area  includes  the  back  of  the  shoulder  and  arm  and  the  outer 
side  of  the  arm  and  forearm  to  the  wrist.  The  nerves  concerned  are 
the  supra-clavicular,  circumflex,  external  and  internal  cutaneous  and 
posterior  spinal  branches.  The  scapular  reflex,  or  contraction  of  the 
scapular  muscles  by  irritation  of  the  skin  over  the  scapula,  implicates 
the  fifth  cervical  to  the  first  dorsal  segments.  The  supinator  longus 
reflex  is  the  flexion  of  the  forearm  by  the  tapping  of  the  tendon  of 
this  muscle. 

Sixth  Cervical  Segment.  Here  again  a  large  number  of  muscles 
are  innervated — namely,  the  biceps,  brachialis  anticus,  subscapular, 
clavicular  pectoralis,  serratus  magnus,  triceps,  extensors  of  the  wrist 
and  fingers  and  pronators.  The  sensory  areas  are  the  outer  side  and 
front  of  the  forearm,  the  back  of  the  hand  along  the  radial  distribu- 
tion. The  nerves  chiefly  concerned  are  the  external  cutaneous,  internal 
cutaneous  and  radial.  In  the  fifth  to  the  sixth  cervical  segments  we 
find  the  center  for  the  triceps  reUex.  If  the  tendon  just  above  the 
elbow  be  tapped,  the  forearm  jerks  in  extension.  The  sixth  to  the 
eighth  cervical  contain  the  center  for  the  posterior  zvrist  reflex,  ex- 
tention  of  the  hand  occurring  when  the  tendons  are  struck. 

Seventh  Cervical  Segment.  Here  we  find  the  innervation  of  the 
long  head  of  the  triceps,  the  extensors  of  the  wrist  and  fingers,  the 
pronators  of  the  wrist  and  its  flexors,  the  subscapular,  the  costal  part 
of  the  pectoralis,  the  serratus  magnus,  latissimus  dorsi  and  teres  major. 
The  sensory  innervation  includes  the  radial  distribution  in  the  hand, 
the  median  distribution  in  the  palm,  thumb,  index  and  half  the  middle 


THE    XOX-XEUROXIC    DISEASES  489 

finger.  The  nerves  involved  are  the  external  cutaneous,  internal 
cutaneous,  radial,  median  and  posterior  spinal  branches. 

The  anterior  zvrist  reflex  depends  upon  the  seventh  to  the  eighth 
cervical,  the  wrist  undergoing  flexion  when  its  anterior  tendons  are 
tapped.  The  seventh  cervical  to  the  first  dorsal  contain  the  centers 
.  for  the  palmar  reUex.    The  fingers  close  when  the  palm  is  stroked. 

Eighth  Cervical  Segment.  Here  are  found  the  origin  of  stimula- 
tion for  the  long  head  of  the  triceps,  the  flexors  of  the  wrist  and  fin- 
gers and  the  intrinsic  muscles  of  the  hand.  It  receives  sensation  from 
the  ulnar  area  of  the  hand,  back  and  palm  and  the  inner  border  of  the 
forearm.  The  nerves  that  preside  over  this  are  the  internal  cutaneous 
and  ulnar. 

First  Dorsal  Segment.  This  innervates  the  extensors  of  the 
thumb,  the  intrinsic  hand  muscles  and  the  thenar  and  hypothenar  mus- 
cles. The  nerves  involved  are  chiefly  the  internal  cutaneous  and  nen"e 
of  Wrisberg,  or  lesser  internal  cutaneous.  The  skin  chiefly  of  the 
inner  side  of  the  forearm  and  arm  up  to  almost  the  axilla  is  the  sensory- 
area  involved. 

Second  Dorsal  Segment.  Sensation  is  supplied  through  this  m 
the  inner  side  of  the  arm  near  and  in  the  axilla  and  the  nerve  impli- 
cated is  the  intercosto-humeral. 

Second  to  the  Twelfth  Dorsal  Seginoits.  These  stimulate  the 
muscles  of  the  back  and  abdomen  and  the  erectores  spin^e.  They  pre- 
side over  the  sensation  of  the  skin  of  the  chest  and  abdomen,  in  bands 
running  around  the  body  and  downward.  These  bands  correspond  to 
the  spinal  nerves.  As  I  have  said,  the  lines  between  them  are  not  sharp. 
The  sensation  from  the  upper  gluteal  region  is  also  marked  by  these 
segments.  The  nerves  that  are  concerned  are  the  intercostals  and  dorsal 
posterior  nerves.  Two  reflexes  of  importance  are  here  represented. 
The  epigastric,  involving  the  fourth  to  the  seventh  dorsal  segments, 
is  the  retraction  of  the  epigastrium  by  the  tickling  of  the  mammary 
region;  the  abdominal,  mvolving  the  seventh  to  the  eleventh  dorsal, 
is  the  retraction  of  the  abdomen,  produced  by  the  stroking  of  its  sides. 

First  Lumbar  Segment.  The  muscles  concerned  are  the  ilio-psoas, 
the  rectus  and  the  sartorius.  The  innervation  of  the  skin  involves 
that  over  the  groin  and  m  front  of  the  scrotum.  The  nerves  are  the 
ilio-hypogastric  and  ilio-inguinal.  The  cremasteric  reflex,  under  the 
control  of  the  first  to  the  third  lumbar  segments,  is  revealed  in  the 
retraction  of  the  scrotum  by  the  stroking  of  the  inner  side  of  the  thigh. 

Second  Lumbar  Segment.  The  muscles  here  stimulated  are  the 
ilio-psoas,  sartorius  and  quadriceps  femoris.  The  skin  on  the  outer 
side  of  the  thigh,  by  way  of  the  genito-crural  and  external  cutaneous 
nerves,  is  here  innervated.  That  most  important  of  ail  reflexes,  the 
patella,  in  which  the  knee  jerks  as  the  result  of  a  tap  on  the  patella 
tendon,  is  here  represented. 

Third  Lumbar  Segment.  The  muscles  that  receive  their  nerve 
supply  thence  are  the  quadriceps  femoris,  anterior  part  of  the  biceps. 
inner  rotators  of  the  thigh  and  the  abductors  of  the  thigh.  The  skin 
area  affected  is  the  front  of  the  thigh.  The  nerves  are  the  middle 
cutaneous,  internal  cutaneous,  long  saphenous  and  the  obturator. 


490 


THE  NON-NEURONIC  DISEASES 


FIGURE  107. 


CVIII 


Sensory  areas   of  the  skin  and  their  segmental  representation   in  the   spinal 
cord.      (After   Head.) 


THE  NON-NEURONIC  DISEASES 

FIGURE  io8. 


491 


CVIII- 


C  VII 


Sensory  areas   of  the  skm   and  their  segmental  representation  in  the   spinal 
cord.     (After  Head.) 


492  THE  XOX-NEUROXIC  DISE;ASES 

Fourth  Lumbar  Segment.  Plere  the  muscles  represented  are  the 
abductors  of  the  thigh,  the  adductors,  the  flexors  of  the  knee,  the 
tibiahs  anticus  and  the  peroneus  longus.  Sensation  is  received  from 
the  inner  side  of  the  thigh,  leg  and  foot;  and  the  nerves  involved  are 
the  internal  cutaneous,  long  saphenous  and  the  obturator.  The  gluteal 
is  an  important  reflex  represented  here,  though  the  fifth  lumbar  seg- 
ment also  is  involved.  Stroking  the  buttock  causes  a  dimpling  in  its 
fold. 

Fifth  Lumbar  Segment.  Here  we  find  the  source  of  the  nerve 
supply  of  the  outward  rotators,  the  flexors  of  the  knee  and  of  the  ankle,, 
the  peronei  and  the  extensors  of  the  toes.  This  segment  is  in  corre- 
spondence with  the  back  and  outer  side  of  the  leg  and  ankle,  the  sole 
of  the  foot  and  the  dorsum.  The  nerves  implicated  are  the  external 
popliteal,  external  saphenous,  musculo-cutaneous  and  plantar. 

The  Achilles-tendon  reflex,  another  most  important  reflex,  is  here 
centralized.    A  tap  on  the  tendon  causes  the  foot  to  extend  on  the  calf. 

First  and  Second  Sacral  Segments.  The  muscles  represented 
here  are  the  flexors  of  the  ankle,  extensors  of  the  ankle,  long  flexor 
of  the  toes  and  intrinsic  muscles  of  the  foot.  The  back  and  outer  side 
of  the  leg  and  ankle,  the  sole  of  the  foot  and  the  dorsum  are  sensitized 
from  these  segments.  The  nerves  involved  are  the  external  popliteal,, 
external  saphenous,  musculo-cutaneous  and  plantar.  From  the  fifth 
lumbar  to  the  second  sacral  segments  is  the  center  for  the  plantar 
reflex.  When  the  sole  of  the  foot  is  tickled  the  toes  are  all  flexed  and 
the  leg  is  retracted. 

Third,  Fourth  a)id  Fifth  Sacral  Segments.  These  represent  the 
perineal  muscles  and  the  muscles  of  the  bladder,  rectum  and  external 
genitals.  Here  are  also  located  the  automatic  reflex  vesical  and  anal 
centers ;  also  the  genital  and  parturition  centers.  From  these  same 
segments  the  skin  of  the  back  of  the  thigh,  the  anus,  the  perineum  and 
external  genitals  is  innervated.  The  nerves  involved  are  the  small 
sciatic,  pudic,  inferior  hemorrhoidal  and  inferior  pudendal. 

Fifth  Sacral  and  Coccygeal  Segments.  From  hence  the  coccygeus 
muscle  is  supplied  and  the  skin  about  the  anus  and  coccyx.  The  nerve 
is  the  coccygeal. 

Symptoms  of  a  Unilateral  Lesion.  Brown-Scquard's  Syndrome, 
As  this  is  a  localization  manifestation,  it  may  well  be  referred  to  here. 
Brown-Sequard  long  ago  noted  that  whenever  a  lesion  severs  the  cord 
half  way  across,  there  is  complete  motor  paralysis  on  the  same  side 
as  the  lesion,  incomplete  sensory  paralysis,  or  auccsthesia  on  the  oppo- 
site side.  The  reason  for  this  is  obvious,  as  the  motor  tracts  decussate 
in  the  pyramids  above  the  lesion  and  the  sensory  tracts,  immediately 
after  they  enter  the  cord,  below  the  lesion.  Some  additional  phenom- 
ena, however,  accompany  the  syndrome.  The  sensory  disturbance  on 
the  side  opposite  the  lesion  is  an  incomplete  one  because  the  muscular 
sense  is  unaffected.  The  muscular  sense  on  the  side  of  the  lesion  is 
diminished  or  lost.  The  paralyzed  side,  moreover,  is  hypenesthetic,. 
hyperalgesic  and  exhibits  a  slight  elevation  of  temperature.  The  re- 
flexes on  this  side  are  exaggerated  :  though  at  first  they  may  be  absent, 
possibly  in  accordance  with  Bastian's  hypothesis.     If  mobility  returns 


THE  NON-NEURONIC  DISEASES 


493 


FIGURE  109. 


Diagram  to  illustrate  Brown-Sequard's  syndrome.     Modified  from  Brissaud. 


494  '^^^  NON-NEURONIC  DISEASES 

to  this  side,  ataxia,  according  to  Botazzi,  Herbold,  Oppenheim,  sets  in. 
On  the  anaesthetic  side,  all  forms  of  sensation  are  lost,  except  that  of 
the  muscular  sense.  Just  above  the  anaesthetic  area  on  the  side  oppo- 
site the  lesion  there  is  a  hyperaesthetic  zone.  Just  in  an  area  on  the 
same  side  of  the  lesion  and  corresponding  with  the  same  root-zone 
there  is  a  semi-girdle  ring  of  pain,  hypereesthesia  or  anaesthesia. 

The  accompanying  diagram,  modified  from  Brissaud,  exhibits  in 
a  schematic  way  the  mechanism  of  Brown-Sequard's  syndrome.  Dorsal 
stab  wounds  are  the  most  common  cause  of  it,  though  it  may  occur  in 
tumors,  hemorrhages,  syphilitic,  sclerotic  and  even  myelitic  processes 
that  involve  the  cord  half  way  transversely.  The  future  of  these 
unilateral  lesions  is  usually  a  good  one.  The  symptoms  largely  disap- 
pear, though  rarely  completely  so. 

Lumbar  Puncture.  As  a  means  of  diagnosis,  and  in  some  in- 
stances, perhaps,  of  treatment,  lumbar  puncture  has  become  an  estab- 
lished procedure.  At  the  beginning  of  the  consideration  of  spinal  cord 
diseases  would  seem  to  be  the  proper  place  to  consider  it.  Quincke 
first  suggested  the  operation  in  1891  in  a  paper  entitled  Hydrocephalus 
presented  to  the  Tenth  Congress  of  Internal  Medicine.  Two  years 
later  Von  Ziemssen  reported  his  experience  with  it  in  reducing  brain 
pressure.  It  was  Lichtheim  who,  about  the  same  time,  called  attention 
to  the  value  of  it  as  a  diagnostic  procedure.  Then  followed  Furbringer, 
Jacoby  and  many  others,  until  now  it  is  a  familiar  manoeuvre. 

An  ordinary  syringe  with  a  hollow  needle  is  employed.  In  insert- 
ing it  the  needle  may  be  used  alone  or  attached  to  the  barrel  of  the 
syringe.  Too  short  a  needle  ought  never  to  be  used,  as  ofttimes  the 
insertion  has  to  be  made  to  a  considerable  depth.  Sometimes  a  thick 
needle  with  a  stylet  is  most  desirable.  Jacoby  used  a  firm,  smooth 
aspirating  needle  of  a  millimetre  to  a  millimetre  and  a  half  in  diameter 
and  eight  centimetres  in  length. 

Of  course,  strict  asepsis  and  sterilization  are  to  be  employed,  and 
in  restless  patients  an  anaesthetic  may  have  to  be  administered. 

The  column  should  be  rendered  convex  by  the  patient  flexing  his 
body  forward  while  sitting  or  lying,  as  Quincke  recommended,  upon 
his  left  side.  The  puncture  is  to  be  made  between  the  third  and 
fourth,  or  fourth  and  fifth,  lumbar  vertebrae,  in  the  middle  line  in 
children,  about  one  centimetre  laterally  from  it  in  adults,  at  the  height 
of  the  lower  border  of  the  spinous  process,  or  at  about  its  lower  third. 
The  needle  is  made  to  pierce  the  skin  and  then  gently  inserted  upward 
and  towards  the  middle  line,  until  there  is  no  further  resistance.  Usu- 
ally the  needle  has  to  be  pushed  to  a  depth  of  from  two  to  eight  centi- 
metres. As  soon  as  the  subarachnoid  cavity  has  been  entered,  the 
cerebro-spinal  fluid  begins  to  appear  drop  by  drop  or  as  a  slight  stream. 
The  latter  is  due  to  pressure  which  may  be  measured  by  attaching  the 
needle  to  a  manometer.  In  adults  the  normal  pressure  is  about  one 
hundred  and  fifty  millimetres.  It  varies,  however,  from  one  hundred 
and  fifty  to  six  hundred  and  eighty.  Quincke  found  it  to  vary  in  chil- 
dren from  seventy  to  four  hundred  and  seventy  millimetres.  The 
flow,  v^hen  it  has  slowed  down,  rarelv  exceeds  four  drops  in  a  minute. 

Inspiration   and   expiration   modify   the   flow.      Raising   the   head 


THE  NON-NEURONIC  DISEASES  495 

increases  it.  Sometimes  a  slight  change  in  the  position  of  the  needle 
will  cause  a  flow  that  has  ceased  to  start  up. 

There  is  no  absolute  rule  about  the  amount  of  fluid  to  be  with- 
drawn. The  object  being  two-fold — namely,  to  reduce  pressure  and  to 
secure  fluid  for  examination — circumstances  must  determine  the 
amount.  Furbringer  has  taken  off  at  one  sitting  one  hundred  and  ten 
cubic  centimetres. 

There  is  very  little  pain  experienced,  if  aspiration  is  not  resorted 
to.  Headache  sometimes  occurs.  Aspiration  almost  always  produces 
pain,  sometimes  pain  that  is  intolerable.  Rarely  do  any  accidents  occur 
during  the  puncture,  if  care  be  exercised.  The  operation,  however, 
should  not  become  a  routine  one,  for  it  is  not  entirely  devoid  of  dan- 
ger. For  instance,  a  local  meningitis  may  be  transformed  into  a  gen- 
eral meningitis  by  it.  A  root  of  the  cauda  may  be  pierced  and  corre- 
sponding pain  and  neuritis  set  up.  In  cases  of  tumor,  aneurism  and 
meningitis  even,  death  has  followed  early  the  operation.  A  vein  may 
be  entered  and  the  needle  become  clogged.  Blood  must  be  avoided, 
as  it  impairs  the  diagnostic  value  of  the  fluid. 

The  needle  should  be  withdrawn  while  the  fluid  is  still  runnmg. 
In  this  way  the  entrance  of  air  is  prevented.  Sometimes  considerable 
effort  is  required  in  pulling  out  the  needle.  This  is  merely  on  account 
of  the  pressure  upon  the  needle  of  the  crossed  fibrillje  of  the  fascia. 

The  after  treatment  of  the  wound  is  simple  and  consists  of  the 
application  of  a  little  iodoform  collodion  and  a  cotton  compress,  held 
in  place  by  a  piece  of  adhesive  strip.  The  patient  should  remain  quiet 
in  a  horizontal  position  for  several  hours  afterwards. 

As  a  therapeutic  measure,  lumbar  puncture  is  of  little  value.  It 
may  be  employed  as  a  palliative  by  reducing  mtra-cerebro-spinal  pres- 
sure. Some  day  it  may  prove  useful  for  the  direct  medication  of  the 
brain  and  cord. 

As  a  means  of  confirming  a  diagnosis,  under  some  circumstances, 
it  is  available.  Even  here,  however,  it  has  its  limitations.  The  state  of 
the  fluid  does  not  always  and  absolutely  indicate  the  pathological  condi- 
tion present.  For  instance,  there  may  be  an  inflammator}^  separation 
of  the  cranial  and  spinal  cavities  and  the  fluid  that  is  drawn  off  be  per- 
fectly normal,  though  the  cerebral  meninges  are  in  a  high  state  of 
disease.  The  thickened,  gelatinous  condition  of  the  fluid,  sometimes 
observed,  impairs  the  value  of  the  criteria. 

Normal  cerebrospinal  fluid  is  colorless  and  alkaline,  and  con- 
tains sodium  chloride  and  other  inorganic  salts.  There  are  o.i  per 
cent.  of.  proteids,  consisting  chiefly  of  proto-albumose  with  some 
serum-globulin  and  rarely  peptone.  It  does  not  contain  any  serum- 
albumin,  fibrinogen  or  nucleoproteid.  There  is  a  non-nitrogenous  re- 
ducing substance  in  it  which  Claude  Bernard  thought  was  sugar,  but 
which  Halliburton  regards  as  pyrocatechin  derived  from  the  proteids. 

Pathologically  we  note  in  the  fluid  an  increased  quantity  and 
change  of  pressure,  change  of  physical  appearance  such  as  cloudiness, 
increase  of  albumin,  coagulability  and  the  presence  of  abnormal  sub- 
stances and  micro-organisms. 

The  pressure  is  increased  in  hydrocephalic  conditions,  whether  due 


496  THE  NON-NEURONIC  DISEASES 

to  tumor  or  meningitis,  or  other  cause.  It  is  not  constant  nor  path- 
ognomonic in  any  way.  Albumin  is  increased  in  the  inflammatory 
conditions. 

The  presence  of  blood  may  be  accidental  from  the  operation,  or 
pathological.  Hemorrhages  into  the  brain  and  cord  are  the  most  fre- 
quent causes  of  it. 

Purulent  meningitis  often  reveals  pus  cells  in  the  fluid  and  ren- 
ders it  cloudy.  It  is  often  cloudy  also  in  tubercular  meningitis.  The 
presence  of  leucocytes  may  indicate  purulent  inflammation  somewhere, 
though  no  pus  cells  are  found. 

More  important  than  all,  however,  are  the  bacteriological  find- 
ings. These  are  not  constant  unfortunately,  but  when  they  are  pres- 
ent a  positive  differential  diagnosis  can  be  made.  The  bacteria  found 
are  the  bacillus  tuberculosis  in  tubercular  meningitis,  the  pneumococ- 
cus  and  meningococcus  intracelhilaris  in  pneumonia  meningitis,  and 
the  streptococcus  and  staphylococcus  in  purulent  meningitis. 

DISEASES  OF  TPIE  SPINAL  COLUMN. 

These  are  practically  all  surgical  disorders  but  they  produce  neu- 
ronic derangements  of  suflicient  significance  to  warrant  their  consid- 
ation  in  a  work  upon  neurology. 

DISLOCATIONS  AND  FRACTURES  OF  THE  VERTEBRA. 

The  great  majority  of  dislocations  occur  in  the  cervical  region 
and  are  the  result  of  blows  and  injuries  of  various  sorts.  In  this  way 
the  atlas  is  displaced  from  the  axis.  Bone  disease  not  infrequently 
causes  dislocation  between  the  fifth  and  sixth  cervical  vertebrae.  Dis- 
placements are  exceedingly  rare  in  the  dorsal  and  lumbar  region^,  and 
when  they  do  occur  there  do  not  give  rise  to  marked  nervous  symp- 
toms. The  displacement  of  the  vertebrae  may  be  in  any  direction  and 
usually  both  adjoining  bones  are  out  of  the  proper  line.  The  displace- 
ment may  be  unilateral ;  as  a  rule,  however,  it  is  bilateral  and  may  be 
complete  or  incomplete. 

Luxations  in  the  cervical  region  may  result  from  blows,  twists, 
wrenches,  falls  and  sudden  turning  of  the  head  when  there  is  a  heavy 
weight  being  borne  upon  it.  The  deformity  consists  chiefly  of  an  in- 
clination of  the  head  forward,  and  of  the  spinous  processes  of  the  ver- 
tebrae below  the  luxated  one  backward.  The  chin  thus  is  brought  in 
apposition  with  the  chest  or  shoulder  and  the  occiput  with  the  nape 
of  the  neck.  Sometimes  a  noticeable  prominence  is  to  be  detected  at 
the  side  of  the  neck.  Palpation  at  the  back  of  the  pharynx  will  some- 
times reveal  the  dislocation.  The  irregularity  of  the  spines  is  always 
noticeable. 

The  cord  may  be  compressed,  bruised  or  completely  divided.  The 
last  is  a  very  rare  accident.  A  temporary  paralysis  caused  by  compres- 
sion may  quickly  disappear  as  soon  as  the  dislocation  is  reduced.  In 
the  bruised  cases  there  is  some  extravasation  of  blood  and  ere  long- 
myelitis.    Ouadriplegia,  anaesthesia,  sphincter   paralysis    and    all    the 


THE  NOX-XEUROXIC  DISEASES  497 

usual  signs  of  transverse  myelitis  then  appear  and  run  their  usual 
course.  If  the  transverse  ligament  of  the  atlas  is  ruptured,  as  has 
occurred  in  hanging  and  in  the  lifting  of  children  by  the  head,  the  odon- 
toid process  may  compress  the  spinal  cord  and  produce  instantaneous 
death. 

Fractures  may  occur  in  any  part  of  the  spinal  column  and  be  due 
to  disease  of  the  bones,  associated  with  blows,  falls,  violent  muscular 
■contractions  and  sudden  forcible  flexion  of  the  spine.  The  middle 
cervical,  upper  dorsal  and  first  lumbar  vertebrae  seem  to  be  the  choice 
victims  of  the  accident.  Dislocation  often  accompanies  the  fracture. 
Crepitation,  fixation  and  distortion  are  the  usual  surgical  symptoms. 
The  cord  is  u^sually  pressed  upon  and  may  be  damaged  even  when  there 
is  no  constriction  of  the  canal.  Rarely  is  the  dura  torn  but  there  is 
almost  always  rupture  of  the  veins  and  abundant  hemorrhage  in  the 
■extradural  space.  In  the  pia  mater  are  slight  extravasations  of  blood. 
The  cord  is  usually  bruised  and  compressed  by  the  lower  fragment. 
It  is  flattened  and  may  even  be  completely  severed.  Rarely  it  has  been 
lacerated  longitudinally.  Thus  extravasation  of  blood  and  cavities  have 
occurred  in  the  cord  substance.  All  of  this  is  more  or  less  localized. 
Immediately  a  myelitis  lights  up  ^vhich  may  spread  beyond  the  bruised 
area.     Caries,  sometimes  of  a  secondarv  character,  follows  the  injury. 

There  are  three  great  groups  of  symptoms  in  spinal  fracture. 
There  is  the  deformity.  Then  there  is  the  general  nervous  shock  with 
its  sudden  and  temporary  loss  of  consciousness,  its  vomiting  and  its 
pains  and  tetanoid  manifestations.  Lastly  there  are  the  signs  of  con- 
tusion, laceration  and  pressure  of  the  cord.  The  last  include  the  symp- 
toms of  both  epidural  and  snbaracJuioidai  hemorrhage,  central  hemato- 
myelia  and  transverse  myelitis. 

The  transmission  of  impulses  through  the  cord  is  usually  stopped 
"by  the  focal  damage.  ^Motion  and  sensation  are  lost  in  those  parts 
whose  nerve  supply  is  from  the  segment  of  the  cord  below  the  one 
that  is  injured.  There  is  a  horizontal  or  segmental  distribution  of  the 
sensory  phenomena,  on  the  surface  of  the  body.  The  upper  edge  of 
the  sensory  disturbance  does  not  reach  as  high  as  the  level  of  the  af- 
fected vertebra. 

For  the  interpretation  of  the  symptoms  in  these  transverse,  seg- 
mental lesions,  the  reader  is  referred  to  the  account  of  the  Localiza- 
tions in  the  Spinal  Cord. 

Sometimes  the  svmptoms  are  not  such  as  to  afford  an  opportunity 
to  make  a  segmental,  localization  diagnosis.  They  are  irregular  and 
anomalous.  In  such  cases  there  is  only  partial  damage  of  the  cord 
and  the  confusion  arises  from  the  associated  central  hemorrhage  in- 
juring the  gray  matter  but  leaving  the  white  tracts  uninvolved. 

In  these  transverse  lesions,  together  with  the  motor  and  sensory 
paralysis  of  all  parts  below  the  level  of  the  lesion,  there  are  loss  of 
the  reflexes  in  the  zone  of  the  lesion,  or  of  the  segment  below  it.  and 
increase  of  the  reflexes  that  have  their  central  seat  still  lower  down. 
Bastian's  law.  supported  by  Bruns,  must  be  taken  into  account  here. 
Bastian's  hypothesis  is  that  the  lesion  is  only  a  partial  one  when  there 
are   exaggerated  reflexes  below  it,    for  he   says  that  in   all   complete 


498  THE  NOX-NEUROXIC  DISEASES 

transverse  lesions,  the  reflexes  below  are  abolished.  The  functions  of 
;he  sphincters  are  always  impaired. 

In  all  complete  transverse  lesions  the  paralysis  in  the  limbs  is  a 
flaccid  one.  If  the  lesion  is  a  partial  one,  it  is  spastic.  All  lesions  in 
the  lumbar  region  produce  a  flaccid  paralysis  in  the  legs.  Disturbance 
of  the  sensibility  with  preservation  of  the  general  motor  system  means 
involvement  only  of  the  nerve-roots.  Pains  and  twitchings,  spasmodic 
jerkings,  contractures  and  atrophic  paralysis  in  the  muscles  innervated 
by  the  special  nerves  involved  are  then  the  objective  phenomena. 

The  clinical  picture  varies  not  only  in  accordance  with  whether 
the  cord  or  roots  are  implicated  and  the  degree  of  the  damage  done, 
but  it  varies  as  the  lesion  occurs  in  dift'erent  parts  of  the  column. 

Death  is  usually  instantaneous  in  fracture  of  the  atlas  or  axis. 
There  may  be  a  very  slight  displacement  and  the  patient  live,  but  he 
is  in  imminent  danger  from  the  slightest  movement.  Death  usually 
occurs  in  such  cases  in  a  few  weeks  from  secondary  myelitis  or  even 
caries. 

Dislocation,  inclination  of  the  head,  rigidity  and  immobility  from 
pain,  dyspnoea  and  bulbar  symptoms  are  the  usual  signs  of  upper  cer- 
vical fractures.  In  all  cervical  lesions  the  penis  is  erected;  ejaculation 
takes  place  at  the  moment  of  injury;  the  temperature  is  elevated,  the 
pulse  increased  and  the  general  vasomotor  apparatus  disturbed. 

In  mid-cervical  fractures,  the  involvement  of  the  phrenic  nerve 
is  a  cause  of  death.  Sometimes  here  there  is  only  a  slight  displacement 
but  there  is  constant  danger  from  the  slightest  movement. 

Symptoms  of  the  disease  in  the  cervico-dorsal  region  are  the 
oculo-pupillary  disturbances  with  myosis  and  narrowing  of  the  palpe- 
bral opening ;  priapism ;  vasomotor  changes ;  early  paralysis  of  the 
legs  and  muscles  of  the  trunk ;  diaphragmatic  respiration ;  later  in- 
volvement of  the  arms,  affecting  special  muscles ;  muscular  spasm  and 
rigidity  in  the  arms  and  hands ;  and  general  hyperpyrexia. 

Dorsal  lesions  leave  the  arms  intact  and  are  usually  accompanied 
by  intense  pains  about  the  body  and  complete  paralysis  in  the  legs. 
Bastian's  rule  about  the  reflexes  applies  here,  namely,  that  they  are 
lost  if  the  lesion  is  complete,  exaggerated  if  it  is  incomplete. 

Lumbar  lesions  provoke  a  flaccid,  atrophic  paralysis  in  the  legs, 
complete  loss  of  reflexes,  paralysis  of  bladder,  rectum,  genitals  and 
anaesthesia  in  the  distribution  of  the  third  and  fourth  sacrel  nerves. 
This  is  the  saddle  type  of  ansesthesia. 

It  is  practically  impossible  to  differentiate  lesions  of  the  cauda 
equina  from  those  of  the  conns  mcduUaris.  for  the  latter  is  surrounded 
by  the  roots  of  the  former.  There  are  radiating  pains  around  the  areas 
of  distribution  of  the  sciatic  and  pudendal  nerves. 

The  prognosis  of  all  these  cases  is  most  serious.  Dislocations 
hold  out  a  better  hope  than  do  fractures.  The  latter  often  kill  in- 
stantaneously or  in  a  very  short  time.  This  is  especially  true  of  the 
cervical  fractures.  The  lower  dorsal  and  lumbar  fractures  may  not 
at  once  destroy  life  but  they  set  up  spinal  disease  that  causes  bedsores, 
contracture,  nephritis,  cystitis  and  all  the  sequelae  of  a  profound  mye- 
litis that  sooner  or  later  does  terminate  fatallv. 


THE  XOX-XEUROXIC  DISEASES  499 

The  management  of  these  diseases  is  practically  a  surgical  ques- 
tion. After  careful  study  of  statistics,  Goldscheider  formulates  the  fol- 
lowing practical  conclusions : 

1.  Recent  cases  should  not  be  operated  on,  except  where  there  is 
merely  a  comminutive  fracture  of  the  vertebra,  fragments  of  which  are 
pressing  upon  the  cord. 

2.  When  the  paralysis  does  not  disappear  and  a  deformity  also 
exists,  indicating  a  fracture  of  the  vertebral  body,  an  operation  may  be 
in  place. 

3.  Hemorrhage  into  the  spinal  canal  is  not  a  sufficient  cause  for 
laminectomy. 

4.  Operation  is  more  justifiable  in  fracture  of  the  lower  lumbar 
vertebrae  than  in  any  other  region. 

CARIES    OF    THE    \"ERTEBR.E.     TUBERCULAR    SPONDY- 
LITIS. 

Pott's  disease  of  the  spine  first  attracted  attention  on  account  of 
the  nervous  manifestations  produced  by  it.  The  old  English  surgeon, 
Percival  Pott,  described  it  as  long  ago  as  1779.  as  a  cause  of  paralysis. 
It  is  strictly  a  surgical,  bone  disease  of  tuberculous  origin  but  which 
secondarily  involves  the  spinal  cord  in  such  a  way  as  to  bring  it  most 
forcibly  under  the  observation  of  neurology. 

Etiology. — A  tuberculous  cachexia  underlies  the  disease,  though 
in  a  few  instances  a  non-tuberculous  traumatic  caries  does  occur.  In 
many  cases  the  tuberculous  trouble  lies  dormant  until  an  injury  to  the 
spine  starts  it  into  activity.  There  is  an  inherited  diathesis  often  pres- 
ent and  not  infrequently  tuberculous  foci  of  disease  are  found  in  the 
lungs  and  other  parts  of  the  body.  Sex  seems  to  have  no  influence 
upon  the  incidence  of  the  disease.  It  may  appear  at  any  age,  though 
it  is  most  frequently  observed  in  childhood  and  early  adult  years.  It 
does  not  always  immediately  follow  an  exciting  traumatism  for  it  is 
so  insidious  that  many  years  may  intervene  between  the  injury  that 
starts  it  and  the  first  manifestations  of  its  presence.  It  is  now  known 
that  syphilis  has  nothing  to  do  with  it.  Nearby  centers  of  suppuration, 
as  a  retro-pharyngeal  abscess  may  initiate  a  spinal  caries.  Non-septic 
inflammation  very  rarely,  if  ever,  causes  it.  Sometimes  no  cause  can 
be  found  for  it. 

Pathology  axd  Pathogexesis. — Csuaily  only  one  vertebra  is 
affected.  Cnder  the  effects  of  a  tuberculous  osteitis,  the  body  of  the 
vertebra  breaks  down  into  a  fungous,  granulation  tissue,  eventuating 
even  in  the  formation  of  liquefaction  products,  such  as  caseous  and 
purulent  matter.  The  bone  softens  and  yields  under  the  superincum- 
bent weight  so  that  the  spine  is  deformed  and  the  cord  is  distorted  or 
pressed  upon.  The  inter-vertebral  substance  participates  in  the  dis- 
ease process  and  like  the  body  of  the  vertebra  may  go  on  to  complete 
necrosis.    The  pus  burrows  in  various  directions. 

Not  infrequently,  and  especially  under  treatment,  the  disease  pro- 
cess ceases,  resolution  takes  place,  new  bone  replaces  that  which  was 
lost,  and  a  complete  recovery  is  effected. 


500 


THE  XOX-XEUROXIC  DISEASES 


The  sl>iiial  cord  is  involved  secondarily  by  compression  and  bv 
the  pus  that  oozes  into  the  spinal  canal.  Sometimes  there  is  an  enor- 
mous accumulation  of  purulent  matter  between  the  cord  and  the  ver- 
tebrse.  involving  the  loose  areolar  tissue  found  there  and  the  outer  sur- 
face of  the  dura  mater  in  a  severe  septic   inflammation.      When   the 

FIGURE  no. 


Pott's  disease.      (Whitman.) 

pressure  becomes  considerable  the  cord  undergoes  a  similar  inflam- 
matory process.  A  myelomalacia  may  first  be  produced  by  the  com- 
pression and  obstruction  of  the  bloodvessels  and  lymphatics  by  the 
external  pachymeningitis.  Usually,  however,  a  focal  myelitis  or  men- 
ingo-myelitis  occurs,  which  becomes  more  or  less  transverse  though 
it  does  not  extend  longituduially  but  a  very  short  distance. 

The  myelitic  symptoms  are  typical  and  need  not  be  described  in 
greater  detail  here  than  to  say  that  there  is  oedema,  softening,  prolifer- 


THE  XOX-NEUROXIC  DISEASES  5OI 

ation  of  the  vessels,  minute  hemorrhagic  spots  and  local  secondary 
neuronic  degenerations.  Occasionally  the  myelitic  foci  are  dissem- 
inated. Inflammation  always  occurs  when  there  is  compression  but 
sometimes  it  may  appear  when  there  is  slight  or  no  compression.  In 
such  cases  it  probably  advances  from  the  spinal  nerve  roots,  a  neuro- 
myelitis, or  it  may  be  the  result  of  the  extension  of  the  disease  along  the 
course  of  the  arteries,  in  which  case  the  primary  process  may  be  a  soft- 
ening from  a  tuberculous  arteritis  obliterans.  The  spinal  roots  of  course 
are  often  affected. 

The  dorsal  cord  seems  to  be  the  favorite  seat  of  the  trouble.  The 
vertebree  being  laterally  displaced  so  that  one  is  moved  to  one  side  in 
relation  to  its  neighbor,  or  the  bodies  being  collapsed,  there  is  a  notice- 
able deformity  of  the  spinal  column  which  often  becomes  very  marked 
in  the  mid-dorsal  region.  One  or  two  spines  stand  out  beyond  the  oth- 
ers giving  the  typical  appearance  of  an  "angular  curvature." 

Symptoms. — The  symptoms  group  themselves  under  the  four 
heads  of  (i)  constitutional  manifestations,  (2)  the  bone  deformity, 
(3)  the  signs  of  involvement  of  the  spinal  roots,  and  (4)  the  signs  of 
co}npression  of  the  cord  and  myelitis. 

Usually  the  disease  is  so  insidious  that  no  constitutional  or  febrile 
symptoms  are  present.  Signs  of  infection  may  appear,  how- 
ever, but  they  belong  to  the  tuberculosis  or  the  general  disease  and 
are  very  variable.  They  need  not  concern  us  here  as  they  are  not  a 
part  of  the  spinal  cord  phenomena. 

In  most  cases  there  is  a  distinct  spinal  deformity.  This  is  of  the 
nature  usually  of  a  kyphosis.  It  is  commonly  known  as  Pott's  hump. 
It  is  an  acute  angled  protrusion  or  con^  exity  backwards  of  the  spinal 
vertebrae,  due  to  the  softening  and  yielding  of  their  bodies  to  the 
superincumbent  weight.  It  is  accompanied  by  a  local  tenderness,  and 
by  which  it  has  usually  been  preceded.  The  pain  and  soreness  can 
be  easily  elicited  by  vertical  press*ire  upon,  and  lateral  movement  of, 
the  spines.  When  the  disease  is  in  the  cervical  region,  movements  of 
the  head  often  provoke  the  pain.  This  of  course  produces  a  peculiar, 
half -voluntary  rigidity  of  the  neck  and  back  that  has  a  remote  resem- 
blance to  a  torticollis.  Deformity  is  not  infrequently  absent  in  cervical 
spondylitis.  The  tissues  are  thickened  about  the  spine  and  a  gravity 
abscess  sometimes  appears.  These  abscesses  burrow  and  break  out  in 
all  sorts  of  unexpected  places.  They  often  confuse  greatly  the  clinical 
picture.  A  retro-pharyngeal  abscess,  for  instance,  may  interfere  with 
swallowing  so  much  as  to  lead  one  to  imagine  there  is  some  bulbar 
paresis ;  or  the  abscess  may  follow  the  psoas  muscle  and  appear  well 
down  upon  the  anterior  part  of  the  thigh.  CEsophageal  obstruction  has 
been  suspected  from  an  abscess  of  spinal  origin. 

The  involvement  of  the  nerve  roots  is  witnessed  by  the  charac- 
teristically distributed  pains  and  their  intensity.  Sometimes  they  are 
absent.  Xot  infrequently  motor  and  sensory  symptoms  show  the  im- 
plication of  both  anterior  and  posterior  roots.  The  pain,  the  hyperces- 
thesia,  the  muscular  zveakness  and  the  slight  atrophy  follow  the  course 
of  the   nerve  distribution.     A  girdle-like   sensation   is  thus  produced. 


502  THE  NON-NEURONIC  DISEASES 

Instead  of  the  hyperaesthesia,  there  is  occasionally  a  neuritic  hyperaes- 
thesia,  or  even  anaesthesia. 

The  neuritic  symptoms  all  occur  only  when  there  is  a  distinct 
pachymeningitis  which,  however,  does  not  mean  the  majority  of  the 
cases. 

When  the  cord  is  iniplicated,  the  symptoms  are  usually  those  of 
a  transverse  myelitis,  most  frequently  of  the  mid-dorsal  type.  There 
is  a  paraplegia  of  the  legs  with  spasticity  and  exaggeration  of  the  knee- 
jerks.  If  the  cord  is  completely  severed  across  by  the  destructive  pro- 
cess the  well-known  exception  of  Bastian  will  be  observed  and  conse- 
quently there  will  be  flaccidity  and  loss  of  the  knee-jerks  in  the  lower 
extremities.  Ancesthesia  below  the  area  innervated  from  the  diseased 
segment  of  the  cord  is  present.  Above  this  a  zone  of  hyperocsthesia 
is  often  noticed.  In  this  vicinity  also  occurs  the  girdle  pain,  so  dis- 
tinctive a  sign  of  myelitis.  The  superficial,  like  the  deep  reflexes  of  the 
lower  limbs  and  lower  part  of  the  body  are  intact  or  exaggerated. 
Sometimes  they  are  lost  in  accordance  with  Bastian's  hypothesis.  The 
vesical  and  rectal  sphincters  are  paralyzed.  Trophic  symptoms  occur. 
In  brief,  the  entire  clinical  picture  is  that  of  a  distinct  transverse  mye- 
litis. 

Oftentimes  the  existence  of  the  caries  is  long  recognized,  some- 
times years,  before  the  myelitic  paralysis  appears.  The  spinal  deform- 
ity has  been  seen  in  early  childhood  and  yet  the  paraplegia  has  not 
occurred  until  well  into  adult  life.  About  a  year  or  two  after  the 
kyphosis  is  discovered  the  paralysis  supervenes.  Occasionally  both 
appear  together.  Rarely  the  paralysis  has  appeared  without  any  ob- 
jective sign  of  bone  disease  for  a  time. 

The  onset  of  the  paraplegia  is  for  the  most  part  gradual  though 
it  has  followed  soon  after  some  strain,  injury  or  other  exciting  cause. 
In  very  rare  instances  it  has  been  instantaneous,  probably  on  account 
of  some  sudden  displacement  after  a  considerable  period  of  bone  dis- 
ease. Both  legs  are  usually  affected,  though  in  some  instances  one 
leg  has  revealed  weakness  before  the  other.  As  a  rarity,  the  Brown- 
Sequard  syndrome  may  even  be  witnessed. 

The  hump  and  tenderness  in  the  spine,  when  observable,  will  help 
to  localize  the  nervous  lesion.  But  often  these  objective  signs  are 
not  marked.  Then  we  can  often  localize  the  trouble  by  the  peculiar 
grouping  of  the  nervous  exhibitions. 

The  nerve  roots  that  are  involved  will  be  shown  by  the  course 
and  location  of  the  pains,  the  peculiar  distribution  of  the  paralysis 
and  atrophy,  the  herpetiform  eruption,  the  hyperaesthesia  and  the 
anaesthesia.  In  other  words,  the  signs  of  a  distinct,  and  local  neuritis 
must  be  made  out  and  then  the  origin  of  the  particular  nerves  involved 
be  traced  back  to  the  cord  center.  Of  course  these  neuritic  symptoms 
will  only  be  observed  when  a  pronounced  pachymeningitis  is  in  ex- 
istence.    This  is  not  often  the  case,  however. 

This,  as  well  as  the  localization  of  the  lesion  from  the  spinal 
cord  symptoms,  can  be  greatly  facilitated  by  a  reference  to  the  table 
presented  under  the  head  of  spinal  localizations  in  the  preceding 
chaptc 


THE  XOX-XEUROXIC  DISEASES  5O3 

If  the  damage  is  Jiigh  up  in  the  cervical  region,  there  will  be  a 
spastic  quadriplegia,  without  atrophy,  with  the  paralysis  more  marked 
in  the  legs.  Bulbar  symptoms  may  be  present  with  nystagmus  and 
interference  with  respiration.  Death  under  such  circumstances  may 
be  imminent  at  any  moment.  The  pains  shoot  up  over  the  occipital 
region  and  there  is  a  stiffness  and  half-voluntary  fixation  of  tne  head 
that  closely  resembles  a  torticollis.  Occipital  anaesthesia  mav  be  de- 
tected. 

A  lesion  in  the  loi<.'er  cervical  area  produces  the  well-known 
oculo-pupillary  changes,  sweating  on  one  side  of  the  head  and  vaso- 
motor disturbances.  The  legs  remain  in  a  condition  of  spastic  para- 
plegia. The  hands  and  arms  undergo  an  atrophic  paralysis  which  pre- 
cedes the  trouble  in  the  legs.  There  are  sensory  disorders  especially 
in  the  ulnar  distribution.  The  phrenic  and  spinal  accessory  nerves  may 
be  implicated. 

When  the  mid-dorsal  region  is  the  seat  of  the  disease,  the  case  is 
as  a  rule  a  typical  manifestation  of  an  ordinary  transverse  myelitis. 
The  paraplegia  with  rigidity  and  increased  reflexes  in  the  legs,  the 
sphincter  disorders,  the  ansesthesia,  the  girdle  pains  and  the  decubitus 
constitute  its  tout  ensemble  of  clinical  presentations. 

As  we  approach  the  lumbar  region,  the  paralysis  of  the  legs  be- 
comes flaccid  in  character  and  the  knee-jerks  are  lost. 

These  symptoms  are  subject  to  considerable  variation  in  details, 
though  when  taken  broadly  as  general  groups  they  maintain  a  high 
degree  of  constancy,  much  more  so  than  one  would  expect  with  si:ch 
a  variable  lesion.  As  the  myelitis  spreads  up  or  down  the  cord  it  in- 
volves this  or  that  part  more  than  another,  s}"mptoms  appear  that  one 
may  almost  be  inclined  to  regard  as  complications.  Thus  in  old  cases 
bedsores  and  cystitis  occur.  Poliomyelitic  changes  occur,  causing 
profound  atrophy  and  paralysis,  with  the  classical  electrical  degenera- 
tive reactions.  Implication  of  the  posterior  columns  may  lead  to 
ataxic  exhibitions.  Pyramidal  and  disseminated  lesions  have  been 
recorded  with  all  their  peculiar  clinical  manifestations. 

DiAGxosis. — The  readiness  with  which  caries  of  the  spine  can 
be  diagnosed  is  very  different  w^hen  the  signs  of  bone  disease  are  ob- 
trusive from  what  it  is  when  they  are  absent.  If  there  is  a  slight -pro- 
trusion of  the  spine  at  one  point  and  this  is  tender  upon  pressure  or 
movement :  if  there  are  neuritic  pains  that  seem  to  be  in  nerves  that 
lead  back  to  that  point  in  the  cord :  if  the  reflexes  are  slightly  exagger- 
ated, both  skin  and  tendon  reflexes ;  and  if,  especially,  symptoms  show- 
ing more  or  less  solution  in  the  continuity  of  the  cord,  as  the  spastic 
paralysis  of  the  legs,  anaesthesia,  and  irregularity  of  the  sphincters. 
the  diagnosis  can  be  made  practically  certain.  The  Rontgen  ra}'  may 
be  brought  into  use  to  reveal  an  obscure  bone  lesion,  but  the  use  of 
tuberculin  to  establish  the  diagnosis  is  liable  to  be  followed  by  disas- 
trous results.  If  a  focus  of  tuberculosis  can  be  found  elsewhere  in 
the  body,  the  diagnosis  of  course  is  strengthened.  It  must  be  remem- 
bered that  traumata  and  other  non-tuberculous  causes  can  sometimes 
set  up  a  simple  spondylitis  with  similar  implication  of  the  nervous 
structures. 


504  THE  NON-NEURONIC  DISEASES 

There  are  cases  of  caries  in  which  the  diagnosis  is  rendered  very 
difficult  by  the  absence  of  objective  deformity.  These  cases  can  rarely 
be  diagnosed  with  absolute  certainty,  though  some  of  them  are  more 
than  merely  suspicious.  If  the  patient  is  youthful  and  shows  tuber- 
culosis elsewhere,  together  with  a  more  or  less  localized  set  of  slow, 
progressive  nervous  manifestations  pointing  to  the  cord  or  some  of 
its  nerve-roots,  the  diagnosis  may  be  made  with  a  fair  degree  of  ac- 
curacy. 

If  all  signs  of  tuberculosis  fail  and  we  have  nothing  to  depend 
upon  but  the  nervous  manifestations,  the  diagnosis  becomes  extremely 
difficult  and  uncertain.  In  such  cases  sometimes  only  waiting  for 
further  appearances  will  clear  away  the  mystery.  The  disease  under 
these  circumstances  is  liable  to  be  confused  with  primary  myelitis,  pro- 
gressive muscular  atrophy,  intercostal  neuralgia,  primary  pachymen- 
ingitis, tubercular  meningo-myelitis,  intraspinal  tumor,  neurasthenia 
and  hysterical  paraplegia.  Repeated  careful  examinations,  with  every 
effort  made  to  elicit  the  slig^htest  evidence  of  tuberculous  bone  dis- 
ease alone  will  enable  one  to  establish  the  true  character  of  these  cases. 

Remember  that  in  caries  there  are  three  great  neurological  fea- 
tures to  be  looked  for,  namely,  a  progressive,  slowly  advancing,  fixed 
lesion,  that  first  irritates  and  then  destroys ;  secondly,  signs  of  nerve- 
root  involvement  such  as  the  pains  and  atrophic  paralyses ;  and  thirdly, 
signs  of  more  or  less  severance  of  the  spinal  cord,  with  corresponding 
phenomena  in  all  parts  of  the  body  below  the  lesion.  Only  in  pachy- 
meningitis, primary  myelitis,  and  tumor  of  the  cord  is  this  clinical  array 
of  events  liable  to  be  closely  duplicated. 

In  pachymeningitis  the  differential  diagnosis  is  sometimes  abso- 
lutely impossible.  The  usual  causes  of  meningitis,  especially  syphilis, 
and  the  age  of  the  patient  must  be  taken  into  account.  In  pachymen- 
ingitis the  cord  symptoms  are  perhaps  less  and  the  root  symptoms  are 
more  pronounced  than  they  are  in  caries. 

Primary  myelitis  does  not  have  the  root  symptoms  to  the  same 
degree  that  caries  has.  The  neuralgic  pains  and  the  local  trophic  signs 
are  less  pronounced.  In  a  word  primary  myelitis  is  more  distinctively 
a  cord  disease  and  exhibits  the  paraplegic,  ansesthetic,  girdle,  sphinc- 
teric  and  trophic  symptoms  that  go  more  particularly  with  cord  lesions. 

In  tumor  the  pains  are  more  intense  and  excruciating,  the  pro- 
gression more  steady  and  definite,  and  the  succession  of  irritation  and 
destruction  more  regular,  as  a  rule,  than  they  are  in  caries. 

In  progressive  ninscnlar  atrophy  there  are  no  pains  and  the 
-atrophy  is  more  systematically  distributed.  Moreover  the  extensive- 
ness  of  the  symptomatology  shows  the  greater  extensiveness  of  the 
disease  process. 

Intercostal  neuralgia  exhibits  no  atrophic  paralysis,  no  cord  symp- 
toms. 

Nenrasthenic  and  hysterical  patients  not  infrequently  complain  of 
spinal  pains  that  might  easily  lead  to  a  suspicion  of  tuberculous  spondy- 
litis. In  neurasthenia  the  spine  is  not  often  focally  painful.  It  feels 
sore  and  heavy  throughout  its  entire  length.  There  are,  moreover, 
no  distinct  organic  manifestations  such  as  caries     almost     invariably 


THE  NON-NEURONIC  DISEASES  505 

shows,  to  some  degree  at  least.  In  neurasthenia  the  symptoms  are  those 
of  fatigue  and  weariness  and  in  a  changeable  sort  of  a  way  involve  the 
entire  nervous  system.  "Spinal  irritation"  as  a  unique  condition,  apart 
from  the  general  neurasthenic  state,  has  no  place  in  modern  neuro- 
logical nosology. 

In  hysteria  there  are  tender  spots  in  the  spine  so  frecjuently  that 
I  have  long  taught  that  they  were  almost  pathognomic.  They  are  mov- 
able, however,  and  are  subject  to  the  patient's  mental  changes.  Hys- 
terical paraplegia  is  sometimes  remarkably  similar  to  organic  paralysis. 
It  is  spastic ;  its  reflexes  are  increased ;  the  sensory  symptoms  are  not 
as  marked  as  is  usually  the  case  in  hysteria ;  and  there  may  even  be 
some  muscular  atrophy,  probably  from  non-use.  It  is  easy  to  com- 
prehend how  this  may  be  mistaken  for  organic  disease.  We  must  de- 
pend entirely  in  such  cases  upon  finding  other  hysterical  stigmata  and 
especially  the  mental  status  must  be  given  close  study.  It  is  too  fre- 
quent an  error,  however,  which  we  should  be  warned  of,  the  calling 
of  an  obscure  case  of  caries  one  of  hysteria.  The  treatment  for  caries 
would  not  hurt  a  hysteric ;  the  treatment  for  hysteria  might  bring  irre- 
parable disaster  upon  a  spondylitic  case.  I  have  seen  a  serious  organic 
disease  of  the  spinal  cord  several  times  made  to  pass  beyond  the  repara- 
tive stage  by  its  treatment  upon  the  erroneous  notion  that  the  trou- 
ble was  a  mere  neurosis.  Caution  is  most  imperative  here  and  from 
my  own  observation  of  some  of  the  sad  errors  that  have  been  commit- 
ted, I  am  prone  to  feel  that  too  much  cannot  be  said  in  urging  the  pro- 
fession to  keep  their  hands  off  of  a  case  of  spinal  disease  when  they 
are  in  doubt  as  to  whether  it  is  an  organic  or  a  functional  trouble. 

Prognosis. — The  course  of  the  disease  is  most  variable  and  un- 
certain. The  deformity  may  precede  or  it  may  follow  the  nervous 
manifestations.  Steady  progression  or  remissions  may  occur.  Even 
sudden  spontaneous  and  complete  cessation  may  not  be  unlooked  for. 
Abscesses  are  always  liable  to  appear  and  in  high  cervical  disease,  bul- 
bar manifestations  and  sudden  death  need  never  cause  surprise.  Af- 
ter the  paraplegic  condition  has  declared  itself,  the  myelitis  is  likely  to 
terminate  in  about  a  year  with  the  usual  signs  such  as  contracture, 
decubitus,  nephritis,  cystitis,  and  death.  Occasionally  the  fatal  issue  is 
more  the  result  of  a  general  septicjemia  and  tuberculosis  than  of  any 
special  local  trouble.  When  resolution  and  cure  take  place,  either 
the  cord  manifestations  or  the  spondylitic  may  vanish  first. 

Youthful  patients,  and  those  in  whom  the  disease  has  not  yet  been 
of  long  standing,  have  a  better  chance  both  as  to  life  and  cure  than 
aged  and  decrepit  individuals  and  those  in  whom  the  history  of  the 
malady  can  be  traced  many  years  back.  The  existence  of  a  general 
tuberculosis  and  the  character  and  location  of  the  abscesses  modify,  of 
course,  very  seriously  the  prognosis.  Mid-dorsal  lesions  offer  the 
most  favorable  prognosis ;  high  cervical  lesions  perhaps  the  worst.  A 
case  once  got  well  after  an  attack  of  erysipelas,  and  Gowers  mentions 
a  complete  recovery  in  a  case  in  which  there  was  paralysis  of  all  four 
limbs  and  the  diaphragm.  Serious  as  the  disease  is,  therefore,  one  is 
never  justified  in  withholding  hope  of  recovery  from  the  patient  and 
his  familv. 


506  THE  XOX-XEUROXIC  DISEASES 

Treatment. — The  two  great  indications  for  treatment  are  the 
bone  disease  and  the  secondary  myelitis. 

For  the  tuberculous  spondyhtis  a  supporting  treatment  and  pro- 
longed rest  are  the  two  great  desiderata.  The  former  involves  rich, 
nourishing,  fatty  food,  plenty  of  air  and  such  well-established  tonics 
as  cod-liver  oil  and  iron.  The  latter  demands  the  recumbent  position 
in  bed ;  best  on  the  back  because  thereby  the  greatest  amount  of  im- 
mobility is  obtained.  Many  months  may  have  to  be  passed  thus  but 
the  importance  of  the  rest  is  so  great  that  no  temxporizing  should  be 
allowed  that  in  any  way  limits  it. 

For  the  detailed  treatment  of  the  spondylitis  the  reader  should 
consult  the  works  upon  surgery.  Suspension,  the  wearing  of  a  jacket, 
and  the  employment  of  revulsive  measures  will  all  be  amply  discussed 
there.  Suspension  seems  to  me  to  have  too  many  disadvantages  to 
cause  it  to  be  adopted  as  a  routine  measure.  The  cases  that  have  ab- 
ruptly had  their  spinal  symptoms  relieved  by  it.  have  in  all  likelihood 
been  cases  with  displaced  vertebras.  The  greatest  disadvantage  against 
it  is  that  the  rest,  which  is  so  necessar\-  and  which  is  more  than  any 
medicine  or  surgical  procedure  to  the  patient,  is  constantly  broken. 
If  the  spinal  extension  could  be  maintained  then  the  method  would 
be  both  logical  and  commendable.  A  certain  degree  of  permanent  ex- 
tension is  obtained  by  a  jacket,  a  jacket  with  a  jur}^-mast  attachment 
and,  better  than  all.  a  weight  attached  to  the  feet  or  to  a  band  about 
the  hips  while  the  shoulders  are  drawn  towards  the  head  of  the  bed 
with  sheeting  passed  under  the  arm-pits  and  around  the  bed  posts. 
To  be  sure,  not  very  great  extension  can  be  thus  secured  and  it  can- 
not be  long  maintained  without  wearying  the  patient.  Its  advantages 
are,  however,  that  it  can  be  easily  accomplished  without  any  disturbance 
in  the  recumbency  of  the  patient. 

Except  in  a  few  cases,  the  plaster  jacket  had  better  be  avoided. 
It  causes  much  mobility  in  getting  it  on  and  off.  and  when  once  on 
it  tempts  the  patient  to  go  about  more  than  is  wise.  An  extension  plas- 
ter-of-Paris  bed.  as  suggested  by  Phelps  and  Lorenz.  or  even  a  suit 
of  plaster-of- Paris  proposed  by  Karewski.  may  not  be  objectionable 
for  they  at  least  infer  the  recumbent  position.  In  my  own  judgment. 
however,  the  bed  alone  is  the  best,  as  necessitating  the  smallest  amount 
of  movement  and  yet  furnishing  a  means  of  securing  prolonged  and 
absolute  rest. 

The  revulsive  measures,  such  as  setons,  cautery-  and  sinapisms, 
are  not  as  much  employed  now  as  they  were  formerly.  In  regard  to 
the  more  violent  forms  of  counter-irritation  I  rejoice  in  this,  but  in 
regard  to  the  steady,  prolonged  use  of  mild  co-jnter-irritation  I  think 
w^e  may  lose  a  valuable  aid  to  the  treatment,  if  it  be  entirely  discarded. 
The  continuous  application  of  weak  mustard  plasters  or  mustard  poul- 
tices may  not  do  much  for  tuberculous  spondylitis,  but  I  am  sure  it 
has  in  my  hands  helped  ver}-  greatly,  and  more  than  once,  the  spinal 
inflammation.  The  skin  must  not  be  damaged,  the  sinapism  must  be 
shifted  about,  and  the  treatment  must  be  prolonged  for  weeks  and 
months.  Cuoping.  wet  or  dry.  is  an  abrupt  treatment  and  has  more 
disadvantages  than  advantages. 


THE  NON-NEURONIC  DISEASES  507 

Operative  procedures,  such  as  laminectomy,  forcible  redressement, 
liave  not  gained  popular  favor  because  their  later  results  have  not  been 
^o  favorable  as  they  promised  to  be  at  first.  These  are  surgical  ques- 
tions, however,  and  their  discussion  does  not  belong  here. 

There  is  no  specific  treatment  for  the  disease  process.  Oleum 
morrhuas  and  iron  about  exhaust  the  list.  The  syrup  of  the  iodide 
of  iron  is  particularly  useful.  Mercury  and  the  iodides  would  of 
•course  come  into  play  if  there  is  a  history  of  syphilis.  I  consider  the 
calcium  salts  as  very  much  over-rated.  I  have  administered  them 
time  and  again  without  seeing  the  results  that  others  have  claimed  for 
them. 

The  treatment  of  the  nervous  lesions  is  fostered  by  the  treatment 
^iven  for  the  tuberculous  bone  trouble.  In  fact,  after  the  bone  disease 
lias  disappeared  the  ijervous  trouble  often  vanishes  also.  If  compres- 
sion merely  is  present,  the  entire  management  of  the  case  resolves 
itself  into  the  management  of  the  bone  disease.  If  myelitis  is  present, 
the  treatment,  secondary  to  that  of  the  bone  trouble,  should  follow  the 
general  principles  laid  down  for  that  of  inflammation  of  the  cord. 
Symptomatic  treatment  is  of  the  greatest  importance  in  combating  the 
iDcdsores,  the  cystitis,  the  contractures.  In  the  cases  that  recover,  mas- 
■sage  and  mild  faradic  stimulation  of  the  muscles  may  be  of  use.  Tenot- 
-omy  may  be  called  for  to  counteract  the  deformities  produced  by  the 
•contractures. 

In  mentioning  electricity,  I  desire  again  to  emphasize  the  fact 
that  it  is  a  most  dangerous  agent  if  miproperly  used.  I  have  sometimes 
^shed  it  had  never  been  introduced  into  general  therapeutics.  With 
some  medical  men,  and  nearly  always  with  the  laity,  nervous  diseases 
are  always  the  indication  for  electrical  treatment.  If  the  trouble  is 
spinal  and  they  don't  know  just  exactly  what  it  is,  they  at  once  be- 
g'in  the  use  of  strong  galvanic  currents  up  and  down  the  spinal  cord. 
I  would  like  to  see  such  practices  made  a  crime.  I  have  been  the  un- 
■willing  witness  of  them  several  times.  Electricity  is  rarely,  if  ever, 
called  for  in  spinal  or  brain  diseases.  It  is  most  religiously  contra- 
indicated  in  organic  acute  diseases  and  where  there  is  a  possible  doubt 
about  the  accuracy  of  the  diagnosis.  To  see  a  mild,  stationary  myelitis 
that  interfered  but  little  with  the  patient's  comfort  suddenly  trans- 
formed into  a  complete  paraplegia,  with  a  rapid  hastening  of  the  pa- 
tient toward  death,  by  a  medical  man  who  gloried  in  the  use  of  his  elec- 
trical paraphernalia,  but  who  could  not  distinguish  a  myelitis  from  a 
rheumatism,  is  a  most  disheartening  and  exasperating  experience. 

Patients  that  have  once  had  caries  of  the  spine  must  lead  a  care- 
ful, hygienic  life  and  must  be  warned  of  the  possibility  of  relapse  from 
a  neglect  to  do  so. 

TUMORS  OF  THE  VERTEBRA. 

Carcinoma^  sarcoma  and  myxoma  are  the  principal  new  growths 
that  attack  the  spinal  column  and  secondarily  affect  the  spinal  cord 
and  its  functions.  Exostoses  growing  from  the  bodies  of  the  vertebrae 
into  the  spinal  canal  may   also  produce   very  slow,  progressive  cord 


508  THE  NON-NEURON IC  DISEASES 

symptoms.  Of  all  these,  however,  cancer  and  sarcoma  are  the  most 
common.  The  same  conditions  for  all  of  them  are  usually  found  else- 
where in  the  body.  Carcinoma  especially  is  generally  due  to  the  same 
disease  in  the  stomach,  womb,  mammary  gland  or  other  organ  from 
which  it  has  spread  by  metastasis.  Sarcoma  and  osteosarcoma  spread 
from  the  surrounding  parts  and  are  found  chiefly  in  those  advanced 
in  years.  Rarely  are  any  of  these  growths  primary  in  the  vertebrae, 
though  when  they  are  primary  they  usually  start  in  the  bodies  and 
spread  from  one  to  the  other.  The  vertebral  bodies  break  down  and 
thus  allow  the  formation  of  an  angular  curvature.  This  kyphosis  is 
not  generally  so  sharp  as  it  is  in  caries,  as  more  bones  take  part  in  it 
and  the  tumor  is  present  to  modify  it. 

From  the  bodies  there  may  be  an  extension  of  the  growth  into 
the  neighboring  ribs,  muscles,  along  the  lateral  processes  of  the  corre- 
sponding vertebrae,  narrowing  the  inter-vertebral  foramina  througk 
which  the  spinal  nerves  pass.  The  nerve  roots  are  pressed  upon,  in- 
flamed and  sometimes  infiltrated  by  the  cancer.  The  disease  may  even 
advance  into  the  areolar  tissue  between  the  dura  and  the  vertebrae  and 
surround  the  cord  completely.  The  cord  is  thus  compressed  and  often 
inflamed.     It  is  never  invaded,  however,  by  the  neoplasm. 

The  nervous  symptoms  of  special  import  are  the  intense  pains 
from  the  implication  of  the  posterior  nerve  roots  and  the  signs  of  com- 
pression of  the  cord.  Most  cases  are  diagnosed  from  the  deformity  of 
the  spinal  column,  the  presence  of  the  disease  elsewhere  in  the  body  and 
these  nerve  root  manifestations. 

The  pains  follow  the  course  of  the  spinal  nerves  and  are  distinc- 
tive for  their  excruciating  intensity.  They  are  far  more  intense  than 
they  are  in  caries.  At  first  there  are  remissions  but  later  on  they  are 
constant  with  paroxysmal  exacerbations.  They  are  sharp,  lancinating 
and  are  increased  by  every  movement.  They  appear  in  the  arms, 
trunk,  and  legs,  according  to  the  site  of  the  tumor.  They  are  accom- 
panied by  cutaneous  hyperaethesia  and  spots  of  anaesthesia.  The  asso- 
ciated muscles  are  thrown  into  a  state  of  spasm  and  rigidity,  are  con- 
tractured,  paralyzed  and  wasted.  Spasms  and  pains  often  appear  to- 
gether in  the  paroxysms.  In  some  cases  paraplegia  develops,  often 
very  rapidly.  In  this  the  cord  manifestations  dififer  from  those  of 
caries,  where  they  progress  more  slowly.  Twelve  or  twenty-four  hours 
may  see  all  power  in  the  legs  lost.  The  intensely  painful  character  of 
this  paralysis  led  Cruveilhier  to  name  it  paraplegia  dolorosa.  Some- 
times the  onset  of  the  paralysis  is  slower.  The  compression  of  the 
cord  is  the  explanation  of  it.  There  is  nothing  distinctive  about  the 
paralysis.  Inflammation  more  often  accompanies  it  perhaps  than  it 
does  the  paralysis  of  caries. 

The  diagnosis  should  carefully  take  into  account  the  age  of  the 
patient,  the  presence  of  the  disease  in  other  parts  of  the  body,  the  spinal 
deformity,  the  intense  character  and  anatomical  distribution  of  the 
pains,  and  the  signs  of  compression  of  the  spinal  cord.  Skiagraphy 
may  be  invoked  to  assist  the  diagnosis.  Caries  is  less  painful,  is  tuber- 
culous in  the  vast  majority  of  cases  and  occurs  in  younger  individuals^ 


THE  NOX-NEUROXIC  DISEASES  5O9 

Jn  intercostal  neuralgia  the  pains  are  not  bilateral  and  there  are  no  mo- 
tor or  cord  phenomena. 

Cancer  is  a  growth  that  often  runs  its  course  in  a  few  months. 
The  other  tumors  last  for  years  and  then  destroy  life  only  secondarilv 
hy  the  trophic  troubles  they  set  up  and  the  intercurrent  maladies  that 
intervene. 

The  prognosis  of  course  is  always  bad. 

The  operative  treatment  so  far  has  not  accomplished  anything. 
Morphine  to  relieve  the  pains  and  general  hygiene  is  about  all  that  can 
he  done. 

SYPHILITIC  DISEASES  OF  THE  \'ERTEBR.T:. 

Syphilitic  exostoses  that  press  upon  the  cord  are  not  common. 
They  produce  deformity  or  rather  a  spondylarthrosis ;  damage  the 
nerve-roots ;  and  compress  the  cord.  There  is.  therefore,  nothing  dis- 
tinctive about  them  but  their  etiology.  This  is  usually  clear.  If  it  is 
only  suspected  it  may  be  cleared  up  by  the  administration  of  the  iodides 
in  large  dosage  for  a  long  period  of  time. 

AXEURISAIAL  EROSIOX  OF  THE  \'ERTEBR.T:. 

This  cannot  be  diagnosed  unless  there  are  other  indications  in 
the  body  of  aneurism.  Symptoms  of  a  neoplasm  such  as  I  have  been 
relating,  involving  the  nerve-roots  and  the  cord,  that  are  suddenly  in- 
terrupted by  a  complete  paraplegia  followed  by  an  ascending  paralysis, 
would  justify  a  strong  suspicion  of  a  ruptured  aneurism  within  the 
spinal  canal.  The  condition  is  of  more  pathological  then  clinical  in-, 
terest. 

SPIXAL  HYDATID  DISEASE. 

Leyden  and  others  have  collected  a  number  of  reports  of  the  de- 
velopment of  hydatid  cysts  in  the  areola  tissue  between  the  cord  and 
the  bones,  and  possibly  even  in  the  bones  themselves.  Double  cysts, 
partly  in  and  partly  outside  of  the  canal,  have  been  observed.  Of 
course  the  cord  is  compressed  and  inflamed,  vvith  the  usual  symptoms. 
The  diagnosis  is  extremely  difficult  from  other  vertebral  diseases  that 
provoke  a  similar  clinical  picture.  We  can  only  depend  upon  the  pres- 
ence of  the  disease  elsewhere.  Practically  all  cases  prove  fatal,  even 
though  puncture  has  been  tried  as  a  means  of  amelioration. 

LATERAL  CCRX'ATURE  OF  TtlE  SPIXE. 

This  rarely,  if  ever,  produces  distinct  cord  symptoms,  even  when 
there  is  slight  pressure.  I  have  seen  it,  however,  cause  decided  weak- 
ness in  the  legs,  neuralgic  pains  and  severe  general  neurasthenic  man- 
ifestations. The  accompanying  picture  is  that  of  a  girl  who  was  a 
sufferer  from  such  symptoms  and  supposed  she  was  a  nervous  wreck. 
A  correction  of  the  spinal  deformity  resulted  in  her  complete  restora- 
tion to  health  and  happiness. 


510  THE  NON-NEURONIC  DISEASES 

ARTHRITIS  DEFORMANS  OF  THE  SPINAL  COLUMN. 

As  a  phase  of  the  disease  rheumatoid  arthritis,  the  articulations  be- 
tween the  vertebrae  may  be  affected  and  even  become  anchylosed.  The 
whole  spine  may  be  involved  but  it  occurs  more  frequently  in  the  cerv- 
ical region.  The  inter-vertebral  cartilages  undergo  atrophy  or  become 
calcified,  the  heads  of  the  bones  become  enlarged,  new  bony  formation: 

FIGURE  III. 


1.- iii 


Lateral  cun-ature  of  the  spine  with  marked  hystero-neurasthenic  symptoms. 
Orthopsedic  treatment  for  the  spinal  trouble  caused  complete  disappearance  of 
the  neurotic  manifestations. 

takes  place  on  the  spinous  processes  and  complete  fixation  occurs.  The 
spine  is  thus  made  rigid.  The  neck  becomes  fixed  and  the  chin  is  in- 
clined toward  the  chest.  The  inter-vertebral  foramina  are  constricted 
and  the  nerves  pressed  upon.  The  spinal  cord  is  not  usually  impli- 
cated.   A  descending  neuritis  is  seen  in  some  of  the  nerves  involved. 

The  symptoms  of  the  disease  include  the  rigidity,  of  the  spine,  which 
does  not  yield  under  chloroform  narcosis,  local  tenderness  in  the  spine. 


THE  XOX-XEUROXIC  DISEASES  5II 

radiating  pains  and  a  partial  neuritic  atrophic  paralysis  in  the  area  to 
which  the  nerves  go  that  are  inflamed.  The  inflamed  nerves  are  lo- 
cally tender,  as  well  as  being  the  seat  of  the  shooting,  lancinating  pains. 
The  sympathetic  may  be  implicated  when  the  trouble  is  in  the  cervical 
region.  The  nerves  of  the  medulla  have  been  affected  in  a  few  in- 
stances. The  diagnosis  of  the  malady  must  be  made  largely  from  the 
presence  of  the  same  disease  in  other  joints  of  the  body. 

The  disease  is  a  chronic  one,  running  its  course  with  remissions 
and  exacerbations.  It  is  incurable.  The  best  we  can  do  is  to  foster 
a  remission  by  the  use  of  massage,  local  applications  of  iodine,  the 
administration  of  potassium  iodide,  the  salicylates,  quinine,  iron  and 
arsenic,  and  the  employment  of  sulphur  and  alkaline  baths. 

DISEASES  OF  THE  MEMBR.\NES  OF  THE  SPINAL  CORD. 
ANEMIA  AND  HYPEREMIA. 

Notwithstanding  the  fact  that  many  of  the  older  neurological 
writings  contain  much  about  anaemia  and  hypergemia  of  the  spinal 
membranes,  we  know  practically  nothing  about  these  conditions.  On 
account  of  the  peculiar  arrangement  of  the  circulation  and  its  rich 
anastomoses  in  and  around  the  spinal  cord,  it  may  well  be  doubted 
whether  anaemia  or  hyperemia  of  the  membranes  ever  occurs  apart 
from  a  similar  condition  in  the  cord.  Of  the  possibility  of  the  latter 
there  is  not  a  little  dispute.  It  is  not  intended  by  this  to  deny  abso- 
lutely that  anaemia  follows  a  severe  hemorrhage,  an  exhaustive  diar- 
rhoea or  an  aortic  obstruction,  or  that  a  hyperaemia  is  associated  with 
certain  sexual  and  muscular  excesses,  uraemic  and  other  convulsions, 
suppression  of  menstruation  and  strychnine  poisoning.  It  is  but  to 
reiterate  that  we  do  not  have  any  positive  knowledge  of  such  an  under- 
lying condition.  It  must  be  presumed  that  in  the  earliest  stage  of 
meningitis,  and  possibly  as  a  residuum  after  the  inflammation,  hyperae- 
mia of  the  membranes  exists  for  a  time. 

The  clinical  description  of  these  conditions  is  full  of  obscurity. 
On  the  one  hand  many  of  the  symptoms  referred  to  by  authors  are  too 
subjective  in  character  to  possess  any  value  as  indications  of  a  gross 
pathological  disturbance ;  and  on  the  other  hand  they  are  very  closely 
like  those  that  are  known  to  be  indicative  of  actual  inflammation  in 
the  membranes.  The  heavy  feeling  in  the  legs,  the  weakness  amount- 
ing to  paraplegia,  the  pains  in  the  back,  and  the  supposed  relief  afford- 
ed by  lying  flat  on  the  back,  are  too  indefinite  and  certainly  too  posi- 
tively assumed,  as  indications  of  ance)nia.  Such  a  pathology  was  at 
one  time  adopted  for  spinal  concussion  and  the  traumatic  neuroses ;  but 
in  addition  to  what  Page  and  others  have  done  to  show  the  untena- 
bility  of  such  a  pathology,  we  now  know  that  the  traumatic  neuroses, 
including  railway  spine,  railway  shock  and  spinal  concussion,  are 
mostly  cases  of  hystero-neurasthenia. 

The  same  general  critcism  is  to  be  made  of  the  clinical  descrip- 
tion of  hypercBmia.  the  heaviness  and  zueight  in  the  limbs,  the  numb- 
ness, the  slight  paresthesia',  the  fugitive  pains,  the  muscular  tzcitch- 
nigs,  the  disturbance  of  the  sphincters,  and  the  asserted  relief  obtained 


512  THE  NON-XEUROXIC  DISEASES 

bv  lying  on  the  face  or  side,  are  too  subjective  in  character  to  be  of 
real' symptomatic  vakte ;  or  are  much  like  the  well-recognized  symp- 
toms of  actual  inflammation.  At  all  events  the  clinical  picture  usually 
accredited  to  spinal  hyperemia  has  not  yet  been  sufficiently  identified 
with  such  a  pathological  basis. 

All  of  which  being  so  it  is  useless  to  discuss  further  the  diagnosis, 
prognosis  or  treatment  of  anaemia  or  hypersemia  of  the  membranes. 

INFLAMMATION  OF  THE  SPINAL  MEMBRANES.     SPINAL 

MENINGITIS. 

Of  the  three  membranes  covering  the  spinal  cord,  two,  the  dura 
mater  and  pia  mater,  undergo  distinct  forms  of  inflammation.  The 
araehnoid  becomes  implicated  with  the  other  two.  Only  in  very  ex- 
ceptional instances  does  the  inflammation  confine  itself  entirely  to  the 
membrane  originally  attacked.  Sooner  or  later  the  neighboring  struc- 
tures are  involved  by  contiguity.  Thus  when  the  dura  is  inflamed 
externaUv  the  bone  above  it  has  usaully  been  damaged  and  the  loose, 
connective  tissue  between  it  and  the  bone  is  involved.  When  it  is 
inflamed  inter nally  the  arachnoid  and  pia  are  almost  certain  to  be  in- 
cluded. When  the  pia  is  the  original  seat  of  the  disease,  the  arach- 
noid above  it,  including  sometimes  the  dura,  and  the  outer  edge  of 
the  cord  below  it,  are  as  a  rule  more  or  less  implicated  in  the  same 
process. 

This  disease  process  may  be  primary  or  seeondary,  simple  or 
purulent,  acute  or  chronic.  The  symptomatic  manifestations  may  var\- 
greatlv,  the  variations  depending  upon  the  character,  and  location  of 
the  inflammation.  A  number  of  types  of  spinal  meningitis,  therefore, 
are  recognized.  Involving  the  dura  mater  we  distinguish  an  acute 
and  chronic  externaU  and  an  acute  and  chronic  i)iternal,  pachym,en- 
■ingitis. 

The  inflammation  of  the  pia  mater  is  known  as  acute  and  chronic 
leptomeningitis. 

Chronic  svphilitic  meningitis  is  sometimes  spoken  of  as  arachnitis 
gummosa. 

The  forms  of  the  disease  deserving  of  further  consideration  by 
reason  of  their  clinical  importance  are  external  pachymeningitis,  hem- 
orrhagic and  hypertrophic  internal  pachymeningitis,  acute  leptomen- 
ingitis, and  chronic  syphilitic  nieningiiis  or  nieningomyelitis.  The 
epidemic  form  of  cerebrospinal  meningitis  will  not  be  discussed  here. 

ENTERNAL  PACPIY^IENINGITIS. 

This  form  of  spinal  meningitis  never  occurs  de  novo.  It  is  a 
secondary  inflammation. 

Etiology. — Tuberculosis  and  caries  of  the  vertebrse,  fractures 
and  dislocation,  septic  processes  and  purulent  inflammations  in  other 
parts  of  the  body,  such  as  purulent  pleurisy,  psoas  abscess,  puerperal 
pyaemia,  are  the  causative  factors  in  external  pachymeningitis. 

Pathology. — A  purulent  inflammation  with    exudation  and  pus 


THE  NOX-NEURONIC  DISEASES  513 

in  most  cases  occupies  the  space  between  the  bone  and  outer  surface 
of  the  dura.  The  latter  is  covered  with  a  tliick,  creamy,  fibrinous  ex- 
udation either  of  pus  or  caseous  matter.  The  dura  itself  is  thickened. 
The  inner  surface  of  the  dura  is  often  implicated,  but  the  underlying 
pia  very  rarely  so.  The  mflammatory  process  is  more  marked  poste- 
riorly than  anteriorly  on  account  of  the  peculiar  arrangement  of  the 
bloodvessels.  The  cord  itself  is  compressed,  flattened,  and  in  excep- 
tional cases  may  show  some  degree  of  peripheral  inflammation.  The 
thickened  membrane  surrounding  the  nerve-roots  constricts  them  and 
causes  them  to  undergo  inflammation,  softening  and  atrophy.  All  of 
this  produces  what  is  sometimes  called  compression  myelitis  and  multi- 
ple neuritis  of  the  nerve-roots.  As  a  rule  the  disease  extends  focally 
along  a  certain  distance,  though  at  times  the  whole  membrane  may 
be  involved.  The  cervical  part  is  not  as  frequently  attacked  as  the 
dorsal  and  lumbar  on  account  of  the  close  attachment  of  the  dura  to 
the  bone  in  the  neck.  The  cellular  tissue  between  the  dura  and  the 
bone  is  sometimes  purulent  throughout  the  entire  length  of  the  canal. 

Symptoms. — The  symptoms  of  external  pachymeningitis  are  oft- 
times  inextricably  confused  with  those  of  the  original  disease.  When 
they  can  be  clearly  distinguished  they  are  the  signs  of  irritation  and 
compression  of  the  cord  and  nerve-roots.  The  spine  is  tender  and 
painful,  especially  over  the  focus  of  the  disease.  Every  movement 
causes  pain.  Pains  shoot  down  the  limbs  and  around  the  trunk.  These 
radiating  pains  may  assume  the  form  of  typical  girdle,  constricting 
bands.  The  pains  show  a  tendency  to  follow  anatomical  lines  of  nerve 
•distribution.  Various  parcesthesicE  are  present  in  the  extremities,  such 
as  numbness,  formication,  pins-and-needles  sensation  and  tingling. 
Hyperesthesia  of  the  skin  is  common.  Among  the  motor  manifesta- 
tions are  tzvitchings  of  the  limbs,  various  degrees  of  paresis,  partial 
paraplegia.  The  reflexes  are  generally  exaggerated  and  the  sphincters 
may  be  incompletely  affected.  If  the  disease  process  is  limited  in  ex- 
tent, its  location  wall  modify  the  symptomatology  somewhat.  When 
the  cord  is  inflamed  myelitic  symptoms  may  appear.  The  tempera- 
ture, respiration  and  pulse  rate  will  all  assume  their  characteristics 
very  largely  in  accordance  with  the  extent  and  nature  of  the  original 
trouble  that  is  the  cause  of  the  pachymeningitis. 

Diagnosis. — When  there  is  a  history  of  injury  or  other  disease 
of  the  spine,  or  of  suppurative  processes  elsewhere,  the  above  general 
clinical  picture  will  make  the  diagnosis  easy  enough.  Myelitis  is  de- 
void of  the  general  history  of  these  cases,  does  not  have  the  same  soil 
of  rachialgia  and  radiating  pains,  nor  the  temperature,  but  on  the 
other  hand  is  the  cause  of  more  complete  paralyses,  trophic  and  vaso- 
motor disturbances  and  distinct  focal  signs.  There  are  no  radiating 
pains,  parsethesia  and  history  of  injury  and  suppuration  in  muscular 
rheumatism.  Tetanus  is  distinguishable  by  its  trismus  and  the  excita- 
tion of  the  muscular  spasms  by  peripheral  irritation. 

Prognosis. — This  is  always  grave.  It  depends  upon  that  of  the 
original  disease,  as  well  as  upon  the  character  of  the  meningeal  in- 
flammation. If  the  original  trouble  were  not  serious,  and  the  menin- 
geal symptoms  indicated  only  irritation,  some  hope  of  recovery  might 


514 


THE  NON-NEURONIC  DISEASES 


be  held  out.  When  the  original  trouble  is  serious,  as  it  mostly  is,  and 
especially  when  the  meningitis  has  been  of  long  standing,  showing 
involvement  of  the  cord,  the  prognosis  is  absolutely  bad. 

Treatment. — The  treatment  is  practically  surgical  and  concerns 
itself  mostly  with  the  primary  disease.  This  once  overcome,  the  men- 
ingitis is  to  be  treated  upon  the  same  principles  as  any  of  the  more 
common  forms  of  the  disease. 

CHRONIC     CERVICAL     HYPERTROPHIC     PACHYMENIN- 
GITIS. 

This  is  an  internal  inflammation  of  the  dura  mater,  chronic  in 
duration,  hemorrhagic  and  hypertrophic  in  character,  and  involves 
sooner  or  later  the  adjoining  arachnoid,  pia  and  cord.  It  was  first  de- 
scribed by  Charcot  and  Joffroy. 

Etiology. — Adults  are  usually  affected  by  this  disease,  though 
cases  have  been  reported  in  children.  Males  are  more  prone  to  it  than 
females.  Cold,  trauma,  over-exertion,  exposure  and  alcoholism  have 
been  said  to  produce  it.  Syphilis,  however,  plays  so  large  a  role  in  its 
etiology,  that  some  have  wondered  whether  the  disease  were  not  a 
manifestation  of  spinal  syphilis.  It  has  been  supposed  to  have  been 
brought  on  also  by  syringomyelia.  In  the  heTiiorrhagic  form,  analogous 
almost  to  the  hematoma  of  the  cerebral  dura,  it  is  not  uncommon  in 
the  chronic  insane. 

Pathology. — The  disease  is  most  frequent  in  the  cervical  re- 
gion, though  rarely  it  may  occur  in  other  parts  of  the  column.  The 
most  striking  pathological  feature  is  the  thickening  of  the  dura,  almost 
five  and  ten  times  as  thick  as  the  normal  membrane.  The  process  is 
a  chronic  one,  is  more  or  less  limited  to  the  internal  layer  of  the  dura, 
and  ultimately  involves  the  underlying  arachnoid,  pia  and  cord.  Pre- 
ceding the  hypertrophic  process,  in  most  cases,  is  the  hemorrhagic, 
which  in  a  way  resembles  a  dural  hematoma  such  as  occurs  on  the 
brain  sometimes.  The  hemorrhage  occurs  on  the  internal  surface  of 
the  dura  and  is  followed  by  a  chronic  inflammation.  After  a  time  an- 
other hemorrhage  with  inflammatory  action  and  deposition  of  new  mat- 
ter takes  place.  By  the  frequent  repetition  of  this  pathological  action, 
layer  after  layer  of  fibrinous  tissue  is  deposited,  gradually  thickening, 
hardening,  almost  ossifying  the  membranes,  binding  them  together 
and  constricting  and  compressing  the  spinal  cord  and  nerve  roots  and 
thus  producing  in  the  latter  atrophy  and  sclerosis.  In  the  syphilitic 
cases  the  deposited  material  is  of  the  gummatous  variety.  As  a  result 
of  the  steady  compression  and  the  extension  of  the  disease  into  the 
substance  of  the  cord,  the  latter  becomes  involved  completely  across. 
Even  cavities  may  form  in  it. 

Symptoms. — A  moment's  consideration  of  the  nature  and  progress 
of  the  lesion  in  this  disease  will  enable  one  to  quite  definitely 
foretell  the  character  and  succession  of  the  symptoms.  There  are  quite 
distinctly  three  sets  of  symptoms  which  follow  one  another  in  a  regu- 
lar progression.  The  first  set  of  symptoms  indicate  irritation  of  the 
cord  and  roots.     There  is  pain  in  the  neck  and  stififness.     Pains  are 


THE  XOX-XEUROXIC  DISEASES  515 

felt  in  the  back  of  the  head  and  between  the  shoulder  blades.  The 
vertebrse  are  tender  upon  percussion.  Hypercesthesia  and  parcesthesia 
occur,  especially  down  the  arms  and  usually  more  in  one  arm  than 
the  other.  Numbness,  tingling,  pricking,  are  complained  of,  especially 
along  the  area  of  distribution  of  the  ulnar  and  median  nerves.  The 
sensory  symptoms  and  particularly  the  pains  are  apt  to  be  worse  at 
night.  Muscular  rigidity,  cramps,  tremor  indicate  the  motor  irritation 
in  the  arms  and  hands.  All  of  these  symptoms  continue  for  many 
weeks  or  months  before  the  next  stage  comes  on  and  are  obviously  due 
to  the  meningitis.  There  may  be  some  slight  disturbance  of  tempera- 
ture and  pulse,  of  the  irregular  type.  Xausea  and  vomiting  are  not 
entirely  unknown. 

Following  this  neuralgic  stage  is  the  second  or  paralytic,  which 
is  purely  neuritic  in  character.  The  arms  are  chiefly  affected.  They 
are  weak,  rigid,  contracted  and  atrophied.  The  extensors  being  unop- 
posed by  the  normal  action  of  the  flexors,  there  is  over-extension  of 
the  wrist.  The  fingers  are  over-extended  in  the  basal  phalanges, 
sharply  flexed  in  the  middle  and  end  phalanges.  This  gives  an  almost 
pathognomonic  appearance  to  the  hand,  known  as  the  preacher's  hand, 
or  main-en- griff e.  This  paralysis  is  of  the  degenerative  type  and  is 
most  pronounced  in  those  muscles  supplied  by  the  ulnar  and  median 
nerves.  Other  nerves  of  course  may  be  involved,  as,  for  instance,  the 
radial,  causing  pronation.  The  pains,  anaesthesia,  hypersesthesia  and 
trophic  manifestations  continue  during  this  stage.  In  some  cases  it  is 
in  this  stage  that  the  ocido-pnpiUary  symptoms  become  marked.  There 
may  be  dilatation  followed  by  contraction.  The  pupillary  signs,  how- 
ever, are  not  distinctive  in  any  way  of  the  disease.  This  is  a  very 
chronic  stage,  even  more  so  than  the  first.  Its  symptoms  are  plainly 
due  to  the  severe  compression  and  beginning  destructive  inflamma- 
tion in  the  roots  and  peripheral  border  of  the  cord.  It  is  not  sharply 
defined  from  the  last,  or  paraplegic  stage. 

In  the  third  stage,  the  paraplegic,  the  cord  is  more  or  less  diseased 
and  damaged  completely  across.  The  pains  and  other  sensory  symp- 
toms now  gradually  decrease  as  the  paralysis  of  the  legs  comes  on. 
This  paralysis  is  spastic  in  character  and  is  associated  with  exagger- 
ated knee-jerks,  increased  niyotatic  irritability,  muscular  rigidity  and 
spinal  trepidation.  Anaesthesia  is  present,  as  well  as  disturbance  of 
the  sphincters.  Gradually  weakness  and  exhaustion  supervene  and  the 
patient  dies  of  this  or  some  intercurrent  malady. 

The  clinical  picture  of  the  disease  which  I  have  just  presented  is 
of  the  more  common,  cervical  type.  The  extension  of  the  inflamma- 
tion up  or  down  the  cord  will  of  course  modify  the  picture  somewhat. 
Involvement  of  the  medulla  and  pons  will  add  corresponding  symp- 
toms, such  as  impairment  of  hearing,  tachycardia,  and  other  special 
bulbar  manifestations.  In  the  so-called  peripheral  type  of  the  disease 
the  symptoms  are  more  distinctly  limited  and  localized  in  the  extrem- 
ities. 

DiAGXOSis. — The  diagnosis  of  cervical  hypertrophic  pachymen- 
ingitis is  at  times  extremely  difficult.  At  first  it  may  be  mistaken  for 
Pott's  disease  of  the  spine.     Later  on  the  atrophy  of  the  muscles  may 


5l6  THE  XOX-NEURONIC  DISEASES 

lead  to  the  erroneous  opinion  that  the  case  is  one  of  progressive  mus- 
cular atrophy.  And  still  later,  the  syringomyelic  lesion  added  to  the 
pachymeningitis  will  be  sure  to  lead  to  confusion.  Moreover  the  dis- 
ease has  to  be  carefully  differentiated  from  myelitis,  spinal  tumor,  tor- 
ticollis, etc. 

When  the  disease  is  of  the  typical,  cervical  type,  the  localization 
of  the  symptoms,  their  bilaterality,  their  chronic,  progressive  charac- 
ter, their  more  or  less  agreement  with  the  succession  of  stages  out- 
lined above  go  far  toward  making  the  diagnosis  positive.  At  times 
tumor  cannot  be  differentiated.  The  safest  way  to  differentiate  this 
from  other  typicaK  diseases  is  to  exclude  this  by  a  careful  considera- 
tion of  all  of  the  symptoms  of  the  others.  A  myelitis,  for  instance,  is 
not  preceded  as  a  rule  by  a  prolonged  meningitic  period  and  a  pro- 
gressive muscular  atrophy  is  practically  devoid  of  all  sensory  phe- 
nomena. 

Widal  and  Le  Sourd  have  suggested  that  an  examination  of  the 
cephalo-rachidian  fluid  should  be  made  in  doubtful  cases.  In  Pott's 
disease,  for  instance,  this  fluid  is  normal  with  respect  to  its  cellular 
contents,  whereas  in  pachymeningitis  it  contains  after  centrifugation 
mononucleated  elements,  lymphocytes  for  the  most  part,  mixed  with 
some  large  cells  having  a  single  nucleus  and  much  protoplasm. 

Prognosis. — This  disease  is  painful,  chronic  and  progressive.  Its 
progress  may  cease  at  any  stage.  Cure  has  been  occasionally  reported. 
Most  of  the  cases,  however,  terminate  in  death  and  a  grave  prognosis 
had  better  always  be  given. 

Treatment. — Syphilitic  cases  of  course  should  be  vigorously 
combated  with  mercury  and  the  iodides.  Other  cases  may  be  helped 
by  the  use  of  local  counter-irritation.  Iodine,  mustard,  cups,  the  act- 
ual cautery,  are  all  indicated.  Hydrotherapy  has  seemed  to  have  been 
useful  in  a  few  cases,  in  giving  relief  if  not  in  producing  a  cure.  The 
pains,  spasms,  etc.,  must  be  treated  symptomatically  with  anodynes, 
narcotics,  antispasmodics.  Electricity  has  a  field  of  usefulness  here 
apparently  and  is  worthy  of  a  trial.  It  is  not  impossible  that  sur- 
gery may  be  of  some  benefit  to  these  cases  some  day.  The  indications 
are  suggestive  and  if  undertaken  early  enough,  before  there  is  serious 
involvement  of  the  cord,  lumbar  puncture,  laminectomy,  or  incision  of 
the  dura  mav  accomplish  something  favorable. 

ACUTE  SPINAL  LEPTOMENINGITIS. 

This  is  an  acute  inflammation  of  the  pia  mater,  rarely  occurring 
apart  from  cerebral  meningitis,  is  secondary,  and  is  due  to  infection. 

Etiology. — Simple,  primary  leptomeningitis  is  practically  un- 
known. When  due  to  a  traumatism,  to  rheumatism,  exposure  and  sun- 
stroke it  is  nevertheless  infective  in  origin.  It  occurs  in  tuberculosis, 
syphilis,  typhoid  fever  and  septicaemia  following  purulent  wounds, 
otitis  and  the  puerperium.  It  is  the  form  of  meningitis  that  occurs 
epidemically  as  cerebrospinal  meningitis.  Children  are  the  most  fre- 
quent sufferers,  and  among  adults  males  predominate.  Dana  remarks 
that  alcoholism  predisposes  to  it. 


THE  XOX-XEUROXIC  DISEASES  517 

Pathology. — The  character  of  the  inflammation  and  its  accom- 
paniments will  naturally  depend  upon  the  cause  and  infective  character 
of  the  original  disease.  Syphilitic  cases  reveal  the  gummatous,  gran- 
ular exudate.  In  the  tuberculous  cases  there  is  not  a  very  abundant 
exudate  and  it  is  of  a  fibrinous  nature,  grayish  in  appearance.  Pus 
of  course  is  absent,  but  there  are  miliary  tubercles  in  the  meshes  of 
the  arachnoid  and  on  the  inner  surface  of  the  dura.  Simple  exudative 
meningitis  is  so  rare  as  to  be  of  but  little  clinical  interest.  In  most 
of  the  cases  an  exudate  is  found  that  is  due  to  various  pyogenic  micro- 
organisms such  as  the  streptococcus  pyogenes,  to  the  pneumon- 
coccus,  etc.  Thus  an  initial  hyperaemia  is  followed  by  a  purulent  exu- 
dation which  spreads  through  the  pia  and  arachnoid  and  clouds  the 
cerebrospinal  fluid.  The  membranes  are  bound  together  by  adhesions 
and  adhere  closely  to  the  cord.  The  spinal  nerve-roots  and  the  peri- 
phery of  the  cord  are  constricted  and  slightly  inflamed.  All  of  this 
is  more  marked  on  the  posterior  than  the  anterior  or  lateral  aspects  of 
the  cord.  Sometimes  the  disease  localizes  itself  focally  at  various 
levels.  When  the  inflammation  ends  there  is  often  left  a  mass  of  new 
connective  tissue,  or  the  disease  passes  into  a  state  of  chronicity.  This 
causes  sclerotic  changes  and  by  the  compression,  irritation  and  destruc- 
tion caused  by  the  thickened,  adhering  membranes  keeps  alive  a  group 
of  subacute,  permanent  symptoms.  • 

Symptoms. — The  chief  symptom  of  spinal  meningitis  is  pain,  and 
is  the  result  of  pressure.  The  pains  are  local  and  radiating,  dull, 
aching,  sharp  and  shooting.  The  spine  itself  is  tender  on  pressure  and 
percussion.  The  tenderness  occurs  sometimes  in  spots,  these  spots 
usually  overlying  the  foci  of  maximum  inflammation.  Sharp,  shoot- 
ing pains  are  felt  up  in  the  neck  and  back  of  the  head,  down  into  the 
arms,  around  the  trunk  and  down  along  the  legs.  They  follow  the 
course  of  the  nerves  and  are  due  to  the  compression  and  constriction 
of  the  posterior  nerve  roots.  The  same  pressure  and  irritation  of  the 
anterior  roots  cause  mnscniar  rigidity.  The  muscles  of  the  back  and 
neck  are  stiff.  The  body  is  sometimes  thus  bowed  forward  in  the  con- 
dition of  opisthotonos  with  the  head  boring  backward  into  the  pillow. 

All  this  usually  starts  abruptly  with  a  chill,  some  elevation  of 
temperature  and  alteration  of  the  pulse  rate.  There  may  be  a  febrile 
headache  and  other  indications  of  cerebral  meningitis  with  nausea  and 
vomiting.  The  urine  is  retained  and  the  bowels  are  constipated. 
Gradually  the  pains  increase  as  well  as  the  muscular  stiffness.  As 
every  movement  of  the  back  provokes  pain,  the  patient  adds  his  volition 
to  the  maintenance  of  the  muscular  rigidity.  The  skin  is  exceedingly 
hypercesthetic  and  painful.  The  reflexes  are  increased  at  first,  but 
diminished  later  on.  On  account  of  the  muscular  stiffness,  Kernig's 
sign  is  present.  The  so-called  tdche  bleudtre  of  the  French  writers 
can  be  elicited  and  indicates  implication  of  the  vasomotor  apparatus. 
It  is  not  important,  however. 

If  the  patient  is  not  cut  oft'  early  by  death,  paralysis,  paraplegia 
or  paraparesis  will  usually  come  on.  The  sensibility  becomes  les- 
sened, the  bladder  grows  weak  and  the  reflexes  become  profoundly 
affected.     The  respiration,  the  heart  beats  and  the  pupillary  activity 


5l8  THE  NON-NEUROXIC  DISEASES 

may  all  be  implicated.  In  the  last  stages  complete  palsy,  atrophy  and 
anaesthesia  may  be  observed.  The  most  severe  and  rapid  onset  of 
symptoms  outlined  above  occur  in  the  septic  cases. 

The  tuberculous  forms  of  the  disease  are  slower  in  their  onset 
and  progress,  while  the  infectious  forms  range  between  the  septic  and 
tuberculous  in  this  respect. 

Diagnosis. — The  diagnosis  of  spinal  meningitis  is  not  difficult. 
The  febrile  symptoms,  the  local  tenderness  and  radiating  pains,  the 
tonic  and  clonic  spasms,  the  Kernig  and  reflex  signs,  when  all  placed 
together  produce  an  unmistakable  picture.  In  myelitis  there  is  no 
spinal  tenderness  and  generally  less  pain  but  much  more  pronounced 
paralysis.  The  sphincters  are  affected  in  myelitis,  the  reflexes  are 
characteristically  exaggerated  and  the  trophic  manifestations  are  more 
prominent.  In  tetanus  the  history  of  an  injury,  the  trismus  and  the 
absence  of  the  irregular,  high  fever  of  meningitis,  ought  to  make  a 
differentiation  comparatively  easy.  Rheumatism  exhibits  mere  mus- 
cular pain,  no  cutaneous  hypersesthesia,  bladder  symptoms  or  trophic 
manifestations.  The  examination  of  the  cerebrospinal  fluid  obtained 
by  lumbar  puncture  may  be  resorted  to  in  very  doubtful  cases.  It 
will  show  in  nearly  every  case  a  cloudiness,  and  a  leucocytosis,  and  pos- 
sibly a  few  bacilli. 

Prognosis. — The  onset  and  course  of  the  disease  are  generally 
acute  and  foudroyant.  In  a  few  days  it  generally  proves  fatal ;  hence 
the  prognosis  is,  as  a  rule,  bad.  Sometimes  the  patients  linger  several 
weeks  before  death  overtakes  them.  These  cases  may  subside  and 
pass  into  chronic  meningitis.  The  cases  with  the  worst  prognosis  are 
those  with  high  fever,  intense  pains  and  rapid  appearance  of  paralysis. 
Septic  cases  are  bad  and  the  tuberculous  cases,  though  ofttimes  slow 
and  prolonged,  cannot  be  expected  to  recover.  Very  rarely,  however, 
recovery  has  occurred ;  more  particularly  among  the  epidemic  and 
otitic  cases.  Partial  recovery,  with  a  remaining  bladder  weakness, 
slight  paralysis,  hyperaesthesia  may  legitimately  be  always  hoped  for. 

Treatment. — The  first  thing  to  do  in  the  treatment  of  spinal 
meningitis  is. to  put  the  patient's  mind  and  body  at  rest.  Perfect 
quietude  of  room  and  environment  must  be  obtained.  The  pains  must 
be  suppressed  by  opiates,  and  sleep  be  induced  by  bromides  and  other 
hypnotics.  The  skin,  bowels  and  kidneys  should  all  be  made  as  active 
as  possible  and  with  the  least  amount  of  disturbance  of  the  patient. 
As  the  patient  is  urged  to  lie  most  of  the  time  on  the  side  or  abdomen, 
local  treatment  of  the  spine  can  easily  be  instituted  and  carried  out. 
An  ice  bag,  of  the  Chapman  type,  may  be  placed  alongside  of  the 
spine,  or  wet  packs  may  be  similarly  employed.  After  the  pain  is 
lessened  somewhat,  dry  cups,  leeches  and  sinapisms  may  be  used.  I 
do  not  favor  too  energetic  measures  for  they  are  apt  to  irritate  and 
disturb  the  patient.  In  most  of  my  cases  I  use  mustard,  even  diluted 
with  flaxseed,  daily  or  twice  a  day  on  alternate  sides  of  the  spinal  ver- 
tebrae. I  believe  more  is  accomplished  by  constant  prolonged  mild 
counter-irritation  than  by  too  hasty  or  severe  methods. 

Notwithstanding  some  opinions  to  the  contrary.  I  am  satisfied  that 
mercury  is  the  best  medicament  now  at  our  disposal  for  the  internal 


THE  NON-NEURONIC  DISEASES  519 

treatment  of  spinal  meningitis,  syphilitic  as  well  as  non-syphilitic.  It 
may  be  used  by  inunction  or  by  the  mouth.  Any  preparation  of  mer- 
cury may  be  used,  though  I  prefer  unguentum  hydrargyri,  calomel  or 
blue  mass.  It  must  be  given  rather  freely,  guarded  by  opium,  and 
for  a  long  period  continuously.  I  have  not  found  it  necessary  to  ex- 
periment with  small  doses  of  potassium  iodide  or  sulphate  of  magne- 
sium, given  at  short  intervals,  though  both  are  highly  indorsed.  In 
the  later  stages  of  the  disease  more  heroic  counterirritation  by  means 
of  cantharides,  the  hot  iron,  the  Paquelin  cautery,  or  even  mere  hot 
douches,  may  be  of  much  advantage.  Lumbar  puncture  with  with- 
drawal of  some  of  the  cerebrospinal  fluid  has  been  reported  to  have 
brought  about  a  cure. 

In  the  treatment  of  meningitis  I  am  convinced  that  time  and 
patience,  with  absolute  quiet  and  the  mercurials,  will  do  more  than 
harsh  or  hasty  methods. 

SYPHILITIC    SPINAL    MENINGITIS.       SPINAL    SYPHILIS. 

Syphilis  affects  the  spinal  cord,  just  as  it  does  the  brain,  in  various 
ways.  Certain  late  products  of  syphilitic  infection,  such  as  the  so- 
called  parasyphilitic  troubles,  like  locomotor  ataxia,  will  not  be  dis- 
cussed here.  Under  the  above  heading,  I  will  consider  rather  the 
true  syphilitic  diseases,  namely,  meningitis,  meningo myelitis,  gumma. 

Our  knowledge  of  spinal  syphilis  is  less  than  our  knowledge  of 
cerebral  syphilis ;  nevertheless  a  sharp  distinction  should  always  be 
made,  when  possible,  between  syphilitic  disease  and  other  affections  of 
the  cord  that  may  resemble  syphilis. 

Etiology. — Constitutional  syphilis,  acquired  or  inherited,  is  of 
course  the  etiological  factor  in  the  production  of  spinal  syphilis.  Other 
determining  influences  are  the  age  of  the  patient,  his  mode  of  life,  the 
manner  of  the  primary  treatment  of  the  constitutional  disease,  trau- 
mata, colds  and  other  infectious  disease. 

Spinal  syphilis  usually  makes  its  appearance  early,  when  it  does 
occur,  after  the  initial  lesion.  Nonne  detected  it  as  early  as  three 
months  after  the  acquisition  of  the  syphilis.  In  most  of  the  cases  it 
appears  in  about  a  year  after,  though  in  some  cases  it  may  not  develop 
until  many  years  after.  In  the  earlier  cases  gummatous  meningitis 
is  the  predominant  lesion  ;  in  the  later  cases  slow  degenerative  processes 
and  sclerotic  conditions  are  more  frequent. 

Pathology  and  Pathogenesis. — ITuebner  enumerates  four  gen- 
eral forms  of  spinal  syphilis: 

First,  neoplasms  of  syphilitic  origin,  including  single  tumors  and 
small  multiple  and  disseminated  formations  on  the  spinal  membranes. 

Second,  syphilitic  callus,  there  being  found  post-mortem  a  cir- 
cumscribed induration  of  the  cellular  tissue  about  the  cord,  generally 
with  adhesions  of  the  dura  mater. 

Third,  simple  softening  of  the  cord.  This  Steenberg  describes, 
though  Huebner  doubts  whether  it  should  be  considered  a  distinct 
syphilitic  lesion.  He  also  doubts  the  existence  of  a  pure  syphilitic 
myelitis. 


520  THE  NON-NEURONIC  DISEASES 

Fourth,  cases  in  which  symptoms  of  acute  ascending  paralysis 
(Landry's  paralysis)  occur  without  discoverable  post-mortem  findings. 

After  giving  a  report  of  a  case  which  manifested  symptoms  to 
classify  it  with  Huebner's  fourth  series,  Wood  states  that  he  doubts 
whether  these  cases  ought  to  be  regarded  as  syphilitic  at  all.  Cer- 
tainly his  own  case,  of  which  it  was  difficult  to  obtain  a  complete 
autopsy,  resembled  one  of  peripheral  neuritis  as  much  as  anything 
else.  The  cases  of  Huebner  and  Kussmaul  were  not  examined  for 
lesions  of  the  peripheral  nerves,  so  that  the  fourth  class,  as  a  form  of 
syphilis,  has  scarcely  been  established. 

In  the  production  of  the  second  and  third  classes  of  Huebner, 
syphilitic  infiltration  and  gummatous  formations  play  an  important 
role ;  so  that  the  softening  of  the  cord  and  the  development  of  callus 
should  be  regarded  in  the  light  of  secondary  effects  rather  than  as 
direct  syphilitic  lesions  of  the  cord. 

This  leaves  only  the  first  class  to  be  considered. 

Syphilitic  neoplasms  are  generally  connected  with  the  spinal  mem- 
branes. They  may  grow  inward  upon  the  cord  and  produce  destruc- 
tion of  the  medullary  elements  and  even  chronic  inflammation  and 
softening;  or  they  may  extend  outward  and  cause  agglutination  of  all 
the  spinal  membranes,  pressure  of  the  nerve  roots,  and  even  disease 
of  the  osseous  vertebrse.  There  are  probably,  therefore,  two  forms  of 
spinal  syphilis  or  gummatous  disease — that  in  which  the  membranes 
are  chiefly  the  site  of  the  disease  (Wood),  and  that  in  which  there  is 
an  infiltration  of  the  cord  from  its  own  vessels  (Rumpf). 

The  meningitis  is  usually  of  the  pia  mater  and  arachnoid,  though 
in  some  instances  it  has  been  seen  to  develop  from  the  inner  surface 
of  the  dura.  The  membrane  is  thickened,  opaque,  clouded  and  more 
or  less  bound  to  the  cord  and  the  nerve  roots.  Granulation  tissue  is 
formed  and  over  the  membranes  is  spread  a  gelatinous,  fibrous  sub- 
stance. The  cord  is  swollen  and  the  dura  is  held  to  it  by  adhesions. 
Yellow,  gray,  soft  or  hard  deposits  are  seen  scattered  here  and  there 
resembling  small,  circumscribed  tumors.  The  process  is  not  uniform 
over  the  whole  membrane  for  in  one  place  it  may  be  highly  vascular 
with  thick  cellular  deposits,  and  in  another  hard  and  fibrous  in  char- 
acter. Usually  it  is  more  pronounced  in  the  region  of  the  posterior 
columns,  a  fact  which  by  comparison  lends  some  color  to  the  theory 
of  Redlich  and  Obersteiner  that  locomotor  ataxia  is  pathogenetically 
primarily  a  chronic  form  of  posterior  spinal  syphilitic  meningitis. 

In  most  of  the  cases  the  periphery  of  the  cord  itself  is  involved  in 
the  inflammatory  process,  so  that  we  have  a  meningo-myelitis  rather 
than  a  simple  meningitis.  Sometimes  the  granulation  tissue  sends 
septa-like  extensions  into  the  cord  substance  which  cause  inflamm.ation, 
atrophy,  destruction  and  sclerosis  in  the  adjoining  tissues.  The  nerve- 
roots  are  usually  implicated,  though  it  is  possible  for  them  to  remam 
normal  where  they  pass  through  the  inflamed  and  thickened 
membranes.  They  usually  show  signs  of  infiltration  and  atrophy. 
Spots  of  softening  and  old  hemorrhagic  inflammatory  foci  are  some- 
times present  in  the  cord,  having  been  caused  by  the  obliteration  of 
the  inflamed  and  thick-walled  bloodvessels.     Oppenheim  is  responsible 


THE  NON-NEURONIC  DISEASES  52 1 

for  the  statement  that  a  shnple  disseminated  and  diffuse  myehtis,  a 
pohomyehtis  (  ?)  may  develop  from  syphiHs.  Isolated  gummata  have 
been  reported  a  number  of  times,  and  Kahler  has  attempted  a  descrip- 
tion of  what  he  calls  a  multiple  gummatous  neuritis  of  the  nerve  roots. 

Specific  gummatous  meningitis,  with  secondary  results,  is  the 
primary  lesion  of  true  spinal  syphilis  as  it  is  of  true  cerebral  svphilis. 
In  fact  the  separation  of  brain  syphilis  from  spinal  syphilis  is  a  mere 
arbitrary  distinction  based  solely  upon  a  convenient  anatomical  classi- 
fication, of  the  parts  of  the  nervous  apparatus.  In  a  large  percentage 
of  cases  both  the  brain  and  the  cord  are  aft"ected  together,  the  brain 
symptoms  merely  over-shadowing  those  of  the  cord. 

Symptoms. — When  examining  a  case  of  suspected  spinal 
syphilis,  it  is  necessary  to  remember  that  the  lesion  may  be  meningeal, 
producing  symptoms  similar  to  those  of  non-specific  spinal  meningitis ; 
and  that,  on  the  other  hand,  it  may  consist  of  an  infiltration  of  the  me- 
dullary substance  itself,  giving  rise  to  symptoms  indicative  of  destruc- 
tion of  the  sensory-motor  tracts.  When  the  gummatous  disease  is  men- 
ingeal, the  earliest  symptoms  will  be  those  of  pain  or  par^esthesia  and 
spasm  or  paresis,  due  to  compression  and  irritation  of  the  anterior  and 
posterior  nerve  roots.  Of  course,  the  sensory  symptoms  will  be  re- 
ferred by  the  patient  to  the  peripheral  terminations  of  the  nerves  whose 
roots  are  undergoing  irritation.  The  principal  dift'erence  between 
gummatous  disease  of  the  meninges  and  simple,  non-specific,  subacute 
or  chronic  meningitis,  is  that  the  symptoms  of  the  former  are  apt  to  be 
more  sharply  defined  or  localized  than  those  of  the  latter.  The  reason 
for  this  is  obvious,  since  the  former  lesion  is  more  in  the  nature  of  a 
tumor  with  comparatively  well-defined  limits. 

According  to  Erb,  the  symptoms  of  syphilitic  disease  of  the  spinal 
cord  closely  resemble  those  of  myelitis  transversa  dorsalis ;  but  the  two 
are,  nevertheless,  distinguishable  by  a  number  of  typical  signs.  The 
walk,  posture,  and  motion  are  quite  characteristic,  and  simulate  those 
of  spastic  paralysis.  The  tendon  reflexes  are  apt  to  be  marked,  with- 
out much  muscular  tension. 

The  pains,  when  present,  are  usually  sharp  and  cutting,  and  when 
the  lesion  is  located  in  the  dorsal  or  lumbar  region  they  assume  the 
girdle  form.  Not  unfrequently  they  resemble  the  lightning  pains  of 
tabes  dorsalis.  Rarely  are  they  dull,  aching,  and  continuous.  Often 
there  is  no  pain  at  all.  On  account  of  the  usual  meningitis  accom- 
panying the  gummatous  deposit,  there  is  more  or  less  local  tender- 
ness of  the  spine  on  pressure.  Wood  states  that  in  several  instances 
this  local  tenderness  was  attributable  to  involvement  of  the  vertebral 
periosteum  and  vertebrae.  All  the  various  sensations  common  to  local 
meningitis  are  characteristic  of  this  form  of  spinal  syphilis,  such  as 
numbness,  formication  of  the  extremities,  "pins-and-needles"  sensa- 
tion, and  other  bizarre  parsesthesise  down  to  the  ultimate  condition  of 
complete  anaesthesia.  There  is  always  distinguishable  impaired  sensi- 
bility, but  severe  pain  is  not  generally  felt,  according  to  the  observa- 
tions of  Erb.  Atrophy  is  not  present.  There  is  little  or  no  involve- 
ment of  the  head  and  cerebral  nerves.  Rarely  are  the  muscles  of  the 
eye  implicated.     There  is  nothing  abnormal  psychically. 


522  THE  XOX-XEUROXIC  DISEASES 

The  motor  symptoms  are  the  same  as  those  of  locaHzed  non- 
specific irritative  meningitis,  such  as  rigidity  of  the  neck  and  Hmbs, 
tremor,  exaggeration  of  the  reflexes,  severe  cramps  excited  by  move- 
ment. Later  on,  complete  paralysis  supervenes.  If  the  palsy  increases 
rapidly  after  long-continued  disturbance  of  sensation,  it  is  almost 
pathognomonic  of  syphilitic  disease,  according  to  Wood.  The  sphinc- 
ters are  generally  included  in  the  final  symptoms.  Bedsores  and  other 
trophic  troubles  occur,  often  with  elevated  temperature  and  general 
septicaemia. 

In  a  case  of  syphiloma  of  the  cord  and  cauda  equina,  reported  by 
Osier,  death  occurred  from  diffuse  central  myelitis.  There  were  pains 
in  the  legs,  particularly  in  the  left,  which  underwent  rapid  wasting 
and  presented  vasomotor  changes.  There  were  pains  in  the  arms, 
especially  the  right,  without  wasting.  There  was  absence  of  control 
of  the  bladder  and  rectum  for  two  months  before  death.  There  were 
bedsores  and  arthritis  in  the  knees  and  ankles.  Toward  the  close  of 
life  high  fever  with  delirium  came  on.  There  was  a  gumma  in  the 
antero-lateral  columns  of  the  cervical  cord,  opposite  the  right  fourth 
anterior  nerve  root.  Gummata  also  involved  the  third,  fourth  and 
fifth  anterior  sacral  nerve  roots,  and  the  second  and  third  posterior 
sacral  roots  on  the  left  side.  Many  of  the  symptoms  in  this  case  were 
due  to  the  accompanying  lesions  resulting  from  the  presence  of  the 
syphilitic  new  formations.  A  differential  diagnosis  in  such  cases, 
though  extremely  difficult,  is  important  if  at  all  possible. 

In  syphilitic  disease  of  the  upper  cord  there  may  be  diplopia, 
amblyopia,  and  pupillary  irregularity.  Tinnitus  aurium  occurred  in  a 
case  reported  by  ^^^eber. 

The  symptoms  of  the  second  form  of  spinal  syphilis,  namely, 
syphilitic  infiltration  of  the  cord,  are  usually  slower  in  their  onset  and 
vary  according  to  the  location  of  the  lesion.  As  the  latter  is  more  or 
less  diffused,  so  will  the  symptoms  be  more  or  less  indefinite.  They 
wdll  range  all  the  way  from  hyperaesthesia  to  anaesthesia,  from  spasm 
to  paralysis.  Spastic  paraplegia  without  much  pain  is  highly  indica- 
tive. Sometimes  the  symptoms  closely  resemble  those  of  locomotor 
ataxia.  True  syphilis  of  the  cord  does  not  follow  the  course  of  the 
sensory  and  motor  tracts  as  do  the  various  systematic  scleroses  and 
subsequent  degenerations.  The  symptoms  are.  therefore,  much  more 
mixed  and  indefinite. 

There  is  a  class  of  cases,  probably  included  in  Huebner's  fourth 
class,  described  by  many  w^riters  under  the  title  of  acute  syphilitic 
myelitis,  acute  syphilitic  paraplegia,  acute  syphilitic  spinal  paralysis. 
They  usually  attain  their  maximum  degree  of  severity  in  a  few  hours 
or  a  few^  days.  They  may  have  prodromal  symptoms  long  before,  how- 
ever. Most  of  these  cases  subside  and  pass  into  a  state  of  partial  re- 
covery ;  a  few  mild  cases  make  a  complete  recovery ;  some  pass  to  a 
ver\-  rapid  fatal  termination.  The  symptoms  are  all  those  of  a  typical 
myelitis. 

There  are  cases  that  resemble  subacute  and  chronic  myelitis  and 
are  progressive  in  character.  Erb  described  a  type  in  which  there 
appears  a  slowly  developed  spastic  paraplegia,  exaggeration    of    the 


THE  NON-NEURONIC  DISEASES  523 

.knee-jerks,  and  disturbance  of  the  bladder.  In  its  pure  form  there 
are  no  sensory  phenomena.  Most  of  the  cases  prove  to  be  not  of  the 
pure  type,  as  sensory  and  other  symptoms  appear  which  Hnk  them  to 
the  great  group  of  variable  cases  of  spinal  syphilis.  Erb  did  not  there- 
fore describe  a  type  of  the  disease,  but  rather  a  particular  symptom 
^roup.  Kuh  says  that  in  Erb's  spinal  paralysis  the  disease  has  its  origin, 
in  all  probability,  in  syphilis  of  the  vessels  of  the  cord  in  the  dorsal  re- 
gion, the  lesions  of  the  cord  being  secondary  and  involving  mainly 
the  lateral  tracts  and  slightly  invading  the  posterior  columns.  Kovva- 
iewsky  affirms  that  the  cases  are  quite  common  in  the  male  sex  be- 
tween the  ages  of  thirty  and  forty-five.  With  Oppenheim  I  am  in- 
clined to  regard  these  cases  of  Erb's  as  merely  representing  a  certain 
.stage  of  the  usual  form  of  syphilitic  meningo-myelitis.  As  Dercum 
well  says,  "When  we  recall  the  fact  that  the  virus  of  syphilis  expends 
itself  mainly  upon  the  membranes  and  bloodvessels,  it  is  not  surprising 
that  most  varied  clinical  pictures  should  present  themselves.  Not  a 
single  symptom  can  be  taken  as  constant  for  all  cases.  Even  the 
spastic  character  of  the  gait  may  be  lacking.  Instead  of  flaccidity,  con- 
tractures may  be  present  and  under  certain  conditions  the  knee-jerks 
may  be. absent."  The  same  remarks  apply  to  the  cases  which  Oppen- 
heim finds  so  similar  to  tabes  and  which  he  has  denominated  syphilitic 
pseudo- tabes. 

A  simple  gliosis,  an  amyotrophic  lateral  sclerosis,  and  other  dis- 
eases have  been  simulated  by  syphilis.  As  in  brain  syphilis,  so  here, 
the  great  diversity  of  symptoms,  their  changeability  and  inconstancy, 
are  one  of  their  characteristic  features  and  go  a  long  way  toward  es- 
tablishing the  diagnosis  of  syphilis  in  doubtful  cases. 

Diagnosis. — There  are  certain  manifestations  of  spinal  syphilis 
that  so  simulate  other  affections  of  the  cord,  and  are  in  themselves 
so  indefinite  and  irregular,  that  a  diagnosis  is  alwa)^s  a  matter  of  ex- 
treme nicety.  In  such  cases  a  course  of  anti-syphilitic  treatment  has 
sometimes  been  resorted  to  before  any  diagnosis  could  be  made.  The 
more  we  can  avoid,  however,  such  indirect,  empirical  methods  of 
making  diagnoses,  and  the  more  we  can  learn  to  depend  upon  the 
•direct  manifestations  of  the  disease,  the  better  it  will  be  for  the  patient 
and  the  more  creditable  to  the  science  of  medicine. 

The  diagnosis  of  spinal  syphilis  is  best  made  by  the  exclusion  of 
other  spinal  affections  and  by  remembering  that  any  one  of  these  other 
affections,  associated  with  a  history  of  syphilis  and  presenting  more  or 
less  unusual  manifestations,  is  very  apt  to  be  syphilitic  in  origin.  If  a 
case  of  apparent  locomotor  ataxia,  for  instance,  shows  an  absence  of  the 
xisual  fulgurating  pains,  or  the  presence  of  the  patellar  reflex,  spinal 
syphilis  rather  than  posterior  spinal  sclerosis  should  at  once  be 
thought  of. 

Simple  myelitis,  compression  myelitis,  multiple  sclerosis  and  dis- 
ease of  the  lateral  and  posterior  tracts,  may  all  be  simulated  by  syphilis. 
Hence  the  differential  diagnosis  can  be  taken  up  better  under  these 
various  heads. 

Prognosis. — The  prognosis  of  spinal  syphilis  should  always  be 
guarded,  even   though  great  improvement   is   obtained   sometimes  by 


524  THE  NON-NEURONIC  DISEASES 

appropriate  medication.  Occasionally  absolute  cures  have  been  made^ 
More  often,  however,  the  delicate  constituents  of  the  cord  have  been 
irreparably  damaged  when  the  case  first  comes  under  observation,  and 
then  only  a  prevention  of  further  injury  can  be  hoped  for. 

The  less  the  cord  itself  is  involved  the  better  the  prognosis.  Whea 
paralysis  has  continued  several  months  no  nnprovement  can  be  ex- 
pected. Spastic  paresis,  bladder  trouble,  etc.,  will  continue.  Relapses- 
are  always  liable. 

Treatment. — The  treatment  usually  resolves  itself  into  the  ad- 
ministration of  mercury  and  the  iodides.  The  object  is  to  neutralize  at 
once  the  syphilitic  poison,  to  sustain  the  vitality  of  the  cellular  struc- 
tures, and  to  remove  as  quickly  as  possible  any  gummatous  enlarge- 
ments that  may  be  exerting  a  deleterious  pressure.  Each  case  is  a. 
law  unto  itself,  but  in  all  cases  bold,  heroic  treatment  is  usually  needed 
to  check  at  once  all  further  damage  of  the  nervous  elements.  Hot  and 
cold  spinal  douches,  suspension,  massage,  all  have  their  applicability 
in  appropriate  cases.  The  indications  are  the  same  as  in  any  of  the 
various  forms  of  organic  disease  of  the  spine.  Spinal  syphilis  should 
be  managed  just  as  any  other  disease  of  the  cord  and  its  membranes, 
plus  the  administration,  heroically  and  for  a  long  period  of  time,  of 
the  requisite  antisyphilitic  remedies.  The  administration  of  these  is 
the  same  as  for  brain  syphilis,  to  which  section  the  reader  is  referred 
for  more  detailed  discussion. 

SPINAL  MENINGEAL  HEMORRHAGE. 

Hematorrhachis.— This  condition  is  so  commonly  secondary  ta 
some  injury  or  other  disease  that  some  authors  do  not  speak  of  it  at 
all  as  a  special  affection.  It  does  occur,  very  rarely,  however,  as  a 
primary  trouble.  Its  symptoms  are  slightly  characteristic.  I  deem  it 
worthy  of  special,  brief  consideration  therefore. 

Etiology. — -The  hemorrhage  may  occur  outside  of  the  dura  mater 
(extra-dural,  extra-meningeal  hemorrhage),  or  it  may  take  place  be- 
tween the  dura  and  the  cord  (sub-dural,  intra-meningeal  hemorrhage). 
The  former  is  the  result  of  traumata,  blows,  falls,  fractures,  disloca- 
tions and  disease  of  the  vertebrse.  The  rupture  of  an  aneurism  may  be 
the  source  of  the  hemorrhage.  The  blood  springs  usually  from  the 
great  venous  plexuses  that  surrotmd  the  dura. 

Sub-dural  hemorrhage  may  result  from  the  same  causes  as  the 
extra-dural,  and  from  all  the  causes  enumerated  under  the  head  of 
hematomyelia  in  a  following  section.  The  clot  may  extend  only 
an  inch  or  so  and  not  compress  the  cord  at  all.  On  the  other  hand  it 
may  reach  the  entire  length  of  the  canal  and  exert  very  severe  pres- 
sure upon  the  cord.  Most  of  these  hemorrhages  occur  from  the  pial 
vessels  in  the  cervical  region.  While  blood  may  pass  up  even  into  the 
ventricles  of  the  brain,  or  vice  versa,  one  must  be  on  his  guard  in  as- 
suming this,  for  the  intra-cranial  and  intra-spinal  hemorrhage  under 
such  circumstances  are  more  apt  to  be  simultaneous  phenomena.. 

Symptoms. — The  symptoms  of  hematorrhachis  are  characteris- 
tically meningitic,  that  is  progressively  irritative  and  paralytic  upon 


THE  NOX-XEURONIC  DISEASES  525 

the  spinal  cord  and  spinal-root  functions.  The  suddenness  of  these 
symptoms  and  their  appearance  at  first  without  fever  indicate  their 
-hemorrhagic  origin.  Preceding  them  there  may  be  slight  premonitory 
manifestations  and  in  a  few  days  after  their  appearance  all  the  signs 
■of  a  meningitis  exhibit  themselves.  There  is  pain  in  the  back  and  pains 
-shooting  along  the  course  of  the  spinal  nerves.  The  nerve  pains  are 
neuralgic  in  character  and  remittent  or  intermitttent.  The  nerves  them- 
-selves  are  not  locally  tender  as  they  are  with  the  pains  of  neuritis. 
The  spine  is  very  tender,  however.  The  cranial  nerves  and  head  and 
mind  are  all  unaffected.  The  skin  is  generally  hypercesthetic,  and  there 
are  usually  various  parcesthesice  such  as  tingling,  pins-and-needles  sen- 
-sation  and  numbness.  The  muscles  are  spasmodic  in  the  same  areas  as 
the  sensory  phenomena.  Soon  they  become  rigid  and  contracted.  The 
back  is  arched  in  opisthotonos.  Finally  in  some  cases  the  condition 
goes  on  to  almost,  but  not  quite,  complete  anaesthesia  and  paralysis,  es- 
pecially in  the  lower  limbs.  Later  on  and  toward  the  close  trophic 
manifestations  appear  and  even  signs  of  a  distinct  meningo-myelitis. 

According  to  the  location  of  the  hemorrhage  so  will  the  clinical 
picture  be  slightly  altered.  If  it  occurs  in  the  himhar  region  the  pains 
are  felt  entirely  in  the  legs.  The  sphincters  are  paralysed.  Paraplegia 
•comes  on  early  and  the  patella  reflexes  are  lost.  Sexual  irritation  may 
be  a  troublesome  symptom  in  the  beginning.  Dorsal  hemorrhage  sends 
the  pains  shooting  around  the  chest  and  abdomen.  When  the 
5eat  of  the  trouble  is  the  cervical  enlargement,  the  pains  are  felt  in 
the  neck  and  arms.  Later  on  the  paralysis  is  spastic  in  the  lower  and 
flaccid  in  the  upper  extremities  though  this  is  rare  and  only  in  very 
advanced  cases  with  considerable  involvement  of  the  cord.  The  neck 
may  be  rigid  and  immovable.  Swallowing  is  difficult.  Respiration  is 
•disturbed.     The  pupils  are  dilated. 

Diagnosis. — The  history  of  an  injury  or  appropriate  cause  for 
a  hemorrhage,  the  onset  of  irritative,  non-febrile  symptoms  of  a  men- 
ingeal character,  ought  to  go -far  towards  making  the  diagnosis  easy. 
Meningitis  itself  approaches  more  slowly  and  insidiously,  and  is  ac- 
companied by  fever,  and  symptoms  that  tend  rather  to  continuously 
progress  and  not  to  recede,  as  they  often  do  in  hemorrhage.  In  mye- 
litis there  is  fever,  more  marked  paralysis  and  anaesthesia  and  not  the 
distinctive  irritative  signs  of  meningeal  trouble. 

"  After  all,  however,  it  must  be  admitted  that  there  is  such  a  close 
relationship  between  all  of  these  troubles,  hemorrhage,  meningitis  and 
"myelitis,  that  a  differential  diagnosis  is  sometimes,  and  under  certain 
conditions,  peculiarly  difficult  and  even  impossible.  At  all  times  it 
can  hardly  amount  to  more  than  a  strong  suspicion,  so  frequently  and 
generally  do  all  three  diseases  overlap  and  run  into  one  another. 

Prognosis. — Most  of  the  severe  cases  prove  fatal  in  a  few  hours. 
Others  recede  somewhat  symptomatically,  then  become  a  meningitis 
and  so  run  their  course.  If  after  a  few  days,  three  or  four,  the  cord 
manifests  no  signs  of  implication,  recovery  may  be  hoped  for.  Cer- 
vical hemorrhage  for  obvious  reasons  is  more  dangerous  than  hem- 
orrhage elsewhere  in  the  spine.  Traumatic  and  infectious  cases  often 
recover.     What  is  called  typhoid  spine  is  sometimes  a  slight  hemor- 


526  THE  NON-NEURONIC  DISEASES 

rhagic  meningitis  or  meningo-myelitis.  I  have  seen  such  cases  recover 
after  one  or  two  years. 

The  cause  of  the  hemorrhage,  its  extent,  its  volume,  the  course 
and  severity  of  the  secondary  meningo-myeHtic  phenomena  will  all 
determine  the  prognosis. 

Treatment. — This  is  about  the  same  as  that  recommended  for 
hematomyelia.  The  posture  should  be  prone  on  the  stomach  or  side, 
and  absolute  quiet  should  be  maintained.  To  obtain  this  sedatives  will, 
have  to  be  rather  freely  given  to  ease  the  pain.  The  bowels  should 
be  freely  moved.  Leeches  may  be  applied  to  the  anus,  or  cups  to  the 
spine.  The  ice  bag  to  the  spine  is  a  regulation  measure.  In  robust 
cases,  venesection  may  be  employed.  Aconite  and  ergot  cannot  do 
much  harm  if  judiciously  used,  but  unfortunately  they  will  do  very 
little  good.  In  purpura  Dana  recommends  the  trial  of  the  mineral 
acids  or  chloride  of  calcium.  The  meningitis  and  residual  phenomena 
are  to  be  treated  on  general  principles  laid  down  for  them  elsewhere. 
Mild  persistent  counter-irritation  to  the  spine  and  the  steady  use  of 
small  doses  of  mercury  for  a  long  time  have  helped  me  much  in  the 
later  management  of  these  cases 


DISEASES  OF  THE  SPINAL  CORD. 


CIRCULATORY  DISEASES. 

The  arrangement  of  the  bloodvessels  in  and  about  the  spinal  cord 
is  such  that  temporary  changes  in  them  are  not  liable  to  occur,  and 
permanent  changes  are  the  result  of  disease  and  not  of  mere  func- 
tional derangement.  Plence.  as  before  mentioned,  ancrinia  and  hyperce- 
mia  of  the  cord  are  unknown  except  under  very  special  circumstances. 
What  is  seen  in  this  respect  after  death  is  absolutely  no  criterion  as 
to  what  is  present  during  life.  In  fact  if  all  hypotheses  were  to  be 
discarded,  all  analogies  cast  aside,  all  logical  deductions  waived,  and 
we  were  to  depend  absolutely  and  entirely  upon  what  the  cord  reveals 
post-mortem,  we  would  probably  say  that  anaemia  and  hyperasmia  never 
occur.  Such  is  the  position  taken  by  some  of  the  more  radical  pathol- 
ogists. They  declare  that  the  few  changes  that  are  observed  in  the 
bloodvessels  and  related  tissues  are  due  to  gravitation,  lethal  changes 
observed  in  all  fatal  diseases,  and  from  various  mechanical  causes  oper- 
ating upon  the  corpse ;  and  that  the  elaborate  symptoms  so  often  noted 
during  life  and  attributed  to  the  alteration  in  the  amount  of  blood  in 
the  cord,  are  really  due  to  other  factors  such  as  toxaemia,  quality  of 
the  blood,  pressure  and  velocity  of  the  flow.  More  conservative  au- 
thorities still  hold  that  anaemia  and  hyperaemia  of  the  cord  may  and 
do  occur,  but  are  rare  and  are  little  comprehended  by  us.  The  symp- 
toms that  have  been  so  elaborately  described  by  the  older  authors, 
cannot  for  a  surety  be  assigned  to  conditions  about  which  we  know 
so  little  and  whose  very  existence  is  problematical. 


THE  NOX-NEUROXIC  DISEASES 


ANEMIA. 


527 


As  a  simple,  primary  condition,  temporary  or  permanent,  we 
know  absolutely  nothing  with  certainty  about  ancBinia  of  the  spinal 
cord.  There  are  some  experimental  observations  and  clinical  facts 
that  are  highly  suggestive,  but  the  conclusions  that  are  drawn  from 
them  must  not  be  regarded  as  the  incontrovertible  actualities.  For  in- 
stance it  is  an  interesting  fact,  and  one  that  leads  to  the  drawing  of 
suggestive  comparisons,  that  the  ligation  of  the  aorta  was.  in  a  few 
moments,  followed  in  the  experiments  of  Herter,  by  complete  para- 
plegia and  paralysis  of  the  sphincters.  Clinically  paraplegia  has  been 
seen  to  follow  either  immediately  or  at  the  end  of  a  few  days,  pro- 
fuse hemorrhages  from  the  stomach  and  uterus.  The  degenerative 
changes  in  the  spinal  cord  in  pernicious  ansemia  are  well  recognized. 
As  a  part  of  a  general  anaemia,  chlorosis  and  debilitated  blood  state, 
the  spinal  cord  may  readily  be  supposed  to  suffer  implication.  As  a 
sequel  to  profuse  hemorrhage,  exhausting  diarrhoea,  and  mechanical 
obstruction  of  any  sort  which  shuts  off  its  blood  supply,  the  anemia 
of  the  cord  may  be  frankly  admitted  as  a  possibility.  Even  local 
ansemia  must  undoubtedly  exist  in  cases  where  the  local  circulation  is 
affected  by  a  tumor  or  other  cause  of  obstruction. 

When,  however,  we  attribute  to  anaemia  zveakness  of  the  legs, 
pains  in  the  hack,  various  parcssthesice.  such  as  numbtiess  and  tingling, 
we  are  reasoning  beyond  the  proofs,  for  these  symptoms  may  be  due 
to  special  changes  in  the  nervous  elements  rather  than  to  the  alteration 
in  the  blood  quantity,  or  they  may  be  toxsemic  in  origin,  or  they  may 
be  a  part  of  the  general  symptom-complex  of  the  general  or  local 
disease  with  which  the  anemia  is  associated. 

HYPER.EMIA. 

Of  this  some  writers  think  we  have  a  little  more  definite  knowl- 
edge, than  we  have  of  ansemia,  and  they  even  discuss  the  condition 
elaborately  under  the  heads  of  etiology,  pathology,  symptoms  and  treat- 
ment. It  seems  to  me  that  in  the  present  state  of  our  knowledge  such 
an  elaboration  of  the  subject  is  unwarrantable.  ]\'Iuch  of  what  is  said 
cannot  be  denied,  to  be  sure,  but  very  little  of  it  can  be  supported  with 
positive  proof.  As  Gowers  well  says,  "volumes  might  be  filled  by  the 
collected  descriptions  of  the  varieties  and  symptoms  of  congestion  of 
the  spinal  cord — descriptions  in  which  the  unrestricted  play  of  'scien- 
tific' fancy  has  elaborated  a  symptomatology  for  the  separate  conges- 
tion of  every  part  of  the  spinal  cord." 

As  a  condition  in  the  beginning  of  myelitis  it  is  undeniable.  It  is 
not  impossible  that  it  may  occur  in  excessive  coitus,  in  certain  forms 
of  violent  exercise,  in  suppressed  menstruation,  in  strychnine  poison- 
ing, as  a  residuum  of  a  meningitis  or  traum.a,  as  a  part  of  the  general 
symptom-complex  of  some  other  disease.  As  I  say,  it  is  not  impossible 
that  such  is  the  case,  but  where  and  what  are  the  proofs  ?  The  symp- 
toms do  not  confirm  it.  The  reputed  heaviness  and  weight  in  the 
limbs,  the  numbness,  the  creeping  sensations,  the  neuralgic  pains,  the 


528  THE  NON-NEURONIC  DISEASES 

weakness  in  the  legs,  the  muscular  tzvitchiiigs,  the  disturbances  of  the 
sphincters,  the  general  tendency  to  paraplegic  phenomena,  the  very 
doubtful  increase  of  distress  when  a  posture  on  the  back  is  assumed, 
may  all  be  due  to  anaemia,  to  circulatory  disturbances  in  the  meninges, 
to  beginning  or  transient  intlammatory  states,  to  irritative  lesions  of 
various  sorts,  to  nutritional  disturbances  in  the  nervous  cells  or  even 
to  other  conditions  in  the  blood  itself,  than  to  the  mere  excess  of  its 
quantity.  No,  it  will  not  do  to  assume  a  hyperaemic  pathology  on  such 
a  diffuse,  indefinite,  loose  basis  as  this  symptomatology  appears  to  be. 
Pathology  and  treatment  suggest  no  proof.  It  is  singular  how  au- 
thors recommend  in  one  paragraph  the  use  of  counter-irritation,  cup- 
ping and  the  ice  bag  to  the  spine,  morphine  and  bromides  internally 
and  in  the  chronic  cases  ergot,  muriate  of  ammonium,  iodide  of 
potassium  and  the  galvanic  current,  when  in  the  paragraph  almost 
immediately  preceding  it  was  admitted  that  these  symptoms  may  be 
due  to  very  different  conditions  from  that  of  congestion  and  that  the 
simple  existence  of  congestion  is  open  to  doubt.  If  the  presence  of 
another  disease  can  be  made  out,  we  may  be  at  liberty  to  suppose  that 
this  therapy  affects  that  disease  and  so  modifies  the  spinal  manifes- 
tations. In  some  cases  the  beneficial  results  may  be  partly  psychic  in 
character.  I  have  often  in  hystero-neurasthenic  cases  obtained  the 
happiest  kind  of  psychic  effects  from  the  use  of  vigorous  cupping  of 
the  spine.  In  such  cases  it  is  a  favorite  trick  to  get  the  patient's 
thoughts  in  regard  to  her  spine  runing  in  another  direction  by  the  use 
of  cups,  galvanism,  etc.  And  I  have  thus  relieved  many  symptoms 
similar  to  those  above  but  I  did  not  fancy  I  was  curing  a  spinal  con- 
gestion. In  fact  I  am  still  of  the  opinion  that  the  treatment  and  its 
good  results  were  alike  largely  psychic. 

EMBOLISM.     THROMBOSIS.     ENDARTERITIS. 

These  conditions  are  comparatively  rare  in  the  spinal  cord. 
Thrombosis  of  the  minor  vessels,  together  with  endarteritis,  undoubt- 
edly underlies  some  of  the  acute  and  chronic  focal  diseases  of  the 
cord,  or  may  be  an  associative  or  complicating  feature  in  the  pathology 
of  these  diseases.  As  a  part  of  general  senile  changes  and  senile 
pathology,  endarteritis  may  be  seen  quite  frequently  in  persons  past 
middle  life.  It  is  not,  however,  a  special  cord  condition  but  the  arteries 
of  the  cord  are  affected  like  those  in  the  rest  of  the  body.  Thus  in 
younger  persons  there  is  a  special  as  well  as  a  general  syphilitic 
nodular  periarteritis  or  endarteritis,  possibly  with  gummatous  menin- 
gitis. Arteritis  obliterans  and  miliary  aneurism  may  be  seen  but  they 
are  far  rarer  in  the  cord  than  they  are  in  the  brain. 

SPINAL  HEMORRHAGE. 

Hematomyelia.  Hemorrhage  into  the  Spinal  Cord. — As  a  primary 
condition,  hemorrhage  into  the  substance  of  the  cord  is  exceedingly  rare, 
even  being  denied  by  some.  It  is  thus  in  marked  contrast  to  hemorrhage 
into  the  brain,  the  difference  being  probably  due  to  the  longer  course 


THE  NON- NEURONIC  DISEASES  52<) 

of  the  Spinal  bloodvessels.  As  a  secondary  condition,  associated  with 
myelitis,  tumors  and  cavities,  or  capillary  hemorrhages  generally  in  se- 
vere tonic  and  clonic  spasms,  heinaioinyelia  is  of  little  clinical  interest 
because  its  symptoms  are  so  masked  by  those  of  the  primary  disease, 
that  the  diagnosis  is  always  uncertain. 

Many  descriptions  have  clearly  been  based  upon  the  secondary 
forms  of  the  trouble.     I  will  discuss  here  only  the  primary  form. 

Etiology. — Men  are  more  subject  to  it  than  women.  It  occurs 
most  often  in  middle  adult  life.  It  has  been  seen  in  infants.  Alcohol- 
ism, degenerated  arteries  in  the  aged,  the  hemorrhagic  diathesis,  pur- 
pura and  other  factors  doubtless  may  predispose  to  it.  The  influence 
of  heredity,  except  through  the  circulatory  apparatus,  is  nil,  and  cer- 
tainly not  what  it  is  in  cerebral  apoplexy. 

By  all  odds,  some  form  of  trauma  is  the  leading  cause  of  spinal 
apoplexy.  Blows  upon  the  spine,  falls,  strains,  wrenches,  lifting  of 
heavy  weights,  excessive  exercise  produce  probably  nine-tenths  of 
the  cases.  Somewhat  traumatic  in  a  way  are  those  cases  said  to  have 
been  due  to  excessive  coitus,  exposure,  suppressed  menstruation,  bleed- 
ing piles,  difficult  parturition.  The  cases  due  to  fractures  of  the  spine, 
dislocations,  inflammations,  syphilis,  neoplasms,  cavities,  tetanus  and 
convulsions  are  of  course  merely  secondary  and  of  very  little  practical 
interest. 

Pathology  and  Pathogenesis. — The  central  vessels  of  the  cord, 
supplying  especially  the  gray  matter  are  the  chief  sources  of  the  hem- 
orrhage. Miliary  aneurisms  are  exceedingly  rare  upon  them.  Their 
coats  of  course  may  be  degenerated  as  the  result  of  disease  or  age. 
Generally,  however,  in  the  primary  form  of  the  trouble,  there  is  no 
very  great  change  observable  in  them.  After  the  rupture  takes  place 
the  blood  pours  out  into  the  surrounding  gray  substance  extending  up 
and  down  the  cord  and  into  the  horns,  especially  the  posterior.  The 
white  matter  is  not  usually  implicated,  certamly  not  to  any  very  great 
extent.  It  is  more  generally  compressed  than  directly  damaged.  Mye- 
litis of  course  soon  lights  up  in  and  around  the  hemorrhagic  focus, 
the  tissues  become  softened,  disappear  and  leave  a  cavity  in  a  few 
cases.  This  process  Van  Giessen  calls  hematomyeloporosis,  to  dis- 
tinguish it  from  hematomyelia.  Sometimes  the  clot  may  be  so  large 
that  the  white  substance  of  the  cord  forms  a  mere  thin,  ragged  wall 
around  it.  It  may  lacerate  its  way  through  the  white  matter  and  ex- 
tend beneath  the  meninges.  The  cord  is  usually  enlarged,  softened 
and  ruddier  in  hue  near  the  extravasation.  In  small  hemorrhages  there 
miay  be  no  noticeable  external  changes. 

Symptoms. — The  first  great  characteristics  to  be  always  noticed 
about  the  symptoms  are  that  they  appear  suddenly  and  are  accom- 
panied by  febrile  phenomena.  As  time  passes,  however,  fever,  pos- 
sibly some  slight  recession  of  the  symptoms  or  the  appearance  of 
others  indicates  that  the  secondary  myelitis  has  begun.  As  the  erup- 
tion of  blood  produces  a  sudden  break  in  the  continuity  of  the  cord, 
all  parts  of  the  body  below  it  are  functionally  paralyzed.  The  patient 
falls,  therefore,  with  a  complete  paraplegia.  This  may  involve  onlv 
bis  arms  or  legs  or  all  four  extremities.    Anesthesia  accompanies  it  and 


530 


THE  NON-NEURONIC  DISEASES 


the  Sphincters  lose  their  control.  In  some  cases  there  are  slight  pre- 
monitory weakness,  tingling  and  numbness  for  a  few  moments,  then 
the  shock  comes  as  just  described  and  is  profound  all  at  once  or  in- 
creases still  more  than  it  was  at  first.  At  first  the  reflexes  are  abol- 
ished but  they  soon  return  and  in  a  little  while  become  highly  exag- 
gerated. The  patient's  consciousness  and  sensorium  are  unaffected 
and  he  often  complains  of  pain  in  the  back. 

The  site  and  size  of  the  clot  of  course  may  vary  and  thus  greatly 
modify  this  clinical  picture  in  different  cases.  The  paraplegia  indi- 
cates a  dorsal  or  lumbar  lesion  when  it  is  limited  to  the  legs.  In  such 
a  case  the  reflexes  may  remain  lost,  the  sexual  functions  be  damao-ed 
and  the  bladder  and  bowels  be  involuntarily  evacuated.  There  may 
be  a  girdle  pain,  especially  when  inflammation  lights  up.     A  quadri- 

FIGURE  112. 


Cross-section  of  the  spinal  cord  in  hematornyelia.     Hemorrhage  into  the  left 
anterior  and  posterior  horns.     (After  Minor  and  Oppenheim.) 

plegia  indicates  a  cervical  hemorrhage.  Here  an  atrophic  paralysis 
occurs  in  the  arms  and  a  spastic  condition  in  the  legs.  Unlike  lumbar 
hemorrhage,  the  patella  reflexes  are  now  exaggerated.  Oculo-pupil- 
lary  symptoms  occur  if  the  lower  cervical  region  is  implicated. 

A  unilateral  hemorrhage  may  cause  the  Brown-Sequard  syndrome, 
typical  in  this  case  of  limitation  of  the  lesion  to  the  gray  matter.  On 
one  side,  the  side  of  the  lesion,  the  leg  exhibits  a  spastic  paralysis, 
while  the  arm  manifests  a  partial,  flaccid,  atrophic  paralysis.  On  the 
opposite  side  appear  anaesthesia,  analgesia  and  thermansesthesia.  There 
may  be  some  hypzesthesia  on  the  side  affected  with  the  motor  paraly- 
sis. In  a  few  days  the  case  assumes  all  the  characteristics  of  a  typical 
myelitis  and  the  symptomatology  of  the  hemorrhage  sinks  intO'  that  of 
this  disease. 

Diagnosis. — The  abruptness  and  paraplegic  character  of  the  on- 
set of  the  trouble  should  be  carefully  noticed.  There  is  no  fever  and 
the  symptoms  tend  to  recede  a  little  for  a  few  days  when  a  change 
takes  place  and  the  case  assumes  a  myelitic  complexion  entirely.     It  is 


THE  NON-NEURONIC  DISEASES  1^31 

difficult,  however,  in  some  cases  to  distinguish  the  hemorrhagic  from 
the  myehtic  manifestations.  Fortunately  the  differentiation  is  rarely  a 
matter  of  any  consequence  as  hemorrhage  almost  always  sooner  or 
later  develops  inflammation  in  the  cord  and  in  myelitis  hemorrhage 
may  or  may  not  occur  without  the  progress  of  the  disease  being  very 
materially  affected. 

Poliomyelitis  is  to  be  distinguished  by  the  febrile  symptoms  and 
the  symptoms  that  indicate  especially  damage  to  the  anterior  horns. 

Hemorrhage  into  the  spinal  membranes  is  different  from  hema- 
tomyelia  clinically  in  that  there  is  pain  in  the  back,  pains  of  a  radiat- 
ing character  along  the  course  of  the  spinal  nerves,  rigidity,  spinal- 
root  signs  and  other  indications  of  meningeal  irritation.  Some  have 
employed  and  recommended  spinal  puncture  to  positively  diagnose 
hematorrhachis.  One  would  fear  an  increase  or  renewal  of  the  hem- 
orrhage in  some  cases  from  the  disturbance  of  the  cerebrospinal  pres- 
sure in  such  a  manoeuvre. 

Prognosis. — This  is  always  serious  for  if  death  does  not  occur 
early,  it  will  in  all  likelihood  later,  from  the  myelitis.  Only  large  haem- 
orrhages destroy  life  early.  Improvement  often  occurs  and  occasionally 
complete  recovery  has  happened.  A  small  hemorrhage  in  the  dorsal 
region  holds  out  the  best  chances  for  recovery.  When  myelitis  de- 
velops, the  prognosis  depends  upon  that.  If  sensation  returns  early 
the  outlook  is  hopeful.  Early  trophic  manifestations  are  discouraging. 
Some  cases  recover  with  permanent  muscular  atrophy  and  degenera- 
tive reactions. 

In  a  word,  the  size  of  the  hemorrhage,  the  extent  and  location  of 
the  clot  and  the  onset  and  severity  of  the  subsequent  myelitis  must 
all  be  carefully  taken  into  account  in  affirming  the  prognosis. 

Treatment. — Absolute  rest  in  bed  for  the  first  few  days  and 
weeks  must  be  enjoined.  The  patient  should  lie  on  his  side  or  abdo- 
men. Ice  should  be  applied  over  the  seat  of  the  hemorrhage,  or  as  near 
it  as  possible.  Aconite  in  small  doses  may  be  given  to  restrain  the 
heart  action.  Ergot  by  the  mouth  in  a  few  large  doses,  or  ergotin 
hypodermically  have  been  recommended.  Their  efficacy  is  doubtful, 
however.     Blood  letting  is  a  more  powerful  measure. 

The  later  treatment  is  the  same  as  that  for  myelitis. 

MYELITIS. 

Myelitis  is  inflammation  of  the  spinal  cord.  It  may  be  acute,, 
subacute  or  chronic.  It  may  occur  in  any  part  of  the  cord.  As  the 
clinical  picture  of  the  disease  undergoes  some  variations  in  accordance 
with  the  character  and  location  of  the  lesion,  subvarieties  of  myehtis 
are  described,  some  of  which  are  of  sufficient  importance  to  be  given 
a  special  chapter. 

When  the  inflammation  surrounds  the  edge  of  the  cord  it  is  known 
as  peripheral  myelitis,  or  meningoniyelitis,  since  it  is  usually  associated 
with  meningitis.  When  it  is  confined  to  the  gray  matter  immediately 
encompassing  the  central  canal  it  is  spoken  of  as  a  periependymal 
myelitis.     When  it  is  confined  to  the  gray  matter  of  the  cord   it  is 


532  THE  NON-NEURONIC  DISEASES 

known  as  poliomyelitis.  Some  authors  regard  acute  anterior  poliomyeli- 
tis as  a  systemic  disease  because  it  is  limited  to  the  column  of  gray 
matter  that  makes  up  the  anterior  cornua.  When  the  disease  extends 
completely  across  the  cord  it  is  a  cotnpletc  transverse  myelitis;  when 
only  part  way  across  it  is  an  incomplete  transverse-  invelitis.  These 
forms  may  all  be  more  or  less  limited  to  the  cervical,  dorsal  or  lumbar 
regions.  Disseminated  viych'tis  shows  the  inflammation  scattered  in 
foci  irregularly  throughout  the  cord. 

All  of  these  forms,  except  the  anterior  poliomyelitis,  will  be  dis- 
cussed in  detail  under  the  head  of  symptomatology. 

Etiology. — Nearly  all  inflammations  O'f  the  spinal  co<rd  are  caused 
by  traumatism  or  infection.  Blows  upon  the  back,  fractures  or  dis- 
locations of  the  vertebrae,  stab  wounds  and  wrenchings  of  the  spine 
are  among  the  former;  acute  infectious  diseases  like  varicella,  sepsis, 
hydrophobia,  tuberculosis,  syphilis,  malaria,  etc.,  are  among  the  latter. 
Gonorrhoea  produces  it  and  it  may  occur  in  pregnancy  and  in  the  puer- 
perium.  It  has  followed  tonsillitis,  dysentery,  erysipelas,  typhoid 
fever,  pneumonia,  cystitis,  influenza,  tetanus  and  phlegmonous  parony- 
chia. 

Primary  acute  myelitis  is  exceedingly  rare.  The  disease  may  oc- 
casionally occur,  however,  as  a  primary  infection.  The  micno-organ- 
isms  are  numerous,  therefore,  that  enter  into  tlie  etiology.  Among  them 
are  the  streptococci,  staphylococci,  pneumococci,  diplococci  and  many 
others.  Whether  the  germs  themselves  or  their  toxines  are  the  direct 
cause  of  the  inflammation  is  still  unsettled.  The  germs  are  not  often 
found  in  the  cord,  but  this  fact  does  not  argue  against  their  being 
the  direct  cause,  for  it  is  a  well  known  fact  that  they  disintegrate  and 
vanish  as  soon  as  they  have  accomplished  their  deleterious  work.  Op- 
penheim  and  Grasset  believe  that  myelitis  really  results  from  a  mixed 
or  secondary  infection. 

An  ascending  neuritis  has  been  charged  as  a  cause  of  myelitis.  It 
certainly  has  followed  certain  diseases  of  the  urinary  apparatus,  caisson 
disease  and  arteriosclerosis.  Some  of  the  so-called  re-Rex  paralyses  fall 
in  here. 

Among  the  intoxicants  found  to  have  caused  myelitis  may  be  noted 
carbon  dioxide,  carbon  disulphide,  illuminating  gas,  chloroform  and 
nitrobenzine. 

Adults  of  early  middle  life  and  of  the  male  sex  are  chiefly  affected. 
Dana  afifirms  that  over  one-half  of  the  non-traumatic  and  non-tuber- 
culous cases  in  adult  life  are  due  to  syphilis.  We  no  longer  lay  any 
stress  upon  cold,  exposure,  over-exertion,  sexual  excesses  or  violent 
emotions  in  the  etiology  of  the  disease,  except  as  general  predisposing 
factors. 

Pathology  and  Pathogenesis. — As  myelitis  is  primarily  a  pure 
inflammation  there  is  at  first  hypersemia,  congestion,  enlargem.ent  and 
proliferation  of  the  bloodvessels,  extravasation  of  the  corpuscles, 
swelling  of  the  perivascular  spaces  with  fluid  and  a  general  softening 
and  obliteration  of  the  normal  appearances.  Sometimes  the  cord  is  so 
softened  that  it  flows  out  when  the  pia  is  cut.  This  extreme  fluidity 
is  partly  a  post-mortem  change.     In  the  early  stage  the  softened  area 


THE  NON-NEURONIC  DISEASES 


533 


FIGURE  X13. 


-  FIGURE  114. 


^i. 


ff^ 


3^ 


FIGURE  115. 


/ 


myl^tS'lff^T"^^^'^"T  'I'-  ^°"^'  '""^^  column-form.  Figure  114,  Chronic 
myelitis  of  the  dorsal  cord.  Figure  115,  "Compression  myelitis,"  due  to  car- 
cinoma of  the  third  dorsal  vertebra.     (After  Jakob.)  -  -     ue  10    car 


534  THE  NOX-NEURONIC  DISEASES 

is  reddish ;  then  as  the  coloring  matter  of  the  extravasated  corpuscles 
breaks  down  the  softened  area  becomes  mottled,  brownish  or  grayish- 
yellow  in  appearance ;  and  finally  with  the  gradual  absorption  of  these 
coloring  matters  it  becomes  paler  and  \vhiter.  The  term  softening 
applied  to  these  three  stages  of  the  process  should  not  be  confounded 
with  the  softening,  or  myelomalacia  from  embolic  or  thrombotic 
obstruction.  Under  the  microscope  the  nervous  elements  are  seen  to 
be  most  seriously  damaged.  The  axis-cylinders  and  cellular  elements 
are  swollen,  which  at  first  causes  a  pufhng  up  of  the  cord  and  an 
obliteration  of  the  distinction  and  line  of  demarkation  between  the  gray 
and  w^hite  substance.  As  degeneration  proceeds  in  these  elements  the 
cord  appears  yellowish,  smaller  and  even  cystic  at  times.  Granular 
cells  are  found  in  abundance,  and  with  the  fat  drops  resulting  from  the 
breaking  down  of  the  myelin  are  here  and  there  heaped  up.  The 
neuroglia  is  proliferated  and  the  spider-like  cells  of  Deiters  are  numer- 
ous and  prominent.  In  a  transverse  myelitis  this  condition  of  the  cord 
extends  about  an  inch  or  two,  shading  oft  above  and  below.  Usually 
the  pia  mater  is  somewhat  thickened  over  the  diseased  area  and  often 
the  whole  cord.  In  severe  and  secondary  cases  the  cord  is  often  reduced 
m  size,  rather  hard  to  the  touch  and  under  the  microscope  shows  little 
but  an  excess  of  connective  tissue.  In  the  cases  less  severe,  or  the 
parts  of  the  cord  less  seriously  affected,  congestion  and  vascular  irri- 
tation are  noticeable,  some  nerve  fibres  are  intact  or  partially  disinte- 
grated, and  cells  in  various  stages  of  degeneration  are  seen.  A  good 
deal  of  amorphous  material  is  present  studded  with  nuclei. 

Symptoms. — In  describing  the  symptoms  of  myelitis,  the  trans- 
verse dorsal  type  is  taken  as  the  model  and  the  variations  from  that 
noted  in  other  types.  There  are  110  prodromata  in  the  true  sense  of 
the  word.  When  the  first  symptoms  make  their  appearance,  the  dis- 
ease has  already  begun  its  regular  course.  These  early  symptoms  may 
be  of  a  very  fugitive  and  indefinite  character  and  may  come  on  prompt- 
ly after  an  injury  or  they  may  be  delayed  and  announce  themselves 
later  in  a  severe  and  definite  manner.  For  some  time  after  a  strain,  I 
have  seen  the  pains  diagnosed  as  rheumatism  and  the  attending  physi- 
cian chagrined  to  observe  all  the  signs  of  a  transverse  myelitis,  with  a 
fatal  issue,  follow.  I  have  seen  in  consultation  a  case  in  which  a  mere 
disturbance  of  the  bladder  with  slight,  fugitive  pains  as  the  only  trouble 
that  sent  the  patient  to  his  doctor. 

It  is  well  to  be  alert  when  such  indefinite,  slight,  changeable  sensory 
phenomena,  with  motor  weakness,  are  complained  of  in  the  history  of 
syphilis  or  after  an  injury,  for  in  many  cases  they  wdl  be  seen  to  be 
the  early  manifestations  of  a  genuine  myelitis. 

In  the  larger  number  of  cases  the  symptoms  appear  rather  abruptly, 
and  in  a  few  hours  or  a  few  days  rapidly  rise  to  their  height.  There 
is  an  initial  numbness  in  the  legs,  beginning  in  the  feet.  Pains  of  a 
dull,  aching  character  are  complained  of  in  the  back,  around  the  lower 
part  of  the  body  and  even  down  the  legs.  The  legs  feel  heavy  and 
weak.  The  patient  notices  that  his  walking  is  growing  stiff  and  labored. 
The  numbness  gradually  increases  in  area  and  passes  into  a  condition 
of  anoesthesia.     The  upper  limit  of  the  anaesthesia,  usually  near  the 


THE  NON-NEURONIC  DISEASES  535 

level  of  the  umbilicus,  is  fairly  well  marked.  Near  this  point  is  felt  a 
cincture  pain  or  constriction  girdle  sensation.  Sometimes  for  an  inch 
or  two  above  this  the  skin  is  hypercusthetic.  The  bowels  are  constipated 
and  there  is  some  incontinence  of  urine.  The  temperature  may  be 
elevated  a  degree  or  two  but  never  as  much  as  in  meningitis.  By  this 
time  the  disease  has  assumed  its  typical  clinical  appearance,  the  symp- 
toms of  which  are  so  characteristic  that  they  call  for  a  little  more  detail 
of   description. 

The  most  obvious  symptom  of  a  fully  developed  attack  of  myelitis 
is  paraplegia.  This  paralysis  is  a  trtie  paralysis,  spastic  in  character, 
and  affects  all  of  the  muscles  of  both  legs.  Both  the  immobility  and 
spasticity  are  of  course  due  to  the  break  in  the  continuity  of  the  cord 
and  the  separation  of  the  brain  from  the  lower  motor  neurones  of  the 
lumbar  area.  The  niyotatic  irritability  of  the  muscles  of  the  legs,  as 
well  as  the  tendon  reflexes,  are  greatly  exaggerated.  A  slight  tap  causes 
lihem  to  contract  violently  and  when  this  is  observed  in  conjunction 
•with  the  profound  anesthesia,  the  symptom  is  most  impressive.  The 
limbs  at  first  lie  extended  but  as  the  rigidity  of  the  muscles  increases, 
contractures  come  on  and  they  become  strongly  flexed  at  all  of  the 
joints.  On  this  account  the  patient  lies  on  his  back  or  side  with  his 
legs  drawn  tightly  up  towards  his  belly.  Often  there  are  twitchings 
and  jerkings  and  other  spontaneous  movements  in  the  legs,  of  which 
the  patient  is  perfectly  unconscious  except  as  he  happens  to  see  them. 

As  a  rule  all  forms  of  sensation  are  lost  in  the  legs  and  lower  part 
of  the  body.  This  anaesthesia  is  complete  and  its  upper  limit  is  clearly 
defined  by  a  ring  around  the  body.  At  a  point  above  this  upper  border 
of  the  ansesthesia  there  is  a  girdle  or  constriction  band  which  at  first 
may  be  painful  but  which  later  on  becomes  a  feeling  of  pressure  or  of  a 
vise-like  band.  For  some  little  distance  above  the  girdle-pain  and 
around  the  body  the  skin  is  hyperaesthetic.  As  this  ancesthetic  border 
xvith  its  hypercusthetic  area  above  moves  up  or  dawn  with  the  exten- 
sion of  the  lesion,  it  enables  one  to  make  a  fairly  accurate  localization 
diagnosis  of  the  site  and  probable  extent  of  the  lesion. 

When  the  ansesthesia  is  not  complete  it  is  most  marked  in  the 
sense  of  touch,  less  so  in  that  of  temperature, ?Lnd\ed.stoisi\\mtha.t  oipain 
The  anaesthesia  involves  the  bladder  and  rectum.  On  account  of  this 
and  the  paralysis  of  the  sphincters,  the  functions  of  the  bladder  and 
rectum  cannot  be  controlled  by  the  patient.  Incontinence  and  reten- 
tion of  urine  and  fceces  are  most  significant  symptoims  of  this  form  of 
myelitis.     Priapism  occurs  as  well  as  sexual  impotence. 

Bedsores  in  most  cases  begin  to  develop  early.  These  are  genuine 
trophic  symptoms,  though  of  course  they  are  favored,  by  weight  and 
pressure,  loss  of  sensation  and  consequent  uncleanliness.  Most  of 
these  sores  occur  over  the  trochanters,  the  sacrum  or  in  the  toes,  and 
sometimes  they  burrow  so  deep  as  to  expose  the  underlying  bone. 
Pyogenic  infection  plays  a  role  also  in  their  production.  Pemphigus 
and  other  trophic  skin  troubles  sometimes  occur. 

Among  the  vasomotor  and  secretory  disturbances  are  the  arthro- 
pathies, oedema  and  anidrosis.  The  skin  is  rough  and  cold  and  con- 
gested.     Sometimes    excessive   perspiration   occurs. 


536  THE  NON-XEUROXIC  DISEASES 

There  is  no  muscular  atrophy  nor  electrical  change. 

.In  a  word  the  cardinal  symptoms  of  the  typical  form  of  myelitis, 
namely,  the  transverse  dorsal,  are  spastic  paraplegia,  anesthesia,  exag- 
geration of  the  superficial  and  deep  reflexes,  cincture-pain,  disturb- 
ance of  the  vesical  and  rectal  sphincters,  bedsores  and  other  trophic 
manifestations,  and  certain  vasomotor  and  secretory  symptoms.  A 
few  words  must  now  be  devoted  to  the  changes  in  the  above  clinical 
picture  caused  by  a  change  in  the  location  of  the  lesion.  When  the 
latter  does  not  extend  completely  across  the  cord,  all  of  the  usual  symp- 
toms are  less  complete.  For  instance,  the  paraplegia  is  more  of  a  paresis 
and  is  irregularly  distributed.  The  same  is  true  of  the  anaesthesia  and 
the  trophic  symptoms.  The  symptoms  may  even  be  unilateral  or  they 
may  be  more  pronounced  on  one  side  than  on  the  other.  In  some  rare 
cases  Brown-Sequard's  phenomenon  is  present,  namely,  paralysis  on 
the  side  of  the  lesion  with  anaesthesia  on  the  opposite  side.  The 
lesion,  moreover,  may  extend  up  and  down  the  wdiole  dorsal,  or  in- 
volve a  part  of  the  dorsal  with  the  lumbar  region.  It  may  be  completely 
or  incompletely  transverse.  The  symptoms  under  these  circumstances 
will  be  slightly  modified  but  in  a  way  that  can  be  easily  imagined.  In 
the  main  they  will  represent  the  general  picture,  but  the  reflexes  will 
be  abolished,  the  paralysis  will  be  more  profound  and  the  atrophy  will 
be  more  distinct.  According  to  Bastian,  when  the  lesion  is  such  that 
there  is  a  total  destruction  of  the  conducting  tracts  above  the  reflex- 
arc,  that  reflex  will  be  decreased  or  annulled,  whereas  in  a  partial  or 
incomplete  destruction  it  will  be  exaggerated.  This  is  not  entirely 
proved,  however.  When  the  disease  is  of  a  slowly  progressive  charac- 
ter, the  reflex  functions  of  the  cord  may  be  retained  and  the  muscular 
tone  may  remain  unimpaired,  thus  modifying  Bastian's  hypothesis  to  a 
certain  extent.  In  compression  of  the  cord,  where  the  anatomical 
lesion  is  slight  or  incomplete,  there  may  be  a  physiological  loss  of 
function,  and  the  same  may  be  true  of  the  functions  of  the  cord  below 
a  transverse  lesion.  At  all  events,  as  Warrington  has  pointed  out, 
no  case  of  incomplete  division  of  the  cord  has  been  recorded  in  which 
all  the  symptoms  described  by  Bastian  were  present,  and  in  which  the 
lumbar  enlargement  was  intact.  It  was  Van  Gehuchten  who  taught 
that  the  reflexes  depend  upon  the  tone  of  the  motor  ganglion  cells,  as 
well  as  upon  the  integrity  of  the  reflex-arc,  and  that  therefore  the 
reflex  may  be  annulled  by  a  complete  destruction  of  conduction  in  the 
spinal  cord,  and  exaggerated  by  a  degeneration  of  the  pyramidal  tracts. 
This  may  explain  in  part  the  exaggeration  of  the  knee-jerks  in  some 
cases  of  transverse  myelitis,  particularly  the  slowly  progressing  or  high 
dorsal  cases,  and  its  abolition  in  some  other  cases,  such  as  the  severe 
and  complete  cases  of  the  lower  dorsal  or  dorsoi-lumbar  type. 

When  the  disease  is  entirely  of  the  Inmbar  or  lunibo-sacral  type, 
the  paralysis  and  anaesthesia  are  profo-und,  the  reflexes  are  lost,  and 
the  implication  of  the  bladder  and  rectum  is  decided.  The  paralysis 
is  of  the  flaccid  type  with  atrophy  and  the  reaction  of  degeneration. 
There  are  shooting  pains  in  the  legs  but  no  girdle  sensation  about  the 
body.     Priapism  followed  by  loss  of  the  sexual  function  occurs. 

A  cervical  myelitis  involves  all  four  extremities,  quadriplegia  or 


TiriC  NON-NEURONIC  DISEASES  537 

paraplegia,  and  trunk  in  the  paralysis  and  ansesthesia.  When  the  lesion 
is  in  the  loiver  part  of  the  cervical  cord  tlie  paraplegia  is  spastic  in  the 
legs  and  atrophic  in  the  arms.  Moreover  there  are  oculo-pupillary 
symptoms  from  implication  of  the  ciliospinal  center.  When  it  is  in  the 
upper  cervical  region  the  arms  as  well  as  the  legs  are  spastic  and 
paraplegic.  Encroachment  of  the  lesion  upon  the  phrenic  center  causes 
a  disturbance  in  the  action  of  the  diaphragm.  Sometimes  in  these  high 
forms  of  myelitis,  there  are  medullary  symptoms  such  as  cardiac  and 
respiratory  disturbances. 

In  a  central  or  periependymal  myelitis  the  symptoms  bear  a  re- 
mote resemblance  to  those  of  syringomyelia,  namely,  muscular  localized 
atrophy,  disturbance  of  pain  and  temperature  sense  with  preservation 
of  tactile  sense,  and  symptoms  referable  to  the  viscera  especially  and 
vasomotor  and  secretory  apparatus.  There  may  be  some  pain  and 
irritation  but  they  are  distinctly  less  than  in  the  other  forms  of  mye- 
litis. 

Compression  myelitis  of  the  periphery  of  the  cord,  is  characterized 
particularly  by  irritative  symptoms  involving  the  spinal  nerve  roots. 
It  is  slow  in  onset  and  usually  being  but  a  part  of  a  meningomyelitis 
it  reveals  meningitic  symptoms  in  addition  to  the  myelitic.  Therefore 
it  is  accompanied  by  muscular  twitchings,  spasms  and  contractures, 
sharp  pains  along  the  course  of  the  nerves,  incomplete  anaesthesia  and 
paralysis,  late  involvement  only  of  the  sphincters  and  slight  trophic 
manifestations.  The  reflexes,  however,  are  exaggerated  and  sooner 
or  later  there  is  a  spastic  paraplegia. 

A  disseminated  myelitis  involving  the  cord,  medulla,  pons  and 
brain  is  the  type  that  follows  as  a  rule  the  infectious  fevers.  These 
cases  are  not  entirely  unlike  multiple  sclerosis  in  their  symptomatology. 
The  motor,  sensory  and  trophic  symptoms  bear  the  same  general  char- 
acteristics noted  under  the  head  of  the  latter  disease,  and  depend  upon 
the  extent  and  location  of  the  foci  of  disease. 

Diagnosis. — The  diagnosis  of  myelitis  is  not  difficult  in  the  typical 
cases.  It  is  the  miodified  and  complicated  forms  that  give  the  most 
trouble  in  this  respect.  In  making  a  diagnosis  special  attention  must 
be  given  to  the  history  of  the  case,  its  mode  of  onset  and  progress, 
the  distribution  of  the  individual  symptoms  and  the  total  clinical  pic- 
ture that  is  presented.  It  is  well,  as  a  rule,  to  keep  in  mind  the  cardinal 
symptoms  of  a  typical  transverse  dorsal  myelitis,  and  with  this  general 
clinical  picture  as  a  sort  of  schema,  to  assign  the  aberrant  symptoms 
that  may  appear  with,  or  in  place  of,  the  sympto^ms  of  this  schema 
to  the  possible  changes  in  location  of  the  inflammatory  focus. 

Most  of  the  cases  of  myelitis  begin  abruptly  and  attain  their  climax 
rapidly.  Paraplegia,  anaesthesia,  altered  reflexes,  disturbed  function 
of  the  bladder  and  rectum,  decubitus,  and  other  trophic,  vasomotor  and 
secretory  manifestations  soon  announce  themselves  in  all  their  com- 
pleteness. There  may  be  a  chill  with  considerable  elevation  of  tem- 
perature. Pain  is  comparatively  slight  in  these  acute  cases.  Less 
frequently  the  cases  are  subacute  and  rarely  they  are  chronic.  Most 
of  the  chronic  cases  turn  out  to  be  multiple  sclerosis  with  predominat- 
ing spinal  symptoms. 


53^  THE  NON-NEURONIC  DISEASES 

From  progressive  muscular  atrophy  and  am^'otrophic  lateral 
sclerosis,  this  disease  can  be  readily  distinguished  by  its  febrile  symp- 
toms, its  rapid  onset  and  course,  its  more  prominent  sensory  mani- 
festations, its  involvement  of  the  sphincters  and  its  lesser  degree  of 
muscular  atrophy.  Spinal  tumor  is  sometimes  accompanied  by  a  focal 
myelitis.  It  is  characterized  by  slow  onset,  unilateral  symptoms  not 
unfrequemtly  of  the  Brown-Sequard  type,  and  signs  of  spinal  nerve 
root  irritation  and  compression.  The  metastatic  origin  of  the  neoplasm 
can  sometimes  be  made  otit  and  in  some  cases  it  can  be  definitely 
localized.  In  locomotor  ataxia  there  is  no  true  paralysis,  but  on  the 
other  hand  a  history  of  syphilis,  ataxia,  Argyll-Robertson  pupil  and 
severe  sensory^  disturbances  of  a  progressive  character.  Brain  palsies 
are  hemiplegic  in  distribution,  spastic,  painless,  without  muscular 
atrophy  or  involvement  of  the  sphincters.  Multiple  sclerosis  often 
resembles  and  sometimes  even  develops  on  top  of  a  disseminated  form 
of  myelitis.  The  differentiation  is  extremely  difficult  when  the  spinal 
symptoms  of  multiple  sclerosis  are  so  prominent  as  to  obscure  the 
cerebral  symptoms.  In  all  cases  the  head  symptoms  should  therefore 
be  most  earnestly  sought  for  and  if  the  case  is  one  of  multiple  sclerosis 
there  will  be  found  some  degree  of  optic  atrophy,  diplopia,  dysarthria 
and  tremor  of  the  so-called  intentional  type.  Cervical  pachymeningitis 
is  slow  and  progressive  as  a  rule,  but  whether  acute  or  chronic  is  char- 
acterized especially  by  the  irritative  and  compression  symptoms  of  a 
typical  meningitis  with  the  symptoms  of  the  peripheral  myelitis  coming 
on  later. 

Spinal  meningitis  is  to  be  differentiated  by  the  irritative  root  symp- 
toms, the  tenderness  of  the  spine  upon  pressure  and  the  somewhat  more 
marked  febrile  s}'mptoms.  The  intense  shooting  pains  along  the  course 
of  the  spinal  nerves  are  characteristic.  ]\Ioreover  the  paralysis  and 
atrophy  are  not  so  segmental  as  neuritic  in  distribution. 

Hysterical  paraplegia  may  have  slight  sensory  symptoms,  some 
atrophy  and  a  spurious  ankle  clonus.  The  special  stigmata  of  hysteria, 
the  psychoneurotic  character  of  the  symptoms  can  scarcely  be  mistaken 
if  care  in  the  examination  is  exercised. 

Other  forms  of  paraplegia  are  the  senile  from  arteriosclerosis ; 
traumatic,  from  operations  on  the  bladder,  etc.,  and  neuritic. 

Prognosis. — The  outlook  of  every  case  of  myelitis  is  problemati- 
cal. Unfavorable  as  it  is  in  many  of  the  cases,  I  am  convinced  that 
generally  too  pessimistic  a  view  is  taken  in  regard  to  its  cure.  Some 
cases,  small  in  number  to  be  sure,  do  get  well,  or  at  least  recede  and  pass 
into  a  mildly  chronic  or  latent  condition.  Some  of  these  cases  improve, 
then  relapse  or  remit,  then  improve  again  only  to  relapse  once  more 
and  so  on  until  in  the  end  they  die  in  the  usual  way.  The  most  hopeful 
cases  are  those  that  follow  the  acute  infectious  diseases,  especially  when 
the  myelitis  is  of  the  disseminated  type.  Intermittent  and  malarial 
cases  often  recover.  Syphilitic  cases  sometimes  do.  Gonorrhosal  cases 
always  get  well  under  propter  management.  The  subacute,  chronic,  in- 
sidious, slow-progressing  complete  types  are  perhaps  the  most  unfavor- 
able.    Patients  sometimes  live  many  years  with  this  type  of  disease. 


THE  NON-NEURONIC  DISEASES  539 

The  rapid  cases,  as  a  rule,  soon  cease  to  progress  and  even  when  asso- 
•ciated  with  meningeal  and  neuritic  symptoms  are  not  unfavorable. 

Much  depends  upon  the  constitution  oif  the  patient,  the  amenability 
to  cure  of  the  underlying  etiological  disease  like  caries,  tumor,  etc.,  and 
the  willingness  to  take  treatment  and  the  patience  on  the  part  of  the 
individual  afflicted.  I  have  seen  simple  myelitis  hurried  to  a  fatal  issue 
by  injudicious  electrical  and  "osteopathic"  treatment. 

Dorsal  myelitis  is  the  most  hopeful  form  of  the  disease  from  the 
standpoint  of  the  location  of  the  lesion.  Bedsores,  cystitis  and  long- 
continued,  complete  paralysis  are  bad  signs.  Recession  or  disappear- 
ance of  sensory  symptoms  is  a  particularly  favorable  sign  and  usually 
prophesies  complete  recovery.  Death,  when  it  comes  on,  usually  is 
the  result  of  exhaustion,  cystitis  and  bedsores. 

Treatment. — Tlie  treatment  of  a  case  of  myelitis  calls  for  a  high 
degree  of  patience  and  skill.  The  value  of  a. masterly  inactivity  is 
sometimes  most  beautifully  exhibited  in  the  management  of  this  trouble. 
On  the  other  hand  when  there  is  a  clear  realization  of  the  origin,  nature 
-  and  extent  of  the  disease  process  a  persistent,  energetic  treatment  of 
the  right  sort  will  sometimes  almO'St  do  wonders.  Therefore  unless 
the  practitioner  knows  exactly  what  he  is  attempting  to  do,  and  is 
familiar  with  the  best  means  O'f  doing  it,  he  had  much  better  leave 
the  case  alone  and  do  nothing.  In  this  way  he  will  at  least  escape 
the  charge  of  having  brought  on  a  complete  paraplegia  and  of  having 
liastened  the  end. 

Under  the  best  conditions  the  treatment  of  myelitis  is  not  a  grate- 
ful task ;  for  it  is  slow  and  tedious  and  is  punctuated  by  most  surprising 
and  at  times  thoroughly  discouraging  relapses.  The  patient  had  better 
be  well  forewarned  of  this  before  the  treatment  is  undertaken  and  also 
be  frankly  told  that  he  may  have  to  lie  in  bed  many  months. 

The  prime  element  in  the  treatment  is  rest,  absolute  rest,  mental 
and  physical.  If  we  could  but  write  a  prescription  for  rest  as  we  do 
for  a  drug,  so  as  to  bring  it  home  to  the  patient's  realization  that  in 
this  disease  rest,  rest,  rest,  is  of  even  greater  therapeutic  value  than  any 
drug,  what  better  results  might  we  not  obtain !  But  to  tell  a  patient 
to  keep  quiet  and  to  do  little  but  lie  down  for  months  and  months 
seems  so  trite  and  inert  that  it  is  hardly  to  be  wondered  at  that  he 
rebels  and  demands  some  positive  form  of  activity.  Here  is  where  a 
large  part  of  the  failure  to  successfully  cope  with  myelitis  is  to  be 
charged.  I  have  had  under  my  own  care  cases  that  under  the  advice 
to  remain  quiet  were  after  several  months  progressing  most  satisfac- 
torily. The  symptoms  were  receding  and  the  outlook  was  becoming 
decidedly  hopeful.  Too  hopeful,  unfortunately,  for  the  patient  fondly 
imagining  that  he  was  about  well,  got  up,  started  on  a  long  walk  or 
some  other  prohibited  exercise,  only  to  hasten  back  tO'  bed  again  in  a 
few  hours  with  the  return  of  pains,  numbness  and  muscular  weakness. 
I  have  had  such  experiences  several  times  in  the  course  of  even  a 
single  case.  Under  such  circumstances  the  discouragement  is  so  great 
that  one  is  almost  tempted  to  abandon  the  case  and  leave  the  patient 
to  his  fate.  On  the  other  hand  I  have  seen  most  happy  results  in  cases 
that  were  submissive  and  that  maintained  the  prone  position  for  a  long 


540  THE  NON-NEURONIC  DISEASES 

period  of  time.  Given  such  a  willing  patient,  I  do^  not  relinquish  all 
hope  of  cure,  or  at  least  amelioration,  until  some  eighteen  months  have 
rolled  around  without  any  evidence  of  improvement.  Cures  have  taken 
place  even  after  such  a  long  and  discouraging  experience  as  that. 

The  second  fact  to  bear  always  in  mind  in  the  early  treatment  of 
myelitis  is  that  the  disease  process  is  an  infectious  inflammation. 
Elimination,  therefore,  is  more  important  than  counter-irritation.  A 
diaphoretic  treatment  is  preeminently  called  for  in  this  progressing- 
period  of  the  disease.  The  bowels  should  be  kept  well  open  with  calo- 
mel, salines  and  other  forms  of  catharsis.  The  kidneys  may  be  stimu- 
lated by  diuretin  or  other  mild  diuretic.  The  activity  of  the  skin  can 
be  provoked  by  tepid  spongings.  Full  baths  had  better  be  avoided 
until  the  disease  has  ceased  to  progress,  and,  even  then  they  must  be 
used  cautiously  and  not  too  frequently.  Only  lukewarm  baths  are 
advisable,  and  generally  they  had  better  be  half-baths  given  in  bed  and 
followed  by  gentle  frictions.  Hot  and  cold  baths,  or  other  form  of 
hot  and  cold  applications,  are  positively  contra-indicated.  Sea-bathing 
must  be  prohibited  and  treatment  at  the  various  hot  springs  and  sana- 
taria  is  of  very  doubtful  utility.  They  necessitate  too  much  movement 
and  are  apt  to  be  too  stimulating. 

Counter-irritation  of  the  spine  is,  in  my  opinion,  of  little  benefit 
unless  it  is  so  mild  that  it  can  be  used  for  a  long  period  almO'St  con- 
tinuously. Iodine,  fly-blisters,  vesicants  of  various  sorts,  the  actual 
cautery  and  the  seton  have  not  been  sufficiently  beneficial  in  my  obser- 
vation to  encourage  me  in  the  use  of  them.  Moreover,  they  have  ad- 
ded too  greatly  to  the  general  distress  of  the  patient.  I  depend  more 
upon  the  constant  application  of  sinapisms,  diluting  the  mustard  some- 
times with  ground  flaxseed  and  changing  them  about  on  the  back  sO' 
that  the  patient  can  wear  them  almost  continuously.  In  this  way  they 
soothe  the  patient  and  relieve  the  pain ;  above  all  they  do  not  materially 
add  to  his  discomfort. 

Among  the  remedies  that  may  be  employed,  iodide  of  potassiunt 
still  holds  the  first  place.  It  must  be  used  steadily  and  in  moderate 
doses.  In  syphilitic  cases  the  iodide  in  large  doses  and  mercury  are 
of  course  indicated.  In  the  non-syphilitic  cases  of  myelitis  I  am  just  as 
urgent  to  contra-indicate  the  use  of  mercury  as  I  am  to  indicate  it  in 
the  cases  of  meningitis.  If  there  are  symptoms  of  meningomyelitis  I 
use  mercury  steadily  for  a  long  period  of  time,  guarding  it  with  a  small 
amount  of  opium. 

The  use  of  opium  or  its  alkaloid  is  sometnues  advisable  to  relieve 
the  pain  and  induce  quietude  for  a  time  in  the  early  management  of 
the  case.  I  have  had  no  experience  with  ergot  and  cannot  understand 
upon  what  principle  it  is  recommended.  Silver  in  the  form  of  the 
nitrate  has  seemed  to  help  some  cases ;  so  have  the  arsenite  of  sodium, 
the  salicylates,  chloride  of  gold,  and  phosphorus.  Later  on  small 
doses  of  strychnia,  or  the  hypodermic  injection  of  strychnia,  may  be 
employed  to  combat  the  paralysis.  Cystitis  must  be  carefully  guarded 
against  by  clean  catheterization  and  flushings  and  the  use  of  buchu,. 
boric  acid,  sandalwood  and  similar  drugs.  The  skin  around  the  scrotal 
region  must  be  carefully  protected  by  a  urinal  or  an  antiseptic  pad. 


THE  NON-NEURONIC  DISEASES 


541 


Por  bedsores  as  well  as  for  the  atrophic  changes  aggravated  by  am- 
moniacal  urine,  Palmer  recomtnends  the  use  of  a  soft  linen  bag  large 
-enough  to  extend  down  the  thighs  and  filled  with  bran  moistened  with 
dilute  sulphuric  acid.  Two  ounces  of  the  dilute  acid  may  be  used 
to  a  quart  of  bran  and  it  should  be  renewed  every  second  day. 

Care  in  avoiding  points  of  pressure,  and  the  use  of  a  water  mat- 
tress or  water  pillows,  will  obviate  the  development  of  bedsores. 

Contractures  cannot  be  forestalled,  even  morphine  and  hyoscin 
usually  failing.  A  permanent  bath  is  sometimes  good  for  them 
Tenotomy  is  of  course  to  be  considered  in  connection  with  severe  forms 
of  contracture. 

Special  forms  of  myelitis  sometimes  call  for  special  lines  of 
treatment  and  such  etiological  factors  as  syphilis,  malaria,  etc.,  indicate 
the  proper  mode  of  medication.  In  chronic  meningomyelitis  much 
benefit  is  sometimes  obtained  from  suspension  and  the  spinal  jacket. 
Stefano  Personali  especially  claims  good  results  from  tMs  treatment 
in  this  form  of  the  disease.  He  employs  the  usual  apparatus  for  sus- 
pension daily  for  one  to  four  minutes  for  four  days,  then  for  four 
minutes  for  twelve  days,  after  which  the  jacket  is  applied  and  worn 
in  bed  for  three  months.  When  the  patient  can  walk  a  little  about  the 
house,  this  jacket  is  removed  and  another  one  applied.  This  is  worn 
for  two  months,  the  patient  not  being  kept  so  strictly  in  bed  as  before. 
A  third  jacket  is  then  put  on  for  three  months,  being  made  of  strong 
muslin.  In  some  cases  the  suspension  may  be  made  on  an  inclined  plane 
and  then  the  jacket  be  applied. 

Surgery  may  have  a  field  of  usefulness  in  myelitis  aside  from  the 
mere  removal  oi  tumors,  carious  bone,  etc. ;  for  in  such  operations  the 
associated  myelitis  has  been   cured. 

In  a  case  of  typhoid  myelitis  in  a  }-oung  man,  rest  in  bed  with 
carefully  arranged  coordinating  and  resisting  exercises,  the  exercises 
being  continued  and  elaborated  after  he  began  to  get  out  of  bed,  pro- 
duced happy  results  in  a  case  of  J.  K.  Mitchell. 

After  recovery  all  cases  must  be  urged  to  avoid  that  which  may 
tend  to  bring  on  a  relapse.  Mountain  climbing  is  therefore  dangerous. 
A  sea-voyage  is  excellent.  A  quiet,  wholesome  life,  without  strain 
and  with  plenty  of  fresh  air  and  nourishing  food  must  be  sought  after. 
In  this  way  a  recovered  case  of  myelitis  may  live  a  normal  age  without 
a*iy  reappearance  of  the  old  symptoms. 

ACUTE  ANTERIOR  POLIOMYELITIS  OF  INFANTS. 

This  is  a  commion  disease  and  is  sometimes  known  as  infantile 
palsy,  acute  atrophic  spinal  paralysis,  or  cornual  myelitis.  As  it  is 
primarily  an  inflammation  it  should  be  treated  of  under  the  general 
head  of  inflammations  of  the  spinal  cord.  By  some  writers  it  is  consid- 
ered among  the  systemic  diseases  of  the  cord,  because  the  primary  dis- 
ease process  is  limited  to  the  column  of  gray  matter  that  makes  up  the 
anterior  horn,  with  mere  secondary  processes  in  the  peripheral  motor 
tiicurones.  In  my  own  opinion,  logical  sequence  demands  that  it  should 
be  distinctly  ranked  under  the  head  of  a  localised  inflauiniation  of  the 


542  THE  NOX-XEURONIC  DISEASES 

cord,  for  reasons  which  will  appear  when  I  discuss  its  pathology  and 
pathogenesis.  The  disease  is  characterized  especially  by  a  ^accid 
paralysis  and  atrophy  with  certain  consequent  manifestations,  the 
paralysis  and  atrophy  being  limited  to  individual  muscles  or  groups  of 
muscles,  because  of  the  damage  to  their  representative  cells  in  the 
anterior  horns. 

Etiology. — The  most  striking  feature  of  the  etiology  of  infantile 
palsy  is  the  age  at  which  it  occu.rs.  Though  it  may  appear  at  any 
period  of  life  it  is  preeminently  a  disease  of  early  childhood.  The 
great  majority  of  the  cases  occur  in  the  second  and  third  years,  when 
the  child  is  beginning  to  walk  and  is  undergoing  the  process  of  denti- 
tion. The  disease  is  very  rare  before  the  fifth  month  and  is  not  often 
seen  after  the  fourth  year.  According  to  Sinkler  it  has  been  known 
to  start  before  birth,  giving  rise  to  a  congenital  type  of  the  disease- 
It  is  slightly  more  frequent  in  boys  than  in  girls.  Heredity  shows  its 
influence,  probably  neuropathically,  in  a  very  small  percentage  of  cases. 
It  has  occurred  in  several  members  of  the  same  family. 

The  great  majority  of  the  cases  take  place  in  the  hot  months  of 
the  summer.  It  would  seem  chat  certain,  time-honored  alleged  causes, 
such  as  sudden  chilling  of  the  body,  over- exertion,  traumata,  etc.,  would 
be  more  operative  at  this  time  when  the  child  is  more  out  of  doors 
and  at  greater  liberty  than  in  the  winter  when  he  is  restrained  and 
closely  protected.  And  yet  it  is  now  pretty  generally  agreed  that  these 
supposed  causes  are  subsidiary  or  at  least  especially  operative  in  only 
a  limited  number  of  cases. 

The  cause  of  infantile  palsy  is  without  doubt  some  form  of  in- 
fection. This  is  shown  by  the  course  of  the  disease,  the  circumstances 
under  which  it  usually  occurs,  its  appearance  with  other  forms  of  in- 
fectious nervous  diseases  like  cerebrospinal  meningitis  and  neuritis, 
and  by  the  fact  that  it  has  been  not  infrequently  observed  to  occur 
epidemically.  ^loreover,  micro-organisms  have  been  introduced  ex- 
perimentally into  the  bodies  of  animals  and  alterations  have  occurred  in 
the  cord  that  simulated  perfectly  those  of  the  disease  under  considera- 
tion. In  addition  to  all  this,  the  disease  has  followed  other  forms  of 
infection  such  as  scarlet  fever,  measles,  whooping  cough,  etc. 

]Mcst  remarkable  and  suggestive,  however,  are  the  epidemics  of 
anterior  poliomyelitis  that  have  been  reported.  In  the  outbreak  in 
Vermont  in  1894,  reported  by  Dana,  some  160  cases  appeared  from 
June  to  September  in  the  country  along  the  Otto  Creek.  In  the  same 
year  Putnam  reported  an  irruption  that  occurred  in  and.  about  Boston. 
Medin,  of  Stockholm,  described  an  epidemic  in  which  there  were  44 
cases  in  the  same  town  within  one  month. 

That  the  disease  is  endemic  rather  than  epidemic  is  suggested  by 
the  fact  that  Oppenheim  voices  when  in  his  own  particular  experience 
he  says  that  most  of  his  cases  have  seemed  to  come  from  Weissensee, 
near  Berlin.  The  Gloucester,  I\Iass.,  epidemic  that  occurred  in  the 
summer  of  1900,  and  was  reported  by  Painter,  occurred  w'ithin  a  radius 
of  four  miles  and  included   some  38  cases. 

Tlie  influence  of  sudden  changes  of  temperature  as  a  contributive 
cause  along  with  the  infection  is  strikingly  shown  in  Painter's  report. 


THE  NON-NEURONIC  DISEASES  543 

The  majority  of  the  cases  occurred  in,  or  more  frequently  twenty-four 
or  thirty-six  hours  after,  periods  of  extreme  heat ;  and  in  some  in- 
stances im^mediately  after  a  sharp  drop  from  an  abnormally  high  tem- 
perature, or  a  bath  in  the  ocean.  The  disease  has  even  attacked  domes- 
tic animals,  such  as  fowls,  dogs  and  horses.  In  the  Vermont  epidemic 
a  typical  case  occurred  in  a  man  seventy  years  of  age. 

Patpiology  and  Pathogenesis. — The  essential  lesion  in  this  dis- 
ease is  an  iniiammation  of  vascular  origin  in  the  anterior  gray  horns 
of  the  spinal  cord,  with  subsequent  degeneration  and  disappearance  of 
the  ganglion  cells  and  their  processes.  The  work  of  Marie  and  Gold- 
scheider,  Redlich  and  Siemerling  seems  to  intimate  that  the  process 
is  primarily  a  general  inflammation  of  the  cord  and  that  while  the 
entire  cross-section  is  involved  the  maximum  point  of  the  trouble  is 
located  in  the  anterior  horns.  An  infection  is  the  origin  of  the  inflam- 
mation, thfe  infectious  material  (an  infectious  embolus  possibly)  reaches 
the  anterior  horns  by  way  of  the  anterior  spinal  artery.  The  peculiarity 
of  the  blood  supply  and  the  relative  abundance  of  the  ganglion  cells 
in  the  lumbar  and  cervical  portions  of  the  cord,  explain  satisfactorily 
the  preference  of  the  disease  for  these  localities,  both  in  its  pathology 
and   symptomatology. 

The  macroscopic  and  microscopic  appearance  of  the  cord  and  lesion 
will  vary  according  to  the  period  of  the  disease  in  which  the  examina- 
tion is  made.  Most  of  the  earlier  examinations  of  Charcot  and  others 
w«re  made  in  the  later  stages  when  the  inflammation  had  long  sub- 
sided and  only  the  atrophic  condition  was  in  evidence,  and  explain 
the  earlier  teaching,  now  known  to  be  erroneons,  that  the  disease  is 
primarily  a  parenchymatous  inflammation  of  the  ganglion  cells  of  the 
anterior  gray  horns.  Since  the  investigations  made  by  Goldscheider, 
Siemerling,  Dauber,  Marie,  Redlich,  Von  Leyden,  Schultze  and  others 
we  now  know  that  the  disease  process  is  primarily  a  vascular  inflamma- 
tion with  the  atrophic  change's  occurring  as  secondary  results.  In  the 
first  stage,  therefore,  we  find  hypersemia,  proliferation  of  the  terminal 
branches  of  the  anterior  spinal  artery,  dilatation  and  hypertrophy  of  the 
vessels,  perivascular  efifusion  and  exudation,  thro^mbotic  obstruction, 
extravasations  of  blood,  and  leucocytosis.  There  is  a  heaping  up  of 
the  round  cells  about  the  vessels  and  a  clouding  of  the  elementary 
structures.  No  suppuration  occurs.  The  outlines  of  the  horn  are  ob- 
scured; it  looks  swollen,  and  in  many  cases  the  adjacent  parts  of  the 
cord  and  meninges  are  softened  and  congested.  As  the  process  ad- 
vances, the  ganglion  cells  become  hazy,  swollen  and  involved  in  an 
incipient  chromatolytic  change.  Their  processes  are  swollen  and  exhibit 
a  beginning  degeneration.  Later  on  the  cells  and  fibres  are  distinctly 
atrophied.  Some  of  them  disappear  entirely  and  their  places  taken  in 
part  by  an  overgrowth  of  connective  tissue.  The  involvement  of  the 
neighboring  white  substance  decreases.  The  anterior  horn  diminishes 
and  shrivels  and  the  cord  seems  in  the  vicinity  smaller  and  harder. 
Sometimes  there  is  an  associated  sclerosis  in  the  lateral  columns.  The 
anterior  roots  and  motor  nerves,  of  course,  are  atrophied  and  the  re- 
lated muscular  tissues  are  zvasted  and  show  an  overgrowth  of  con- 
nective tissue.     Alterations  of  this  same  character  have  been  observed 


544  THE  NON-NEURONIC  DISEASES 

in  the  motor  nuclei  of  the  medulla  oblongata,  since  these  nuclei  are 
but  the  upward  extension  of  the  anterior  gray  matter  of  the  cord. 
When  the  disease  is  among  the  lower  medullary  nuclei  it  is  known 
as  inferior  polioencephalitis ;  when  among  the  upper  or  nuclei  of  the 
motoroculi,  it  is  spoken  of  as  superior  polioencephalitis  (ophthalmo- 
plegia). 

It  is  to  be  noted  that  the  branches  of  the  anterior  spinal  artery 
are,  in  Cohnheim's  sense,  terminal  arteries  and  that,  as  Schaefer  has 
shown,  no  one  set  of  arterioles  is  limited  in  its  distribution  to  any  one 
group  of  cells.  The  supply  of  the  posterior  parts  of  the  cord  by  the 
posterior  spinal  arteries  is  comparatively  scanty.  These  facts  help  to 
explain  the  peculiar  limitation  of  the  maximum  focus  of  the  disease 
to  the  anterior  or  motor  part  of  the  cord  and  the  symptoms  of  paralysis 
and  atrophy  in  particular  muscles  or  groups  of  muscles. 

Symptoms. — The  symptomatology  of  acute  anterior  poliomyelitis 
is  marvelously  definite  and  uniform.  The  clinical  picture  develops  and 
progresses  through  stages  that  are  singularly  distinct  and  logical.  A 
typical  case,  except  in  the  very  earliest  onset  of  the  disease,  presents  no 
great  difficulties  in  diagnosis.  Remembering  the  pathology,  one  can 
readily  understand  why  every  case  should  show  progressively  the  fol- 
lowing four  symptomatic  stages,  namely,  (i)  infections  fever,  (2) 
widespread,  sudden,  flaccid  paralysis,  (3)  recession  of  the  widespread 
paralysis  with  permanent  paralysis  and  atrophy  in  certain  individual 
muscles,  and  (4)  deformities  resulting  from  wasting  of  the  muscles 
and  contractures. 

Such  is  the  regular  clinical  picture  and  progress  of  infantile  palsy. 

I  will  now  discuss  the  symptoms  of  these  four  stages  of  the  dis- 
ease a  little  more  in  detail. 

The  beginning  of  the  disease  is  usually  abrupt  and  unexpected. 
After  a  happy  day  with  its  playmates,  romping  in  the  open  air,  the 
child  comes  in  and  complains  of  extreme  weariness  and  distress.  Its 
head  begins  to  ache.  It  is  nauseated  and  may  vomit.  It  is  listless  and 
clings  to  its  mother's  arms.  Perhaps  it  has  a  znolent  chill.  The  face 
becomes  hot,  dry  and  flushed.  It  may  soon  become  stuporous  and  even 
slightly  delirious.  There  may  be  a  general  convulsion.  The  child  re- 
fuses all  food  and  in  every  way  shows  that  it  is  decidedly  sick  and 
feverish.  With  or  without  the  advice  O'f  the  family  physician,  the 
mother  regards  and  treats  the  condition  as  probably  a  cold,  an  acute 
attack  of  indigestion,  distress  from  the  teeth  or  the  possible  beginning 
of  an  attack  of  measles.  It  is  put  to  bed  and  passes  a  feverish  and 
restless  night.  The  temperature  has  been  anywhere  from  102  degrees 
to  104  degrees  F.  In  the  morning  the  child  wakes  with  perhaps  a 
slight  diminution  of  the  febrile  symptoms  but  completely  paralysed  in 
the  legs  or  arms.  This  is  the  frequent  way  that  the  disease  starts. 
The  febrile  stage  lasts  from  a  few  hours  to  a  few  days.  Sometimes 
it  is  so  brief  and  the  paralysis  comes  on  so  suddenly,  that  one  involun- 
tarily thinks  of  a  hemorrhage.  At  other  times  it  is  so  prolonged  that 
for  many  days  no  diagnosis  is  possible.  For  his  own  credit's  sake, 
the  physician  will  always,  in  such  doubtful  cases,  keep  in  mind  the 
possibility  of  acute  poliomyelitis  and  inform  the  family  of  that  pos- 


THE   XOX-XEUROXIC  DISEASES  543 

9ibilitv  To  the  average  lavman  paralysis  is  a  most  awful  disaster,  and 
diou-h  when  the  paralvsis  comes  on,  the  physician  may  assure  the 
f  amity  'that  it  will  in  a  'large  measure  disappear  or  recede,  it  will  not 

FIGURE  1x6. 


Anterior   poliomyelitis,    showing    atrophic    condition    of   the    right    leg.      Dr. 
Fitch's  case. 

re==tore  the  confidence  shaken  by  the  shock  of  seeing  their  child  sud- 
denly paralyzed  and  by  their  not  having  been  torewarned  ot  such  a 

^°''mer;  the  paralysis  is  discovered  the  general  febrile  disturbance 


546 


THE  NON-NEURONIC  DISEASES 


has  usually  subsided  somewhat.     There  may  be  some  rheumatoid  pains 
complained  of  in  the  back  and  extremities  for  a   few  days,  or  there 


FIGURE  117. 


Anterior  poliomyelitis,  showing  the  atrophic  condition  of  the   right  leg. 

may  be  retention  of  urine  or  some  slight  gastro-intestinal  trouble.    The 
paralysis,  hoiwever,   is   the    dominant   symptom.      This   is  Haccid   and 


THE  NON-NEURONIC  DISEASES  547 

complete  from  the  beginning.  Usually  it  is  paraplegic  in  distribution, 
involving  both  legs  entirely.  Sometimes  it  involves  only  one  leg,  or 
one  leg  and  one  arm,  or  one  arm  alone,  or  both  arms.  Paralysis  of  one 
leg  or  of  one  arm  is  by  far  the  most  frequent  way  it  appears.  Paralysis 
of  bcth  legs  is  perhaps  the  third  most  common  distribution.  Paralysis 
of  the  four  limbs,  quadriplegia,  or  of  the  two  arms  alone,  crossed 
paralysis,  or  hemiplegic  paralysis,  is  very  rare.  Usually  the  paralysis 
includes  the  whole  limb  and  reaches  its  height  in  a  few  hours  or  a  few- 
days.  In  a  short  time  it  is  noticed  that  some  of  the  muscles  of  the 
limb  are  regaining  their  mobility  while  others  continue  immoble.  In 
other  words  the  volition  of  the  patient  can  exercise  itself  upon  some  of 
the  muscles  or  muscle-groups  but  not  on  others.  The  extreme  paralysis 
in  the  latter  may  last  from  six  to  eight  weeks,  when  there  is  a  little 
recession  in  their  paralytic  state.  These  muscles  now  begin  to  degene- 
rate, waste  and  undergo  a  progressive  and  rather  rapid  atrophy.  Their 
electrical  examination  reveals  the  phenomena  of  the  reaction  of  de- 
generation. The  reflexes  in  which  the  atrophied  muscles  are  concerned 
are  lost. 

Thes€  four  symptoms,  flaccid  motor  paralysis,  loss  of  the  tendon 
reflex,  atrophy  and  the  reaction  of  degeneration  are  pathognomonic  of 
disease  of  the  lower  or  peripheral  motor  neurones.  Hence  the  pre- 
eminent characteristic  of  the  paralysis  of  infantile  palsy  is  that  it  is 
a  degenerative  one,  and  that  it  picks  out  particular  muscles  and  muscle 
groups.  The  muscles  of  the  leg  that  are  mostly  affected  are  those  of 
the  anterior  tibial  group.  Sometimes  only  the  extensors  of  the  leg  are 
involved.  The  sartorius  usually  escapes.  In  the  arm  the  deltoid  and 
shoulder  muscles  are  chiefly  inplicated.  The  deltoid  may  be  paralyzed 
alone,  or  in  combination  with  the  biceps,  internal  brachial  and  supinator 
longus.  All  kinds  of  combinations  are  possible.  In  a  few  cases  the 
motor  cranial  nerves  have  been  included.  A  slow  improvement  may 
take  place  in  some  of  these  muscles  up  to  the  end  of  a  year.  After 
that  no  further  improvement  is  to  be  expected.  Gowers  says  that  we 
should  never  forget  that  after  six  months  the  lesion  in  the  cord  has 
practically  become  a  cicatrix. 

There  are  no  sensory  symptoms  that  belong  to  this  disease.  Some- 
times in  the  beginning  there  are  dull  pains  of  a  rheumatoid  character 
in  the  muscles.  If  these  pains  become  severe  or.  the  muscles  are 
unusually  tender  on  pressure,  there  is  probably  some  degree  of  peri- 
pheral neuritis  with  the  poliomyelitis.  In  a  word  the  sensations  are 
absolutely  normal  in  uncomplicated  infantile  palsy.  The  slight  de- 
crease in  sensibility  in  the  paralyzed  limb  is  undoubtedly  due  to  the 
vasomotor  disturbance  and  lowered  temperature  of  the  skin.  Some- 
times this  decrease  of  surface  temperature  amounts  to  several  degrees, 
and  is  associated  with  a  bluish,  mottled  appearance  of  the  skin. 

There  are  no  psychic  troubles  except  the  early  febrile  stupor  and 
delirium  and  the  sphincters  are  never  involved. 

The  whole  limb  ceases  to  grow  as  rapidly  as  the  well  limb;  the 
bones  do  not  continue  to  develop :  and  as  a  result  the  whole  extremity 
appears  stunted,  shortened  and  awkward  in  movement.  On  account 
of  the  atrophy  and  contractures  in  certain  of  the  muscles,  antagonistic 


548 


THK   NON-NEUKONIC  DISEASES 


groups  do  not  work  together  as  they  should  and  deformities  and  curva- 
tures result.  Talipes  equinus,  talipes  varus  and  valgus  are  thus  pro- 
duced, as  well  as  deformities  about  the  knees  and  curvatures  in  the 
spine.  The  most  common  form  of  foot  deformity  is  pes  equino-varus 
on  account  of  the  paralysis  of  the  extensors  of  the  foot  and  toes. 

FIGURE  1 1 8. 


When 


Anterior  poliomyelitis,  showing  the  wasting  of  the  right  leg  and  foot-drop. 

the  tibialis  anticus  alone  is  affected,  there  is  a  condition  of  talipes  valgus. 
When  the  calf  muscles  are  stricken,  pes  calcaneus  obtains.  The  claw- 
hand  is  a  far  less  frequent  form  of  distortion  than  are  any  of  those 
of  the  feet.  In  the  spinal  column  there  may  occur  lordosis  or  scoliosis. 
Diagnosis. — In  the  early  or  febrile  stage  the  diagnosis  of  acute 
anterior  poliomyelitis  is  always  uncertain  and  sometimes  quite  iinpos- 


THE  NON-NEURONIC  DISEASES  549 

sible.  Even  after  the  discovery  of  the  paralysis,  there  may  be  doubt 
as  to  the  exact  cause  of  it.  Very  rarely,  therefore,  is  the  diagnosis 
of  infantile  palsy  ever  made  early.  The  symptoms  at  this  period  of 
the  disease  are  made  light  of.  They  are  attributed  to  dentition,  gastro- 
intestinal trouble,  over-exertion  and  heat,  intestinal  parasites  or  some 
other  trifling  ailment.  The  parents  are  assured  that  the  little  one  will 
soon  be  all  right.  One  can  easily  imagine  the  feelings  of  the  parents 
and  the  chagrin  of  the  physician  under  these  circumstances  when  the 
paralysis   is  recognized  at  last. 

The  early  diagnosis  of  the  disease  is  most  desirable  therefore  for 
more  reasons  than  one.  The  physician  will  do  well  to  remember  that 
the  paralysis  is  the  special,  significant  symptom  and  after  forewarning 
the  family,  be  on  the  alert  for  the  first  indication  of  it.  It  usually  comes 
on  quickly,  even  sometimes  with  the  beginning  of  the  fever,  rarely 
later  than  a  few  hours  or  days.  An  appeara.nce  of  weakness,  listless- 
ness,  exhaustion,  disinclination  to  move  the  limb  should  be  prompt  to 
awaken  suspicion.  A  close  examination  will  sometimes  show  very 
early  a  little  more  voluntary  mobility  on  one  side  than  on  the  other. 
Such  indications,  faint  as  they  may  be,  had  better  be  regarded  as  the 
forerunner  of  a  paralysis  than  be  erroneously  attributed  to  the  mere 
malaise  of  the  febrile  state. 

When  the  paralysis  does  frankly  declare  itself,  certain  characteris- 
tics about  it  render  the  diagnosis  certain.  Its  suddenness  of  onset,  its 
completeness  from  the  beginning,  its  involvement  of  one  of  the  limbs 
with  later  limitation  to  particular  muscles,  its  gradual  improvement, 
and  its  association  with  atrophy,  loss  of  reflex  action  and  the  reaction 
of  degeneration  render  its  nature  perfectly  clear. 

In  the  later  stages  of  the  disease,  the  history  of  the  case,  the  local- 
ization of  the  paralysis,  the  muscular  atrophy,  the  vasomotor  disturb- 
ances, the  retardation  of  growth  and  the  contractures  and  deformities 
in  the  limb  make  the  diagnosis  positively  easy. 

A  few  atypical  forms  of  the  disease  may  cause  some  confusion  in 
differentiating  them  from  hematomyelia,  acute  rachitis,  coxitis,  osteo- 
myelitis, syphilitic  pseudo-paralysis,  acute  myelitis,  acute  disseminated 
myeloencephalitis,  birth  palsies,  cerebral  palsies,  progressive  muscular 
atrophy,  lumbar  spinal  gliosis,  congenital  muscular  defects,  and  multiple 
neuritis  or  neuritis  of  special  nerves. 

In  hemorrhage  and  acute  myelitis  there  are  prominent  sensory 
symptoms,  exaggerated  reflexes,  involvem.ent  of  the  sphincters  and 
bedsores.  Hemorrhage,  of  course,  is  sudden  but  does  not  occur  often 
without  trauma.  Moreover  the  paralysis  is  not  preceded  by  or  im- 
mediately associated  with  a  fever.  Myelitis  is  slower  in  its  onset ;  its 
fever  is  not  so  high  usually  and  is  longer  in  duration ;  its  paralysis  does 
not  recede  and  remain  permanent  in  particular  muscles  as  it  does  in 
poliomyelitis.  It  should  be  remembered  in  this  connection,  however, 
that  the  earliest  symptoms  of  infantile  palsy  are  so  indicative  of  a  trans- 
verse myelitis  in  many  cases  that  some  authorities  believe  that  the  lesion 
of  anterior  poliomyelitis  begins  as  a  more  or  less  complete  transverse 
myelitis  of  a  mild  degree,  with  the  inflammation  soon  receding,  except 
from  the  anterior  horns  where  its  maximum  foci  were  located.     This 


55^  'i"HE  NON-NEURONIC  DISEASE^ 

is  doubtless  the  explanation  in  part  of  the  early  sensory  symptoms  like 
the  rheumatoid  pains  often  complained  of  in  poliomyelitis  and  of  the 
initial  paraplegic-like  distribution  of  the  paralysis.  The  hypersesthetic 
condition  of  the  involved  limb  duiring  the  first  few  days  of  the  disease 
is  of  much  assistance  in  the  making  of  the  diagnosis.  Of  course  as  the 
inflammation  subsides  these  sensory  manifestations  disappear  and  as 
I  have  said  above  the  further  course  of  the  disease  is  notable  for  the 
complete  absence  of  sensory  phenomena. 

As  Oppenheim  has  well  pointed  out  acute  rachitis,  coxitis,  and 
ostcouiyelitis  are  distinguished  from  the  early  stage  of  poliomyelitis  by 
the  resistance  offered  by  the  child  when  passive  movement  is  attempted. 
He  contracts  his  muscles  and  holds  them  in  a  state  of  rigidity  to  avoid 
the  pain  of  movement. 

Syphilitic  pseudo-paralysis  is  to  be  established  by  the  history  of 
infection,  other  signs  of  specific  disease,  and  the  character  and  distribu- 
tion of  the  paralysis. 

Cerebral  palsy  comes  on  abruptly,  is  hemiplegic  in  character  and 
is  accompanied  by  rigidity  and  exaggeration  of  the  reflexes.  There  is 
mental  depression  of  a  profound  sort  and  stupor,  while  a  series  of  local 
or  Jacksonian  convulsions  may  occur. 

Birth  palsies  are  flaccid  and  degenerative  and  involve  usually  only 
the  arm. 

Progressive  muscular  atrophy  rarely  occurs  in  children.  It  is 
gradual  in  its  onset,  slow  and  steady  in  its  progress,  without  febrile 
or  sensory  phenomena. 

Peripheral  neuritis,  and  especially  multiple  neuritis,  are  rare  though 
they  do  occur  in  diildren  alone  or  as  complications  of  poliomyelitis. 
The  similarity  of  many  of  the  symptoms  sometimes  leads  to  much 
difficulty  in  the  making  of  a  differential  diagnosis.  They  are  more 
gradual  in  onset  than  infantile  palsy,  are  marked  by  local  pain  and 
tenderness  on  pressure  and  have  slight  or  no  febrile  phenomena.  When 
there  is  fever  it  lasts  longer  than  the  fever  of  poliomyelitis.  The 
paralysis  assumes  the  bilateral  type  in  multiple  neuritis  and  the  mono- 
plegic  type  in  simple  neuritis.  It  is  tardy  in  its  development  as  com- 
pared with  the  paralysis  of  poliomyelitis.  The  atrophy  is  not  quite 
as  pronounced  and  is  slower  in  appearing,  while  vasomotor  disturbance 
such  as  oedema  may  be  present.  In  neuritis  there  is  a  greater  tendency 
of  involvement  of  the  cranial  nerves.  It  is  to  be  remembered  that 
peripheral  neuritis  and  poliomyelitis  may  be  associated  in  the  same 
patient. 

Prognosis. — The  prognosis  of  acute  anterior  poliomyelitis  in  re- 
gard to  life  is  absolutely  favorable.  In  regard  to  the  recession  of  the 
paralysis  in  part  and  improvement  within  the  first  six  months  or  a 
year  it  is  favorable.  In  regard  to  any  further  improvement  after  the 
first  year  it  is  absolutely  bad. 

Death  has  been  reported  in  the  first  stage,  possibly  by  involve- 
ment of  the  bulbar  nuclei  or  other  complication.  Neither  the  disease 
nor  its  sequels  cause  a  fatal  issue  except  in  the  rarest  instances.  A 
few  complete  recoveries  have  been  observed.  Improvement — and  some- 
times a  great  deal  of  improvement — is  what  may  be  usually  looked  for. 


THE  NON-NEUROMIC  DISEASES  55  I 

The  amount  and  character  of  the  improvement,  and  the  degree  and 
nature  of  the  sequelae,  can  be  influenced  by  the  early  treatment.  Elec- 
trical examination  helps  much  in  forecasting  the  probable  improvement. 
Muscles  that  still  respond  to  the  faradic  current  after  two  or  three 
weeks  will  resume  their  normal  functions.  When  they  show  the  re- 
action of  degeneration  they  will  remain  paralyzed  and  later  on  become 
atrophied. 

Treatment. — The  early  treatment  of  infantile  palsy  is  antipyretic 
2indconstitutional; the  middle  treatment  [siieurological  and  orthopcedic ; 
the  later  treatment  is  orthopaedic  and  surgical. 

In  the  beginning  of  the  disease  the  clinical  picture  is  that  of  an 
infectious  fever.  Every  effort  at  this  time  should  be  made  to  check 
the  infective  inflammation.  The  child  should  be  put  toi  bed  and  kept 
absolutely  at  rest.  The  bowels  should  be  opened  freely  with  calomel ; 
the  kidneys  stimulated  by  some  simple  diuretic ;  and  the  skin  kept  active 
by  the  use  of  hot  drinks  and  warm  coverings.  A  few  leeches  may  be 
used  on  the  spine,  or  mustard  or  iodine  applied.  It  is  useless  and  in- 
advisable in  an  infectious  inflammation  of  this  sort  to  apply  extreme 
heat  or  cold  to  the  spine,  as  is  done  is  meningitis.  The  spinal  ice  bag 
should  never  be  used.  Full  baths,  hot  or  cold,  produce  too  much  dis- 
turbance and  excitement ;  do  very  little  good ;  and  may  do  a  great  deal 
of  harm.  The  fever  can  best  be  controlled  by  aconite  and  sweet  spirits 
of  nitre.  The  salicylates  and  belladonna  in  full  dosage  have  been  recom- 
mended in  this  initial  stage  of  the  disease.  I  have  found  rest  and 
quiet,  gentle  but  steady  elimination,  with  mild  local  counter-irritation 
with  mustard  the  most  advantageous  way  of  managing  the  first  or 
febrile  stage. 

Usually  the  paralysis  is  complete,  and  has  existed  for  some  little 
time  when  the  patient  first  comes  under  medical  observation.  The  treat- 
ment now  becomes  almost  entirely  mechanical.  It  consists  of  the  steady 
use  of  massage,  aided  by  electricity.  Of  course  the  patient's  general 
health  and  nutrition  must  be  kept  up,  but  except  for  assisting  in  doing 
this  the  further  use  of  drugs  is  uncalled  for.  As  the  result  of  my 
own  personal  observation,  I  consider  the  steady  use  of  massage  the 
prime  factor  in  the  management  of  this  stage  of  the  disease.  Every 
day,  sometimes  twice  a  day,  I  have  the  paralyzed  limb  rubbed  and 
stroked  up  towards  the  body.  The  hand  of  the  operator  may  be  well 
oiled  with  olive  or  cocoanut  oil.  Ten  minutes  should  be  occupied  in 
each  seance.  The  muscles  later  on  may  be  kneaded  as  well  as  stroked. 
Passive  movements  of  the  limb  should  be  instituted  early  and  gymnastic 
exercises  with  slight  resistance  to  the  movements  should  be  persistently 
carried  out  to  avoid  as  much  as  possible  the  late  contractures  and  de- 
formities. It  may  even:  be  necessary  tO'  use  stiff  bandages,  splints,  rub- 
ber muscles  and  other  forms  of  apparatus  to  assist  in  this.  The  early 
and  persistent  treatment  of  these  cases  in  this  way  cannot  be  too  stren- 
uously insisted  upon.  Many  of  the  later  deformities  and  loss  of  function 
are  due  to  the  neglect  or  bad  management  of  these  cases  in  the  begin- 
ning. Massage  and  electricity  may  be  cautiously  begun  as  early  as  two 
v^eeks  after  the  first  appearance  of  the  paralysis. 

The  use  of  electricity  two  or  three  times  a  week  at  first,  and  then 


552  THE   XOX-XEUROXIC  DISEASES 

daily,  is  highly  commendable.  The  only  rule  is  to  employ  that  cur- 
rent and  that  strength  that  will  just  produce  a  muscular  contraction. 
If  the  galvanic  current  is  used  the  cathode  may  be  placed  anywhere 
upon  the  body,  while  the  anode  is  applied  to  the  affected  muscles.  Use 
mild  currents  at  first  and  increase  gradually  to  the  point  of  causing 
muscular  contraction.  The  child  must  not  be  allowed  to  get  frightened. 
When  contraction  can  be  obtained  with  the  faradic  current,  it  is  to  be 
preferred.  Static  electricity  is  useless.  The  electricity  need  not  be 
applied  longer  than  for  two  or  three  minutes  at  each  sitting  and  after 
every  two  or  three  weeks'  treatment,  it  is  well  to  allow  a  week  or  two 
of  rest   without   the   electricity. 

In  this  way  the  massage  and  electrical  treatment  should  be  kept 
up  for  a  year  and  at  occasional  intervals  during  the  next  year.  After 
that   it  is   of  no   further   use. 

I  regularly  advise  the  frequent  immersion  of  the  limb  in  warm 
water,  say  from  90  degrees  to  95  degrees  F.  I  have  had  no  experience 
with  the  subcutaneous  injection  of  strychnine,  as  has  been  sometimes 
recommended. 

If  the  above  line  of  treatment  be  started  early  and  carried  out 
with  care  and  watchfulness  there  will  be  comparatively  little  in  the 
way  of  deformity.  Many  cases  are  so  neglected,  however,  that  the 
deformities  become  so  prominent  that  orthopaedic  and  surgical  measures 
have  to  be  invoked  for  their  relief.  Tenotomy  and  the  wearing  of 
plaster  casts  and  specially  fitted  apparatus  are  the  measures  employed. 
The  methods  of  doing  this  are  described  in  the  books  upon  surgery 
and  orthopaedics.  When  a  shortened  tendon  has  been  cut  and  an 
extension  apparatus  fitted  to  the  limb,  it  must  be  carefully  noted  that 
the  latter  is  comfortable,  does  not  impede  the  circulation,  cause  pres- 
sure or  chafe  the  skin.  It  must  be  changed  as  the  limb  grows.  Some- 
times the  plan  of  Drobnik  may  be  tried  of  partial  or  complete  trans- 
plantation of  the  tendon  of  a  paralyzed  muscle  to  a  neighboring  healthy 
muscle. 

POLIOMYELITIS  OF  ADULTS. 

The  only  excuse  for  devoting  a  special  section  to  the  considera- 
tion of  anterior  poliomyelitis  in  adults  is  that  it  is  so  comparatively 
rare  and  that  its  clinical  exhibition  varies  slightl}-  from,  that  of  the  more 
common  infantile  form  of  the  disease.  It  occurs  in  adults  as  an  acute, 
subacute  and  chronic  affection. 

Etiology. — The  disease  occurs  more  frequently  in  men  than 
women  and  between  the  ages  of  twenty-five  and  thirty-five.  It  is  be- 
coming more  and  more  conclusively  established  that  the  predominant 
cause  of  the  disease,  in  practically  all  cases,  is  an  underlying  toxcemia. 
The  acute  infectious  fevers,  especially  measles,  the  puerperium,  severe 
gonorrhoea,  etc.,  have  been  followed  by  acute  poliomyelitis.  An  under- 
lying toxic  state  of  the  blood  has  probably  co-operated  with  exposure 
to  cold,  over-exertion,  and  traumata,  to  which  the  disease  in  some 
instances  has  been  attributed.  The  subacute  and  chronic  cases  have 
been  associated  with  exposure,  syphilis,  lead-poisoning  and  diabetes. 
Oppenheim  once  saw  an  acute  case  follow  prolonged  chloroform  nar- 


THE  NON-NEURONIC  DISEASES  553 

cosis.  As  these  same  causes  play  a  large  role  in  the  production  of 
multiple  neuritis,  and  as  this  form  of  poliomyelitis  has  been  less  fre- 
quently noted  since  we  have  learned  that  polyneuritis  is  responsible  for 
many  of  the  symptoms,  caution  must  be  exercised  in  the  diagnosis  espe- 
cially when  a  frank  intoxication  is  existent. 

Pathology  and  Pathogenesis. — In  the  few  cases  that  have  been 
examined  after  death  the  pathological  findings  were  identical  with 
those  seen  in  the  infantile  form  of  the  disease.  The  gray  matter  of 
the  anterior  horns  revealed  a  condition  of  primary  acute  oir  chronic 
inflammation,  with  secondary  degeneration  and  atrophy  of  the  nervous 
elements.  In  so^me  quarters  the  belief  is  growing  that  a  primary  wast- 
ing of  the  cells  is  pnovoked  in  some  of  the  severer  toxsemic  cases  and 
that  the  inflammation  and  vascular  changes  are  secondary,  or  rather 
concomitant,  phenomena.  At  all  events  the  twoi  associated  processes, 
vascular  inflammation  and  cellular  atrophy,  constitute  the  pathological 
basis.  The  white  matter  remains  unaffected  or  is  only  slightly  degen- 
erated secondarily. 

Symptoms. — The  onset  of  the  acute  cases  is  the  same  as  that  in 
the  infantile  forms  of  the  disease  except  that  the  early  fever  lasts  a 
little  longer,  one  or  two  weeks,  some  pain  especially  in  the  back  is  more 
apt  to  be  present,  and  the  initial  paralysis  is  more  widely  extended. 
If  there  is  pain  in  the  limbs  a  polyneuritis  is  probably  present.  The 
beginning  of  the  subacute  and  chronic  cases  is  insidious,  usually  with- 
out febrile  phenomena  and  pain  and  without  the  usual  initial  tem- 
porary extensive  paresis. 

In  the  acute  cases  the  paralysis  appears  about  the  time  that  the 
fever  is  subsiding.  At  first  it  is  widely  distributed,  though  not  equally 
profound  everywhere.  Gradually  this  recedes  leaving  some  groups  of 
muscles  completely  paralyzed  while  others  regain  their  normal  power 
of  action.  The  paralysis  is  flaccid  and  is  remarkable  for  picking  out 
individual  muscles  or  groups  of  muscles.  Sometimes  a  whole  limb  may 
be  involved  and  more  frequently  it  is  the  leg.  In  a  few  days  the  re- 
action of  degeneration  can  be  elicited  by  an  electrical  examination  oi 
the  diseased  muscles.  They  begin  to  atrophy  and  feel  soft.  On  account 
of  fatty  degeneration  they  may  assume  the  appearance  of  a  pseudo- 
hypertrophy. The  paralysis  may  partially  recede  even  in  them  during 
the  course  of  the  first  month  or  so.  They  never,  however,  undergo 
complete  recovery.  If  they  do  recover  the  trouble  was  probably  due  to 
peripheral  neuritis.  The  further  progress  of  the  disease  is  the  same 
as  it  is  in  acute  anterior  poliomyelitis  of  children. 

In  the  chronic  type  of  the  disease  there  is  merely  an  initial  weak- 
ness in  the  legs  or  the  arms,  which  progresses  slowly  and  gradually 
towards  paralysis.  Usually  one  or  two  limbs,  and  more  particularly 
certain  groups  of  muscles  in  them,  only  are  paralyzed.  In  other  cases 
all  four  extremities  may  be  involved.  The  paralysis  is  Haccid,  elective, 
atrophic  and  associated  with  electrical  reaction  of  degeneration  and  loss 
of  reiiex  action  if  the  muscles  concerned  in  the  reflex  arc  are  implicated. 
Almost  any  muscle  or  muscle  group  in  the  arm  or  leg  may  be  afflicted 
and  it  is  therefore  needless  to  specify.     Fibrillary  tzvitching  is  often 


554  'f'^I'-   \()X-NKUKONIC  DISEASES 

present  and  annoying.  There  are  no  other  symptoms  in  typical  cases 
though  sometimes  dull  aching  pains  are  complained  of. 

The  disease  is  so  varied  in  its  manifestations  that  an  effort  has 
been  made  to  establish  particular  types.  This  it  seems  to  me  is  un- 
necessary though  it  is  well  to  remember  perhaps  that  some  cases  ad- 
vance rapidly  to  a  climax,  then  recede  and  ultimately  return  to  almost 
complete  health.  Other  cases  advance  slowly  and  with  sharply  limited 
atrophy  and  paralysis,  causing  them  to  bear  a  striking  resemblance 
to  progressive  muscular  atrophy.  In  still  other  cases  there  is  a  less 
rapid  but  more  steady  advance  of  the  trouble  until  death  occurs  in  a 
year  or  two. 

In  all  of  these  forms  of  the  disease  there  are  resemblances  of  a 
striking  sort  to  multiple  neuritis,  progressive  muscular  atrophy,  acute 
ascending  myelitis,  Landry's  paralysis,  etc.  Indeed  it  is  beginning 
to  be  strongly  suspected  that  some  of  these  latter  affections,  either  in 
part  or  whole,  are  ]X)liomyelitic. 

Diagnosis. — The  symptomatic  diagnosis  of  poliomyelitis  is  readily 
made  even  though  the  case  is  not  strictly  typical ;  the  pathological  diag- 
nosis, however,  is  often  a  matter  of  the  greatest  difficulty.  The  etiolo- 
gical precedents,  the  initial  fever  and  paralysis,  the  distribution,  char- 
acter and  progress  of  the  latter,  the  muscular  atrophy,  the  electrical 
reactions  and  the  absence  of  sensory  symptoms  are  distinctive  if  studied 
en  masse  in  the  clinical  presentation  of  the  case.  The  underlying  cause 
of  these  symptoms,  however,  may  be  confused  with  polyneuritis,  pro- 
gressive muscular  atrophy,  amyotrophic  lateral  sclerosis  and  gliosis. 

In  polyneuritis  there  are  peripheral  and  local  pains  in  the  nerves 
and  muscles  of  the  limbs. '  There  is  ataxia.  The  paralysis  is  not  so 
sharply  elective  but  involves  the  ends  of  the  low^er  limbs  first,  gradually 
ascends  and  ultimately  attacks  the  arms  in  the  same  way.  Other  nerves 
besides  those  of  the  extremities,  as  for  example  the  cranial  nerves,  may 
be  involved  in  neuritis.  There  are  some  cases,  however,  in  which  a 
differential  diagnosis  is  quite  impossible.  This  is  probably  due  to  the 
fact  that  in  toxic  cases  there  may  be  both  neuritic  and  poliomyelitic 
processes  going  on  at  the  same  time.  Not  a  few  authorities  believe  that 
in  some  of  these  cases,  if  not  all  of  them,  the  peripheral,  neuritic  de- 
generative process  is  a  mere  secondar_y  result  of  a  profound  toxic  dis- 
turbance in  the  anterior  cornual  cells  and  their  nutritive  function. 

Progressive  muscular  atrophy  is  especially  liable  to  be  confused 
with  chronic  poliomyelitis.  It  is  to  be  remembered,  however,  that  a 
low  grade  poliomyelitic  process  possibly  underlies  many  of  the  spinal 
atrophies.  In  typical  progressive  muscular  atrophy  the  atrophy  runs 
ahead  of  the  paralysis  and  not  vice  versa,  as  in  poliomyelitis.  Moreover 
there  is  no  real  initial  stage  as  in  the  latter  disease  and  the  atrophy 
usually  begins  in  the  small  muscles  of  the  hands. 

Amyotrophic  lateral  sclerosis  is  characterized  by  increased  reflexes, 
a  less  degree  of  atrophy,  selection  of  the  arms  with  merely  early  weak- 
ness in  the  legs  and  marked  bulbar  symptoms.  In  general  gliosis 
sensory  symptoms  are  prominent  and  there  are  trophic  manifestations 
in  the  skin  as  well  as  the  muscles. 

Prognosis. — The  prognosis  is  good  in  pure  cases  so  far  as  life  is 


THE  NON-NEURONIC  DISEASES  555 

concerned.  In  regard  to  the  paralysis,  the  hope  of  a  considerable  de- 
gree of  restitution  may  be  held  out  up  to  a  month  or  two  after  the 
onset  of  acute  symptoms.  Some  cases  may  even  partially  recover  after 
that  or  until  a  year  or  two  has  rolled  around.  Complete  recovery  is 
so  exceptional  as  to  almost  warrant  the  assertion  that  it  is  never  to  be 
expected.  As  the  outlook  for  the  paralysis  in  multiple  neuritis  is 
peculiarly  favorable,  the  more  nearly  these  cases  of  poliomyelitis  ap- 
proach a  multiple  neuritis  the  more  hopeful  is  their  prognosis.  Death 
is  not  a   common   result  of  this   disease. 

Treatment. — The  management  of  these  cases  is  practicallv  the 
same  as  it  is  in  the  infantile  form. 

ABSCESS  OF  THE  CORD. 

Abscesses  rarely  form  in  the  spinal  cord  as  they  do  in  the  brain. 
Only  a  very  few  cases  have  been  put  upon  record,  and  they  followed 
purulent  spinal  meningitis  of  both  the  cord  and  brain,  or  were  the  re- 
sult of  a  metastatic  transference  of  the  disease  from  some  near  or 
remote  focus  of  suppuration.  Myelitis  scarcely  ever  goes  on  to  the 
production  of  an  abscess.  Putrid  bronchitis,  gonorrhoea,  abscess  of 
the  prostate  gland  and  traumatism  have  seemed  to  be  responsible  for 
it  in  some  cases.  Minute  collections  of  pus  have  been  noted  in  a  few 
instances  of  poliomyelitis.  The  gray  matter  is  usually  the  seat  of  the 
abscess,  especially  when  associated  with  purulent  meningitis.  In  such 
cases  the  brain  is  very  often  also  the  seat  of  the  suppurative  process. 
The  majority  of  the  abscesses  appear  in  the  upper  part  of  the  cord 
though  they  may  locate  anywhere. 

Paraplegia,  anccsthcsia,  sphincter  paralysis,  girdle  pai)is  and  all 
the  usual  signs  of  a  severe  meningoinyditis  are  present.  Weakness, 
tremor  and  incoordination  in  the  arms  have  been  seen  in  other  cases 
along  with  the  symptoms  in  the  lower  extremities.  The  usual  signs 
of  infection  are  commonly  present,  such  as  the  irregular  fever,  the 
chills,  the  foul  tongue,  the  subnormal  temperature,  the  debility  and 
general  typhoid  state. 

The  diagnosis  is  easy  as  a  rule  but  the  localization  of  the  abscess 
is  extremely  difficult. 

As  the  condition  is  associated  usually  with  a  diffuse,  or  gener?] 
septicaemia,  surgical  intervention  would  be  of  little  avail.  Death  usu- 
ally takes  place  in  a  few  days. 

TUMORS  OF  THE  SPINAL  CORD. 

By  the  term  tumor  I  do  not  mean  all  forms  of  excrescences  and 
protuberances  that  may  compress  the  cord  or  damage  it  anatomically 
and  functionally  withm  a  limited  area.  The  symptoms  of  these  may 
at  times  be  identical  with  those  of  tumor.  The  ultimate  results  upon 
the  cord  may  even  be  the  same.  Vertebral  disease,  displacements, 
caries  and  exostoses  of  syphilitic  or  traumatic  origin  may  affect  the 
cord  and  its  membranes  very  much  as  a  tumor  w'ould.  Focal  hem- 
orrhage, thrombosis,  embolism,  may  in  their  after  eff'ects  exhibit  an 


556  THE  NON-NEURONIC  DISEASES 

obscure  resemblance  to  a  spinal  neoplasm.  This  is  because  at  times 
all  of  these  troubles  may  be  limited  and  unique,  though  obscure  in 
their  symptomatology,  while  obscurity  and  total  absence  of  symptoms 
obtain  sometimes  even  in  tumor.  These  conditions  must  therefore 
always  be  carefully  excluded  in  the  diagnosis. 

By  tumor  of  the  spinal  cord  I  mean  those  circumscribed  morbid 
growths  that  appear  in  the  spinal  canal  and  spring  from  the  membranes 
or  develop  within  the  cord  substance  itself.  The  interest  in  these  for 
a  long  time  was  merely  pathological  and  post  mortem.  Erb  suggested,, 
in  1878,  that  they  might  be  operated  upon.  It  was  the  successful  case 
of  Gowers  and  Horsley,  in  1887,  however,  that  renewed  the  interest 
in  these  conditions  and  caused  them  to  be  studied  clinically  so  thor- 
oughly that  now  a  fairly  definite  symptomatology  attaches  to  them. 
They  certainly  offer  a  more  tempting  field  for  the  surgeon  than  do  the 
brain  tumors.  Disheartening  as  are  the  total  results  of  opf^rative  pro- 
cedures, and  especially  of  medical  treatment  in  both,  the  results  are 
better  in  the  tumors  of  the  cord  than  they  are  in  those  of  the  brain. 
This  is  significant  in  view  of  the  fact  that  the  literature  would  seem 
to  indicate  that  the  latter  are  much  more  common  than  the  former. 

Etiology. — This  is  not  the  place  to  go  extensively  into  the  etiol- 
ogy of  tumors.  Outside  of  certain  diathetic  conditions,  like  syphilis 
and  tuberculosis,  congenital  influences  as  observed  in  certain  glioma- 
tous  and  fatty  tumors,  parasites  like  echinococci,  and  a  few  obscure 
traumatic  incidents,  we  know  very  little  about  their  causation.  Wet 
and  cold  have  been  followed  by  the  sudden  appearance  of  their  symp- 
toms but  it  is  probable  that  these  agencies  merely  provoked  the  men- 
ingitic,  myelitic  and  other  secondary  accompaniments  of  them.  Mul- 
tiple tumors  exhibit  a  faint  degree  of  heredity.  I\Iost  all  spinal  tu- 
mors appear  between  the  ag-es  of  thirty  and  fifty.  Tuberculous  tu- 
mors appear  earlier.  Men  give  a  history  of  them  more  often  than 
women.  The  etiological  incidence  that  belongs  to  the  tumor  per  se  is 
not  materially  altered  by  its  being  located  in  the  spinal  canal. 

Pathology  and  Pathogenesis. — A  tumor  may  arise  from  the 
vertebrae,  the  spinal  membranes,  or  the  cord  itself.  All  kinds  of  neo- 
plasms occur,  though  there  are  differences  in  regard  to  the  frequency 
of  certain  types  and  their  location.  The  great  majority  of  them  are 
meningeal  in  origin ;  next  in  frequency  arc  the  intraspinal ; 
least  in  frequency  are  the  vertebral.  Glioma  and  sarcoma 
are  the  commonest,  and  next  after  them  fibroma,  myxoma^ 
gumma  and  tubercle.  Some  of  the  tumors  manifest  a  choice  of  loca- 
tion and  it  is  always  well  to  try  and  differentiate  those  that  are  be- 
tween the  bony  column  and  dura  (extra-dural).  those  between  the 
dura  and  cord  (intra-dural),  and  those  that  are  within  the  cord  itself 
(intra-medullary).  There  is  a  slight  difference  in  their  symptoma- 
tologies. 

Extra-dural  growths  may  originate  in  the  membrane,  the  tissue 
between  the  membrane  and  bone,  or  outside  and  grow  in  through  the 
inter-vertebral  foramina.  The  parasitic  tumors,  echinococcus  and  cys- 
ticercus,  occur  here.     Lipomata  usually  select  this  site. 

The  intra-dural  tumors  are  sarcoma,  myxoma,  psammoma,  fibro- 


THE  NON-NEURONIC  DISEASES  557 

ma,  syphilom?.  and  tubercle.  A  sarcoma  may  be  single  and  extended 
or  multiple.  Rarely  tubercular  and  parasitic  tumors  have  been  seen 
within  the  meshes  of  the  arachnoid.  Myolipomata  have  been  found 
here  also.     Multiple  neuromata  sometimes  occur  on  the  nerve  roots. 

The  more  common  intra-niednUary  growths  are  the  gliomata,  syph- 
ilomata.  sarcomata  and  tubercle.  Every  variety  of  neoplasm  has  de- 
veloped within  the  cord.  These  tumors  are  single  or  multiple  and 
spring  from  the  pia  mater  or  the  wall  of  the  central  canal. 

FIGURE  119. 


FIGURE  120. 


i  111 


'"^"'^  Tumor   in  the   dura  of  the   upper 

Tumor    of    the    medulla    spinalis.  part     of     the     lumbar     enlargement. 

<After  iBraubach.)  (After  Gowers.) 

The  size  of  these  growths  is  necessarily  small,  ranging  from  that 
of  a  pea  to  an  inch  or  two  in  length  and  an  inch  in  thickness.  Some 
spread  longitudinally  along  the  cord,  notably  the  gliomata,  which  may 
stretch  the  entire  spinal  length.  The  sarcomata  also  diffuse  them- 
selves but  not  quite  so  much  as  the  gliomata.  Sometimes  the  tumor 
■ensheaths  the  cord  as  in  a  tube. 

The  upper  and  lozver  dorsal  regions  of  the  cord  are  the  favorite 
location  of  tumor.  The  morbid  growths  that  attack  the  cauda  equin-a 
are  rather  frequent  and  large  relatively.  In  the  neighborhood  of  the 
tumor  the  shape  of  the  cord  is  altered.     The  cord  will  feel  soft  if  the 


55o  THE  XOX-XEUROXIC  DISEASES 

tumor  is  a  soft  one.  but  as  a  rule  the  tissues  are  denser  and  harder  than 
normal.  Extra-medullary  tumors  rarely  absorb  the  substance  of  the 
cord,  though  they  may  press  it  extremely  out  of  shape.  Intra- 
medullary tumors  both  absorb  and  distort  the  spinal  tissues.  Some- 
times the  intra-spinal  tumors  are  sharply  demarkated  .  at  other  times 
they  shade  ofif  into  the  normal  tissue.  The  latter  may  be  but  little 
altered  at  times  but  usually  it  is  the  seat  of  secondary  alterations,  inflam- 
mation, softening,  hemorrhage,  etc. 

Symptoms. — There  is  a  certain  degree  of  constanc}'  and  uniform- 
ity about  the  symptomatology  of  all  tumors,  and  as  that  is  often  as  far 
as  we  can  carry  the  diagnosis,  the  exceptional  differentiations  are  only 
possible  in  a  limited  number  of  cases. 

For  operative  purposes  a  differential  diagnosis  between  extra- 
and  intra-dural  tumors  should  always  be  attempted.     The  former  pro- 

FIGURE  121. 


Neuroma  of  the  Cauda  equina.   (After  Lanceraux.) 

duce  more  particularly  pressure  symptoms  and  are  often  accompanied 
by  pronounced  root  symptoms,  local  tenderness  of  the  spine  and  evi- 
dences of  bone  disease.  The  latter  add  to  these,  signs  of  greater  im- 
plication of  the  cord  itself,  pressure,  irritative  and  destructive.  Intra- 
medullary tumors  are  not  marked  by  such  severe  initial  pains  as  are 
the  meningeal  tumors,  and  their  motor  phenomena  are  more  prone  to 
be  unilateral,  especially  in  the  beginning.  Xevertheless  it  must  be 
admitted  that  in  most  cases  only  an  approximation  can  be  attained  in 
these  dift'erential  diagnoses.  Fortunately  such  refinement  of  diagnosis 
is  not  absolutely  called  for  in  the  majority  of  the  cases. 

The  two  essential  points  to  be  established  in  the  diagnosis  are  ( i ) 
the  actual  presence  of  a  tumor,  and  (2)  its  longitudinal  or  segmental 
position  in  the  cord. 

In  the  order  of  their  usual  development  the  symptoms  of  a  spinal 
tumor  are  sensory,  motor,  visceral,  trophic  and  topical.  The  first  to 
appear  are  the  signs  of  spinal  root  compression  and  irritation.  This 
consists  of  constant,  severe  and  continuous  neuralgic  pain  shooting 
along  the  course  of  the  spinal  nerves.  About  the  trunk  there  is  uni- 
lateral or  bilateral  intercostal  neuralgia.  Sometimes  there  is  a  typical 
girdle  sensation.     Sharp,  lancinating  pains  may  shoot  down  the  arm. 


THE  NON-NEURONIC  DISEASES  55q 

more  rarely  in  the  legs.  The  nerve  trunks  themselves  are  not  sensi- 
tive to  pressure.  These  pains  have  caused  such  mistaken  diagnoses  to 
be  made  as  appendicitis,  gallstone  colic,  indigestion  and  angina  pec- 
toris. In  not  more  than  ten  per  cent,  of  the  cases  are  these  charac- 
teristic pains  absent.  Their  course  is  highly  suggestive.  For  instance, 
slight  at  first,  they  become  keen  and  penetrating,  and  paroxysmal, 
then  finally  continuously  dull  but  with  sharp  exacerbations.  They  are 
so  distressing  that  they  have  driven  their  victims  to  suicide.  They  con- 
tinue throughout  the  entire  course  of  the  disease.  Pain  may  be  pres- 
ent in  the  spine  if  the  tumor  is  one  of  the  dura ;  not  so  if  it  is  intra- 
medullary. 

Hyperccsthesia  very  often  accompanies  the  pain.  Between  the 
exacerbations  various  parcestheskc  may  be  present,  such  as  numbness, 
tingling,  pins-and-needles  sensation,  formication.  These  posterior  root 
signs  may  occur  just  as  prominently  when  the  tumor  is  in  the  anterior 
part  of  the  cord  as  when  in  the  posterior  part  and  actually  in  touch 
with  the  posterior  roots.  Later  on  ancESthesia  takes  the  place  of  the 
parsesthesia  and  serves  as  a  means  of  localizing  the  tumor. 

As  sensory  disturbances  thus  result  prominently  from  implica- 
tion of  the  posterior  spinal  roots,  so  motor  symptoms  indicate  the  in- 
volvement of  the  anterior  roots.  Muscular  spasm,  tzvitching  and  con- 
tracture appear  in  parts  of  the  body  supplied  with  motor  innervation 
from  the  same  segments  of  the  cord  which  supply  the  corresponding 
sensory  innervation.  Tenderness  and  rigidity  of  the  spine,  abdominal 
pain  and  tenseness,  in  the  limbs  pain  and  contracture  are  thus  seen 
often  together.  Hemiparesis,  hemiparaplegia,  paraplegia  involving  all 
four  limbs  may  all  appear  in  orderly  succession.  The  Brown- 
Sequard  paralysis  with  loss  of  motion  and  muscular  sense  on  the  side 
of  the  lesion  and  loss  of  the  cutaneous  sense,  especially  pain  and  tem- 
perature, on  the  opposite  side  is  rather  a  frequent  incident  of  spinal 
tumor.  It  is  never  pronounced,  however,  soon  disappears  and  occurs 
only  when  the  tumor  is  above  the  lumbar  region.  If  the  tumor  is 
in  the  latter  region  the  reflexes  may  be  lost,  but  when  it  is  in  the  cer- 
vical region  they  will  be  exaggerated.  The  electrical  excitability  of 
the  afifected  muscles  undergoes  alteration  on  account  of  the  degener- 
ation in  the  anterior  roots.  Atrophy  of  the  muscles  may  occur,  espe- 
cially in  the  legs,  from  the  same  cause. 

Vasomotor  symptoms,  involvement  of  the  bladder  and  rectal  func- 
tions, and  later  on  intractable  bedsores  may  all  be  observed.  Dilata- 
tion and  contraction  of  the  pupils  are  observed  in  high  cervical  tumors. 

When  the  cauda  equina  is  the  seat  of  a  morbid  growth  there  is  pel- 
vic pain,  especially  in  the  anal  and  perineal  region,  and  out  along  the 
sciatic  nerve.  Ataxia,  loss  of  the  knee-jerks  and  paralysis  of  the  blad- 
der may  be  seen. 

From  this  description  it  will  be  readily  seen  that  no  absolutely 
uniform  clinical  picture  can  be  drawn  to  fit  all  cases  alike.  Only  a  thor- 
ough knowledge  of  the  anatomy  and  physiology  of  the  cord  can  enable 
the  physician  to  appreciate  most  clearly  the  presence  of  a  tumor.  The 
symptoms  must  be  studied  always  together ;  the  entire  picture  pre- 
sented by  the  case  must  be  looked  at  in  toto ;  and  while  under  observa- 


560  THE  NON-NEURONIC  DISEASES 

tion  every  change  in  the  syniptoniatology  must  be  carefully  noted,  cor- 
related carefully  with  what  precedes  and  follows  it,  and  compared  with 
the  normal  functions  of  the  cord.  As  the  lesion  is  a  changing-  one.  the 
cause  of  the  symptoms  will  undergo  variations. 

In  regard  to  the  symptomatic  diagnosis  of  the  location  of  the 
tumor  the  reader  is  referred  to  the  chapter  in  the  earlier  part  of  the 
book  devoted  to  spinal  localization.  The  careful  determination  of  the 
limits  of  the  anaesthesia  affords  the  best  guide,  and  next  to  this  the 
muscles  that  may  be  paralyzed.  These  should  then  be  compared  with 
the  table  of  spinal  functions  reproduced  in  an  earlier  chapter.  As  a 
rule  the  tumor  is  located  from  two  to  four  inches  above  the  upper- 
most border  of  the  area  of  ancesthesia.  Spinal  sensitiveness  may  also 
help  slightly  to  localize  the  tumor.  The  peripheral  neuralgic  pain,  if 
sufficiently  constant  and  localized  in  the  area  of  a  nerve  distribution, 
may  assist  by  leading  back  to  the  corresponding  nerve-root.  Unfor- 
tunately, however,  pain  is  far  too  diffuse  a  symptom  to  be  of  much  aid. 

Diagnosis. — This  is  much  more  difficult  than  in  brain  tumor,  for 
the  reason  that  there  is  a  wider  variability  in  the  symptomatology. 
Note  should  be  carefully  taken  of  the  signs  indicating  gradual,  pro- 
gressive compression  of  the  cord  and  nerve-roots.  The  pain  and  its 
special  character,  the  progressive  paralysis,  the  rigidity  of  the  spine, 
the  muscular  contractions  in  the  limbs,  the  early  and  marked  exaggera- 
tion of  the  reflexes  of  the  leg,  the  extension  of  the  symptoms  from  one 
side  to  the  other,  and  the  possible  existence  of  metastatic  conditions  of 
similar  import  in  other  parts  of  the  body,  such  as  syphilis,  tubercu- 
losis, multiple  sarcomata  and  neuromata,  are  all  suggestive  of  a  spinal 
neoplasm. 

Caries  of  the  spine  is  to  be  dift'erentiated  from  tumor  by  the  ab- 
sence, or  less  severity,  of  the  root  signs,  by  the  lesser  degree  of  paraly- 
sis, by  the  presence  of  bone  disease  with  external  tumor  or  kyphosis, 
by  pain  upon  movement,  the  age  of  the  patient  and  the  existence  of 
the  tubercular  diathesis. 

The  symptoms  of  hypertrophic  pachymeningitis  are  bilateral  from 
the  beginning,  and  represent  a  much  more  extensive  lesion  longitu- 
dinally in  the  cord.  The  sensory  symptoms  in  the  arms  are  more 
marked  and  there  is  more  often  early  and  limited  anaesthesia.  The 
distinction  between  this  form  of  meningitis  and  cervical  tumor,  how- 
ever, is  at  times  extremely  difficult  and  for  obvious  reasons.  Menin- 
gitis is  often  a  part  of  the  symptom-complex  of  tumor. 

In  transverse  myelitis  the  pains  are  not  so  severe  and  radiatmg, 
but  there  is  more  of  a  girdle  phenomenon.  The  trouble  does  not  pro- 
gress and  exhibit,  like  tumor,  the  intense  initial  pains,  followed  by 
motor  paralysis  and  anaesthesia  and  the  signs  of  more  or  less  definite 
localization.  Here  again,  however,  a  differentiation  is  often  difficult 
because  myelitis  is  one  of  the  secondary  effects  of  tumor.  Occasion- 
ally the  cause  of  such  an  obtrusive  myelitis  can  be  discovered  to  be  a 
tumor,  by  the  manifestations  and  history  of  the  case,  before  the  appear- 
ance of  the  myelitic  symptoms. 

Neuralgia  of  special  nerves  ought  not  to  give  much  trouble  in 
the  differential  diagnosis  for  it  is  distinctlv  unilateral,  limited  to  the 


THE  NON-NEURONIC  DISEASES  561 

nerve  involved,  and  is  devoid  of  the  motor  and  spinal  symptoms  of 
tumor. 

Skiagraphy  should  always  be  kept  in  mind  as  a  possible  means 
of  diagnosing  and  locating  some  of  the  spinal  tumors. 

Prognosis. — Except  in  syphilitic  cases  the  prognosis  of  spinal 
tumor  is  bad.  The  course  and  duration  of  the  trouble  depend  verv 
largely  upon  the  character,  size,  and  location  of  the  neoplasm.  Most 
cases  run  from  three  to  five  years,  two  or  three  years  being  the  aver- 
age. Tubercles  have  been  known  to  cease  growing.  All  other  forms 
of  tumor  continue,  as  a  rule,  to  steadily  progress.  Rapid  increase  of 
symptoms  and  stationary  periods  often  alternate  in  the  course  of  the 
disease.  Even  transient  improvement  may  awaken  false  hopes. 
Syphilomata  are  the  only  growths  that  are  amenable  to  medicinal  in- 
fluence, and  even  these,  if  long  neglected,  offer  an  insurmountable  re- 
sistance. In  a  few  other  types  of  tumor  lives  have  been  saved  by 
surgical  intervention.  Death  is  caused  by  exhaustion,  bedsores  and 
all  the  usual  sequelae  of  a  severe  meningomyelitis  of  a  high  degree. 

Treatment. — There  is  only  one  form  of  spinal  tumor  that  is 
directly  amenable  to  medicinal  treatment,  and  that  is  syphiloma ;  and 
in  this  form  the  results  are  usually  in  inverse  ratio  to  the  length  of 
time  the  trouble  has  existed,  and  the  destructive  damage  already  done 
to  the  cord.  Therefore  the  earlier  the  treatment  is  instituted  the  bet- 
ter will  be  the  results.  It  is  a  good  rule,  unless  the  indications  point 
absolutely  away  from  syphilis,  to  put  every  case  of  spinal  tumor  upon 
a  trial  antisyphilitic  treatment.  This  is  especially  advisable  if  there 
has  been  exposure  and  a  possibility  of  infection.  The  frequently  evanes- 
cent character  of  the  primary  and  secondary  manifestations  in  cases 
of  tertiary  syphilis,  may  give  ground  for  the  denial  honestly  on  the 
part  of  the  patient  that  he  has  the  disease.  If  he  admits  circumstances 
"by  which  the  disease  may  have  been  acquired,  a  most  thorough  course 
•of  antisyphilitic  medication  should  at  once  be  begun  and  tried  for  a 
while.  It  cannot  do  the  slightest  harm,  should  the  tumor  be  of  any 
other  nature  than  syphilitic,  and  it  may,  in  case  it  is  the  latter,  save 
the  patient's  life.  Of  course  when  there  is  a  clear  history  of  infection, 
the  treatment  should  not  be  delayed  a  moment.  A  day  or  two  delay 
may  eventuate  in  irreparable  damage  to  the  cord.  The  treatment 
should  be  both  prompt  and  vigorous.  Increasing  doses  of  the  iodide 
of  potassium,  from  sixty  grains  a  day  on  up,  should  be  started,  just 
as  I  have  recommended  in  the  chapter  on  syphilis  of  the  nervous  sys- 
tem. If  in  a  few  days  there  is  no  marked  change  in  the  symptoms 
mercurial  enunctions  had  better  be  added  to  the  treatment.  In  some 
old  cases,  known  to  be  syphilitic,  the  treatment  just  suggested  may 
tail  to  modify  the  symptoms.  In  these  cases  the  changes  in  the  cord 
are  beyond  all  human  means  of  repair. 

Most  of  the  other  forms  of  tumor  suggest  the  possible  interven- 
tion of  surgery  but  their  medicinal  treatment  does  not  extend  beyond 
the  administration  of  tonics  and  remedies  for  the  symptoms.  A  tuber- 
culous condition  may  call  for  tonics,  iodine,  oleum  morrhuse,  but  not 
much  direct  effect  will  be  thus  exerted  upon  the  spinal  tubercle.  The 
same  may  be  said  of  the  use  of  arsenic  and  nitrate  of  silver  in  glioma 


562  THE  NON-NEURONIC  DISEASES 

and  sarcoma.  The  iodides  are  often  despairnigly  tried  in  all  cases, 
with  the  vague  idea  of  causing  absorption  of  the  growth.  The  idea  is 
as  poorly  founded  as  the  results  will  undoubtedly  be. 

Surgery  should  always  be  considered,  not  merely  as  a  last  resort, 
but  as  offering  in  some  cases  a  positively  hopeful  outlook.  While  the 
general  results  are  not  brilliant,  in  individual  cases  some  splendid  re- 
turns have  been  secured.  In  capable  hands  the  operation  is  not  now 
so  dangerous  as  it  used  to  be.  Even  an  exploratory  operation  is  to  be 
commended  where  so  desperate  a  disease  is  under  consideration  and 
there  is  doubt,  leaning,  however,  towards  the  diagnosis  of  tumor.  The 
extra-dural  tumors  are  of  course  the  most  favorable  for  operation, 
though  even  the  unfavorable  intra-medullary  growths  may  be  wisely 
enucleated  if  they  are  single  and  of  recent  development.  According  to 
Gowers  and  Horsley,  who  led  the  way  to  the  surgical  treatment  of 
these  tumors  with  their  first  brilliant  case,  almost  all  intra-dural  tu- 
mors are  operable.  Multiple,  metastatic  and  advanced  medullary  tumors 
are  beyond  all  aid,  and  therefore  should  not  be  subjected  to  the  knife. 

The  diagnosis  of  the  location  of  the  tumor  must  be  very  definite 
before  an  operation  is  undertaken.  In  most  cases  the  tendency  is  to 
locate  the  tumor  too  low  in  relation  to  the  guiding  symptoms.  In  Gow- 
ers and  Horsley's  first  case,  the  tumor  was  higher  than  the  symptoms 
suggested,  four  inches  above  the  level  of  the  pains  and  anaesthesia. 
According  to  Bruns,  generally  only  the  segmental  height  of  the  upper 
border  of  the  tumor  can  be  determined.  The  highest  point  of  the 
sensory,  motor  and  painful  manifestations  should  be  carefully  estab- 
lished and  this  compared  with  the  known  physiological  functions  of  the 
various  segments  of  the  cord.  The  chapter  on  spinal  localization  and 
topical  anatomy  of  the  cord  can  be  consulted  for  further  details.  The 
Rontgen  ray  is  a  modern  means  of  great  value  in  some  cases  for 
locating  the  tumor  and  should  always  be  resorted  to  to  add  if  possible 
further  confirmation  to  what  may  be  nevertheless  an  almost  positive 
topical  diagnosis. 

In  all  cases,  operable  or  inoperable,  the  pains  will  have  to  be 
controlled,  bedsores  will  have  to  be  guarded  against  and  properly 
treated  when  present,  disease  of  the  bladder  will  need  attention  and 
other  symptoms,  complications  and  sequelae  will  have  to  be  continu- 
ally looked  to.  The  management  of  a  case  of  spinal  tumor  is  never  a 
very  grateful  task. 

CAVITIES  OF  THE  SPINAL  CORD. 

The  formation  of  cavities  within  the  spinal  cord  is  intimately  re- 
lated to  the  presence  of  gliomatous  tumors.  They  are  the  result  of 
congenital  defects.  The  cavity  may  appear  as  a  primary  defect  and 
be  the  only  abnormality  present.  This  is  hydromyelia  and  is  homolo- 
gous with  hydrocephalus.  Gliomatous  tumors  may  form  within  the 
spinal  cord,  become  absorbed  and  thus  leave  a  cavity,  or  gliosis  may 
take  place  in  the  walls  of  a  congenital  cavity,  enlarge  into  a  tumor 
distending  and  deforming  the  original  cavity  and  then  undergo  partial 
or  complete  absorption,  thus  leaving  a  cyst  but  one  somewhat  differ- 


THE  xox->;euroxic  diseases  563 

ent  in  shape  from  the  original.  This  is  known  as  syringomyelia. 
Finally,  the  remains  of  old  hemorrhages  and  foci  of  inflammation  may 
undergo  partial  resorption  and  leave  small  cavities.  These  may  or 
may  not  be  congenital.  These  myelitic  and  hemorrhagic  remains  may 
be  traumatic  in  origin  or  may  accompany  hydromyelia  and  gliosis.  For 
the  sake  of  convenience  then,  the  cavities  of  the  cord  may  be  discussed 
under  the  three  heads,  (a)  Hydrotnyelia,  (b)  gliosis  and  syringomyelia 
and  (c)  myelitic  and  hemorrhagic  cxcazations. 

Hydromyelia  is  primarily  a  dilatation  of  the  cord,  especially  of 
the  central  canal.  It  is  lined  therefore  with  epithelium.  It  is  of  the 
nature  of  a  developmental  defect  and  may  be  associated  with  hydro- 
cephalus and  spina  bifida  or  exist  alone.  It  is  an  anatomical  curiosity 
without  clinical  importance.  As  a  rule  it  only  presents  symptoms  when 
gliosis  or  gliomatosis  takes  place  within  its  walls  and  it  becomes  occu- 
pied by  a  growing  tumor.     Then  it  becomes  clinically  interesting. 

Gliosis  axd  Syrixgomyelia. — ]\Iany  believe  that  this  and  hydro- 
myelia are  identical  conditions  primarily.  The  hydromeylia  of  child- 
hood evolves  in  the  course  of  time  and  from  various  factors  into  the 
syringomyelia  of  adults.  As  syringomyelia  develops  behind  the  cen- 
tral canal,  and  sometimes  around  it,  it  is  not  always  a  mere  modified 
hydromyelia.  It  is  a  posterior  spinal  defect  of  development.  In  most 
cases  it  is  a  persistent  patulency  of  the  anterior  portion  of  the  posterior 
limb  of  the  primitive  developmental  sulcus. 

Etiology. — Typical  syringomyelia,  as  I  have  intimated,  is  a  con- 
genital trouble  associated  with  or  following  a  gliomatous  neoplasm. 
Dana  says  it  is  more  frequent  than  amyotrophic  lateral  sclerosis  but 
less  frequent  than  multiple  sclerosis.  It  is  far  more  common  in  men 
than  in  women.  In  Schlesinger's  190  cases,  133  were  men,  57  women. 
Most  of  the  cases  begin  prior  to  the  thirtieth  }-ear ;  usually  about  the 
age  of  twenty  or  twenty-five.  It  is  commonly  affirmed  that  heredity 
-  does  not  constitute  an  etiological  factor  in  this  disease,  and  yet  three 
members  in  the  same  family  have  fallen  victims  to  it.  In  the  non- 
gliomatous,  traumatic  syringomyelias  there  is  believed  to  exist  an  in- 
herited or  congenital  predisposition  on  account  of  which  the  trauma 
operates  in  the  way  that  it  does.  The  disease  cannot  be  connected 
with  alcoholism,  syphilis  or  dissipation.  It  has  followed  pregnancv  and 
certain  infectious  diseases.  Dana  observes  that  it  seems  to  occur  to  a 
large  extent  among  those  who  follow  manual  occupations,  such  as 
butchers,  tailors,  etc.  I  observed  it  in  a  man  who  after  recovery  from 
influenza  went  to  work  in  the  fields  and  daily  plunged  into  cold  water 
while  he  was  hot  and  perspiring.  Oppenheim  says  that  spinal  cavities 
have  often  been  observed  in  syphilitic  individuals  and  accompanying 
other  disease  of  the  cord.  These  cases  are  not  typical,  however,  as 
are  the  non-syphilitic  gliomatous  cases. 

Pathology  axd  Pathogexesis. — Upon  taking  the  cord  out  of 
the  spinal  canal  nothing  abnormal  may  appear  about  it.  It  may  seem 
a  little  larger  in  some  places,  softer  than  normal,  and  fluctuating.  The 
essential  finding  of  the  disease  is  only  obser\-ed  when  the  cord  is  cut 
across  transversely.  At  once  a  cavernous  formation  is  seen  in  the  gray 
matter.     It  usually  occupies  the  center  of  the  cord,  obliterating  and 


564 


THE  XOX-XEUROXIC  DISEASES 


FIGURE  122. 


FIGURE  123. 


FIGURE  124. 


Figure  122,  H3^dromyelia  of  upper  dorsal  cord.    Figures  123  and  124,  Syringo- 
mj^elia.     Sections  rnade  in  upper  and  middle  cer\ncal  cord.     (Striimpell — Jakob.) 


THE  NON-NEURONIC  DISEASES  565 

including  the  central  canal.  It  may  extend  in  the  lateral  gray  mat- 
ter or  into  the  horns,  especially  the  posterior  horns.  In  the  latter  it 
has  been  seen  to  reach  almost  to  the  edge  of  the  cord.  The  white 
matter  is  not  touched  by  it.  The  shape  of  the  cavity  is  irregular  and 
various.  It  may  be  angular,  round,  oval,  stellate,  diamond  or  any 
imaginable  shape.  It  is  most  frequently  seen  in  the  cervical  part  of 
the  cord,  though  it  may  be  in  any  part,  or  even  extend  throughout  its 
entire  length.  The  bore  of  the  cavity  when  thus  extended  is  never 
perfectly  uniform.  There  are  apt  to  be  here  and  there  wide  lacunce 
with  narrow  connecting  channels.  Lining  the  cavity  is  a  well-formed 
membrane  and  around  it  a  layer  of  gliomatous  tissue.  In  some  places 
this  gliomatous  tissue  is  proliferated  and  extends  into  the  lumen  of 
the  cavity.  Occasionally  it  may  be  seen  to  occupy  the  whole  cavity 
and  even  be  distending  it.  The  primitive  ciliated  epithelium  of  the 
original  central  canal  may  be  noted  here  and  there  on  the  cavity  wall. 
The  cells  of  the  gliomatous  tumor  are  seen  to  be  in  various  stages  of 
formation  and  decay.  Hemorrhagic  and  inflammatory  foci  may  be 
observed  in  certain  cases.  In  some  cases  other  developmental  defects 
have  been  observed  outside  of  the  cord.  Thus  the  brain  has  revealed  an 
internal  hydrocephalus  and  the  cerebellum  has  been  absent.  Tumors, 
probably  gliomatous,  have  also  been  seen  in  the  pons,  the  cauda 
equina  and  elsewhere,  showing  that  the  gliomatous  growths  of  the 
cord  proper  constitute  but  a  part  of  a  widespread  pathological  tendency. 

The  original  cause  of  these  cavities  is  a  congenital,  developmental 
defect  in  the  posterior  part  of  the  spinal  cord.  There  is  a  defective 
closure  of  the  central  canal  and  posterior  septum,  with  the  remains 
of  epiblastic  tissue  in  the  walls  of  the  imperfect  closure.  Just  to 
what  extent  the  entire  syringomyelic  formation  is  congenital  in  its 
origin  is  not  easy  to  determine ;  nor  can  it  be  stated  positively  just  how 
much  it  has  been  enlarged  and  altered  by  the  over-growth  and  sub- 
sequent degeneration  of  the  gliomatovis  tissue.  The  process  of  cavity 
formation  is  thus  a  complicated  one,  always  primarily  congenital  or 
hydromyelic,  but  secondarily  enlarged  and  distorted  by  the  intra- 
cavernous  growth  and  degeneration  of  a  neuroglia  tumor. 

The  primitive  furrow  in  the  embryo  deepens,  its  sides  rise  up, 
arch  inward,  coalesce,  and  thus  transform  it  into  a  tube.  At  about 
the  sixth  week  this  central  canal  is  comparatively  very  large,  is  dia- 
mond shaped  and  reaches  from  the  anterior  to  the  posterior  surface  of 
the  cord.  Its  walls  are  thinner  in  front  and  behind  than  they  are  at 
the  sides.  As  the  posterior  columns  develop,  the  posterior  part  of  this 
canal  becomes  narrow  and  elongated,  almost  to  the  point  of  being  a 
mere  fissure.  The  surrounding  structure  consists  of  embryonal-  cells 
which  afterward  are  transformed  into  the  proper  nerve  elements. 
Finally  the  canal  becomes  divided  into  an  anterior  and  a  posterior  por- 
tion. The  former  ultimately  constitutes  the  permanent  central  canal, 
the  sides  of  the  posterior  coalesce  and  form  the  posterior  septum. 
When  either  of  these  divisions  of  the  primitive  central  canal  fail  to 
close  properly,  there  is  a  surplus  of  the  embryonal  epiblastic  tissue 
present  which  is  ver}'  liable  later  on  to  undergo  hyperplasia  and  tumor 
formation.    The  cells  are  small,  round  or  irregular  in  shape,  with  large 


566  THE  NON-NEURONIC  DISEASES 

nuclei  and  numerous  fine  fibrillary  prolongations.  Bloodvessels  pene- 
trate these  gliomatous  growths  and  being  diseased  rupture  and  leave 
hemorrhagic  debris.  I'he  tumors  themselves  arc  very  prone  to  degen- 
eration and  disintegration,  transforming  an  originally  limited  cavity 
into  a  much  more  extensive  one.  The  disintegration  and  disappearance 
of  the  gliomatous  tumor  are  due,  in  a  measure,  to  the  liquefactive  de- 
generation of  the  glia  cells.  The  oedema  of  the  cord  may  be  partly  re- 
sponsible for  and  partly  the  result  of  this. 

Symptoms. — Some  cases  of  syringomyelia  do  not  seem  to  produce 
any  symptoms  arid  they  are  only  discovered  upon  post  mortem  examina- 
tion. It  is  probable  they  are  cases  of  hydromyelia  in  which  no  gliosis 
has  taken  place.  The  latter  process  in  the  majority  of  cases  probably 
begins  spontaneously,  though  in  some  cases  it  would  not  occur  at  all 
if  there  had  not  been  some  exciting  initiative  cause,  like  trauma,  hem- 
orrhage, meningitis,  etc. 

The  symptoms  of  syringomyelia  are  the  result  of  the  pressure 
and  destruction  of  gray  matter  caused  by  the  tumor.  This  explains 
why  the  infantile  form  of  the  trouble  is  without  clinical  manifestation 
generally,  whereas  the  adult  form  almost  always  exhibits  outward  signs. 

The  clinical  picture  of  the  disease  is  subject  to  wide  variations. 
This  would  naturally  be  expected  from  so  variable  and  extensive  a 
lesion.  The  establishment  of  types  of  the  disease,  such  as  Schlesinger 
and  others  have  made,  seems  to  me  to  be  arbitrary,  burdensome  and 
dangerouslv  suggestive  of  the  types  being  different  diseases  dependent 
upon  different  lesions.  The  only  anatomical  basis  for  the  separation 
of  these  types  is  the  accidental  location  of  the  pressure  and  destructive 
influences  within  the  cord.  Hence  while  the  clinical  features  are  in  a 
way  complex,  it  is  not  due  to  the  complexity  of  the  disease  but  to  the 
complexity  of  the  physiological  functions  of  the  cord  and  their  dis- 
turbance by  the  particular  location  of  the  disease  process. 

As  the  cavity  usually  appears  first,  and  is  most  extensive  in  the 
cervical  part  of  the  cord  the  symptom.s  appear  most  prominently  in 
the  upper  part  of  the  chest,  the  lower  part  of  the  neck,  in  the  shoulders, 
arms,  and  hands. 

Perhaps  the  most  striking  symptom,  due  doubtless  to  the  destruc- 
tion of  the  gray  matter  of  the  central  cord,  is  the  progressive  muscu- 
lar atrophy.  It  usually  begins  in  the  hands,  sometimes  in  the  shoul- 
ders and  upper  arms.  Sometimes  it  develops  in  the  legs.  It  is  a  true 
atrophy  and  is  liable  to  be  mistaken  for  the  ordinary  form  of  spinal 
progressive  muscular  atrophy.  The  smaller  muscles  of  the  hand  waste 
first  and  the  inain-en-griife,  or  claw-hand,  develops.  The  muscles  on 
the  back  of  the  scapulae,  the  deltoid,  the  biceps  and  triceps,  diminish 
in  size.  The  wasting  is  usually  bilateral  and  is  accompanied  by  a 
fibrillary  tremor.  There  is  a  partial  reaction  of  degeneration  and  dis- 
turbance of  the  reUexes.  Weakness  and  paresis  proceed,  pari  passu, 
with  muscular  wasting.  In  the  legs,  which  are  usually  aft"ected  later, 
there  is  atrophy  with  more  or  less  spastic  paraplegia;  in  other  words  a 
condition  resembling  amyotrophic  lateral  sclerosis,  and  probably  pro- 
duced by  the  same  sort  of  a  disease  process.  The  face  and  throat  mus- 
cles are  not  often  affected  and  the  sphincters  remain  intact.     On  ac- 


THE  XOX-XEUROXIC  DISEASES  56? 

count  of  the  unequal  wasting  of  the  muscles  of  the  back  spinal  curva- 
tures occur,  especially  scoliosis.  The  drooping  of  the  scapula  and  the 
lessening  of  the  shoulder  joint  cause  unilateral  deformities  often  about 
the  shoulder. 

The  sensory  disturbances  are  unique  and  almost  pathognomonic. 
There  is  a  dissociation  hetzi'een  the  tactile  and  pain  senses,  a  simple 
analgesia  without  ancesthesia  or  hypercesthesia.  The  temperature  sense, 
like  the  pain  sense,  is  also  lost.  A  hot  iron  and  a  piece  of  ice  placed 
agamst  the  skin  awaken  only  the  sense  of  contact.  AMth  the  iron  hot 
enough  to  burn  the  skin,  it  still  does  not  cause  any  distress.  This 
explains  the  many  scars  and  marks  of  traumatism  so  often  carried  by 
the  patients  about  on  their  bodies.  The  exact  anatomical  basis  for  this 
remarkable  symptom  is  not  fully  known.  It  is  thought  to  be  due  to 
the  destruction  of  the  gray  matter  of  the  posterior  commissure,  through 
which  course  the  fibres  of  Gowers'  tract  that  carry  the  pain  and  heat 
impulses.  In  some  instances  the  conducting  functions  of  the  cord  for 
sensory  impulses  of  all  sorts  are  so  profoundly  damaged  that  wide 
areas  of  complete  anaesthesia  are  observed.  The  Brown-Sequard  type 
of  hemianccsthesia  is  accordingly  noted.  Parcesthesia  is  not  infre- 
quent and  in  rare  instances  actual  pain  may  be  present.  The  special 
senses  do  not  participate  in  the  trouble. 

This  dissociation  of  the  tactile  and  pain  sense,  with  the  progres- 
sive muscular  atrophy  above  and  the  amyotrophic  sclerotic  manifesta- 
tions below,  constitute  the  pathognomonic  picture  of  the  disease. 

Other  symptoms  of  great  variety  may  also  be  looked  for.  Among 
these  the  vasomotor  and  trophic  signs  stand  prominently  forth.  Thev 
must  be  distinguished  of  course  from  the  mere  injuries  which  these 
patients  so  often  cause  themselves  on  accotmt  of  the  absence  of  the 
pain  and  heat  senses.  CEdema,  redness,  sweating,  slow-healing  sores 
appear  on  the  hands  and  arms.  Eczema,  bullae,  herpetiform  eruptions 
break  out  on  the  skin  of  the  body.  The  latter  is  sometimes  dry  and 
leathery  and  unhealthy  looking.  Whitlows  occur  on  the  fingers,  and 
the  nails  become  brittle  and  fall  out.  In  about  ten  per  cent,  of  the 
cases  arthropathies  occur.  The  bones  become  fragile  and  necrosed. 
and  ankyloses  take  place  in  the  joints.  Spontaneous  fractures  are  not 
to  be  forgotten  as  unfortunate  possibilities.  The  mutilations,  scars, 
deformities  often  render  these  poor  creatures  a  sorry  sight. 

Inequality  of  the  pupils,  and  later  on  distinct  bulbar  symptoms 
with  implication  also  of  the  rectal,  vesical  and  sexual  functions  show 
the  gradual  and  progressive  extension  of  the  lesion, 

]\Iany  changes  may  be  rung  upon  the  above  more  or  less  typical 
clinical  picture,  and  some  novel  combinations  in  the  symptomatology 
make  their  appearance.  These  are  not  types  of  the  disease,  but  mere 
atypical  presentations  of  the  symptoms.  Mor^^an,  for  instance,  de- 
scribed what  he  supposed  was  a  new  disease,  but  \\'hich  is  now  acknowl- 
edged to  be  but  a  particular  presentation  of  syringomyelia.  In  the  cases 
that  Alorvan  described,  analgesia,  thermo-an^esthesia,  tactile  anaesthesia, 
muscular  atrophy  and  felons  on  the  fingers  all  occurred. 

A  rare  group  of  symptoms  that  have  been  separately  seen  in  dift'er- 
ent  cases  are  facial  hemiatrophy,  anaesthesia  of  the  trigeminal  region, 


568  THE   NON-NEURONIC  DISEASES 

early  bulbar  phenomena,  cranial  nerve  palsy,  nystagmus  and  mellituria. 
A  sharp  limitation  of  the  symptoms  may  be  due  to  the  confinement  of 
the  gliosis  to  the  posterior  or  anterior  horns  of  one  side.  In  three  cases 
Oppenheim  observed  the  disease  to  be  restricted  to  the  lower  limbs  in 
the  beginning.  I  saw  a  case  in  which  in  the  beginning  there  was  pain  in 
the  left  hip,  passing  down  the  leg  and  followed  by  a  very  slight  degree 
of  atrophy,  oedema  and  changes  in  the  joints.  Later  on  the  pain  ceased 
in  the  leg  and  marked  atrophy  appeared  in  both  shoulders,  in  the  back 
muscles  and  muscles  of  the  scapulse,  and  part  way  down  the  muscles  of 
the  arm..  Arthropathies  were  marked  in  the  knee  of  the  left  side  and 
shoulder  joints.  The  other  symptoms,  trophic  and  sensory,  were  not 
unusual. 

Optic  neuritis  and  choked  disc  have  been  seen,  and  some  still 
maintain  that  in  part,  at  least,  the  symptom-complex  of  Morvan's  dis- 
ease is  due  to  a  complicating  peripheral  neuritis. 

If  there  is  involvement  especially  of  the  po'sterior  tracts,  the  disease 
may  asume  the  complexion  of  tabes  dorsalis. 

Diagnosis. — Progressive  muscular  atrophy,  dissociation  of  the 
sensory  symptoms,  general  vasomotor  and  trophic  symptoms,  the  amyo- 
trophic lateral  sclerosis  symptomatolo gy  in  the  lozuer  limbs  and  spinal 
curvature  constitute  the  decisive  indications  of  syringomyelia.'  The 
numerous  atypical  combinations  and  presentations  of  its  symptoms  may 
easily  delude  one  into  mistaking  it  for  some  other  disease.  This  was 
much  more  common  in  the  past  than  it  is  to-day,  and  we  now  recognize 
that  there  were  named  and  described  many  separate  affections  that  were 
really  instances  of  syringomyelia. 

Both  ordinary  progressive  mnscnlar  atrophy  and  amyotrophic  lat- 
eral sclerosis  are  very  liable  to  be  mistaken  for  it.  The  former  is  de- 
void of  sensory  symptoms  entirely,  and  the  latter  is  not  characterized 
by  flaccid  atrophic  paralysis  with  preservation  or  diminution  of  the 
knee-jerks.  The  sensory  phenomenon  when  present  will  indicate  con- 
clusively syringomyelia. 

Hypertrophic  cervical  pachymeningitis  causes  muscular  wasting, 
sensory  loss  and  other  resemblances  to  syringomyelia.  It  may  be  dif- 
ferentiated, however,  by  the  local  spinal  tenderness,  the  spinal  root 
symptoms,  the  lesser  extent  of  the  anses'thesia  in  relation  to  the  wasting 
and  the  absence  of  the  characteristic  indications  oi  the  cord  disease. 

Chronic  transverse  myelitis  should  give  no  very  great  trouble  in  the 
diagnosis. 

Caries  of  the  spine,  with  atrophy, .  sensory  disturbances  and 
pupillary  changes,  is  nevertheless  separated  by  the  history  of  tubercu- 
losis and  disease  of  the  vertebrae. 

Gliosis  and  glioma  of  the  cord  are  two  separate  conditioiis,  accord- 
ing to  Hoffmann.  The  former  is  a  rapid,  the  latter  a  slow  process. 
They  are  not  necessarily  syringomyelic. 

Various  peripheral  nerve  diseases  may  be  confused  with  syringo- 
myelia. Morvan's  disease  does  not  call  for  a  differential  diagnosis,  as 
it  is  syringomyelia  with  possibly  a  complicating  neuritis.  It  is  the  form 
of  syringomyelia  that  is  most  likely  to  be  confused  with  ancesthetic  lep- 
rosy.   The  detection  in  the  skin  of  the  lepra  bacillus  is,  oi  course,  final. 


THE  NON-XEUROXIC  DISEASES  569 

In  leprosy  the  cutaneous  evidences  are  in  plaques,  including  the  face 
and  lower  limbs  as  much  as  the  arms.  There  is  no  dissociation  of  the 
sensory  symptoms  as  in  syringomyelia,  but  the  sensory  phenomena  fol- 
low the  innen^ation  particularly  of  the  peripheral  nerves.  In  leprosy 
the  amyotrophic  paraplegia  of  the  lower  extremities,  the  bulbar  symp- 
toms, the  nystagmus  sometimes  seen  in  syringomyelia  are  wanting. 

Neuritis  of  the  brachial  plexus  has  all  the  earmarks  of  peripheral 
neuritis  and  very  few  of  those  of  the  spinal  cord  cavity. 

Hematomyelia  has  its  own  clinical  manifestation,  though  it  may 
later  on  develop  into  a  syringomyelia. 

Hysteria,  Raynaud's  disease,  acroparccsthesia  are  easily  distin- 
guishable from  the  affection  under  consideration  if  emphasis  is  laid 
upon  the  characteristic  symptoms  of  each  respectively. 

Prognosis. — In  regard  to  recovery  this  is  bad.  The  disease  is  a 
progressive  and  congenital  one.  Periods  of  temporar}^  cessation  and 
even  remissions  occur.  It  ma}'  continue  to  advance  for  many  years.  It 
is  doubtful  if  the  case  with  lues,  reported  as  cured  under  the  use  of 
potassium  iodide,  was  typical.  Death  occurs  from  exhaustion,  blood- 
poisoning  and  bedsores. 

Treatment. — This  is  of  no  avail  and  for  reasons  that  are  quite 
obvious.  Warn  the  patient  against  injuring  himself;  maintain  the 
nutrition  of  the  muscles  as  far  as  possible  by  massage  and  electricity; 
administer  general  tonics ;  and  try,  if  you  are  in  a  hopeful  state  of 
mind,  arsenic  or  silver  nitrate.  Lumbar  puncture  entertains  the  sur- 
geons without  in  the  least  helping  the  patient,  and  the  finding  of  some 
drug  or  serum  that  will  check  the  gliomatosis  is  a  dream  the  realiza- 
tion of  which  is  more  to  be  hoped  for  than  actually  anticipated. 

Myelitic  and  Hemorrhagic  Cavities. — The  names  of  these  suffi- 
ciently indicate  their  nature.  They  may  occur  alone  or  with  typical 
syringomyelia.  They  are  not  large,  are  apt  to  be  multiple  and  are  gen- 
erally lined  with  connective  tissue. 

SPINA   BIFIDA   AND   OTHER   CONGENITAL   MALFORMA- 
TIONS OF  THE  CORD  AND  ITS  MEMBR.\NES. 

Spina  Bifida  or  racJiiscJiisis  is  an  embryonal  defect  depending  upon 
a  failure  of  the  spinal  canal  to  close.  It  belongs  to  the  same  class  of 
troubles  as  hare-lip,  cleft  palate  and  exstrophy  of  the  bladder.  The  bony 
canal  being  open  iDehind,  the  contents  protrude  under  the  skin  and  pro- 
duce a  tumor,  varying  in  size  from  a  nut  to  a  child's  head.  The  lum- 
bar region  is  its  most  frequent  site.  In  some  cases  only  the  membranes, 
filled  with  cerebro-spinal  fluid,  protrude.  This  is  a  meningocele.  Some- 
times the  cord  protrudes  with  the  membranes,  giving  rise  to  a  myelocele 
or  meningomyelocele.  When  the  cord  is  syringomyelic,  as  it  occasion- 
ally is,  the  cavities  inside  and  outside  of  the  cord  form  one  and  thus  is 
established  a  syringomyelocele.  The  simple  meningoceles  and  meningo- 
myeloceles are  the  most  common  and  are  sometimes  called  hydrorrhachis 
externa.  When  the  cord  and  nerves  are  in  the  sac,  they  lie  on  the 
posterior,  median  surface.  The  lining  of  the  sac  is,  of  course,  the  dura 
and  the  subdural  arachnoid.     Outside  of  it  the  skin  is  usuallv  normal. 


570  THE  NON-NEURONIC  DISEASES 

fhin  and  covered  somewhat  with  hair.  The  tumor  itself  is  elastic  and 
fluctuating.  Pressure  upon  it  has  caused  unconsciousness  and  other 
cranial  disturbances. 

Other  developmental  anomalies  and  signs  of  degeneracy  are  often 
seen  in  these  patients.  They  are  usually  mentally  defective  and  are 
feeble,  badly  nourished  and  badly  developed  individuals. 

In  simple  meningocele,  the  cord  being  intact,  there  are  often  no 
special  neurological  symptoms.  In  the  myeloceles,  however,  there  is 
usually  complete  paraplegia,  with  muscular  atrophy,  more  or  less  an- 
aesthesia, bladder  and  rectal  trouble,  diminution  of  the  knee-jerks  and 
the  paralytic  type  of  talipes,  especially  pes  varus.  Very  few  cases  live 
to  old  age.    The  prognosis  is  always  grave,  with  or  without  treatment. 

The  treatment  is  entirely  surgical.  Unless  hydrocephalus  is  pres- 
ent, extirpation  of  the  sac  may  be  attempted.  The  results  are  not  very 
encouraging.  Morton's  fluid,  consisting  of  iodine  gr.  x,  potassium  iodide 
gr.  XXX,  glycerin  oj,  has  been  injected  into  the  cyst  in  3j  quantities.  The 
injection  should  be  made  at  the  side  of  the  sac  and  the  child  be  kept 
still.  There  is  nothing  to  be  gained  by  simple  puncture  and  with- 
drawal of  the  fluid.  It  is  a  dangerous  procedure.  Only  several  months 
after  birth  should  surgical  interventio'n  be  thought  of. 

MALFORMATIONS. 

There  are  certain  malformations  of  the  spinal  cord  that  are  only 
of  anatomical  and  pathological  interest.  Such  is  amyelia  or  absence  of 
the  cord.  It  is  morphologically  and  biologically  interesting  that  when- 
ever the  cord  is  thus  wanting  the  brain  also  is  wanting,  but  that  oc- 
casionally the  brain  may  be  absent  without  the  absence  of  the  cord. 
In  these  cases  of  amyelia  the  spinal  nerves  are  present  and  their  inner 
roots  swing  loosely  in  the  spinal  cavity.  These  monsters,  who,  of 
course,  never  live,  demonstrate  most  clearly  that  the  nerves  are  not 
intrinsically  developments  of,  or  parts  of,  the  cord,  and  that  the  brain 
is  practically  a  hyper-development  of  certain  anterior  segments  whose 
homologues  are  the  segments  of  the  so-called  spinal  cord.  An  atelo- 
myelia  is  the  failure  of  development  of  a  certain  segment.  When  the 
cord  is  bifurcated,  the  condition  is  spoken  of  as  diastematomyelia. 
Rarely  is  the  whole  cord  involved  in  this  condition.  Sometimes  the 
cord  is  asymmetrical.  A  double  cord,  with  two-  central  canals,  lying 
side  by  side,  is  known  as  a  diplomyelia.  None  of  these  are  of  any 
clinical  interest,  but  as  indications  of  development  and  biological  evo- 
lution of  this  part  of  the  nervous  system  they  are  of  entrancing  interest. 
Micromyelia  is  an  abnormally  small  cord.  Van  Giesen's  heterotopia  is 
an  abnormally  situated  mass  of  gray  matter.  In  most  cases  it  is  a 
post-mortem  artefact. 

CAISSON  DISEASE. 

This  is  sometimes  called  diver's  paralysis  and  compressed  air  dis- 
ease. It  is  probably  an  affection  of  the  entire  nervous  system  or  cerebro- 
spinal axis,  though  it  is  usually  discussed  as  a  spinal  cord  trouble  be- 
cause its  symptoms  are  largely  paraplegic  in  character,  and  what  few 


THE  NOX-NEUROXIC  DISEASES  57T 

lesions  have  been  found  after  death  were  seen  in  the  cord.  As  diver's 
palsy  the  disease  has  doubtless  long  been  known.  In  these  modem 
days  of  industrial  activity  and  great  engineering  projects,  with  their 
mining,  bridge-building  and  harbor  construction,  in  which  caissons 
filled  with  compressed  air  under  water  are  made  use  of,  the  trouble  has 
become  more  frequent  and  awakened  a  corresponding  interest.  Much 
study  has  been  made  of  it,  both  clinically  and  experimentally,  so  that 
the  literature  is  of  no  mean  proportions. 

Etiology. — The  essential  cause  of  the  disease  is  the  high  atmos- 
pheric pressure  which  the  victims  must  perforce  undergo  in  their  occu- 
pation. It  is  therefore  an  acute  disease  with  one  specific  cause,  and 
all  such  factors  as  age,  sex,  race,  etc.,  are  of  no  significance,  except  so 
far  as  they  are  determined  by  the  occupation.  Those  who  work  in 
caissons,  bells  and  diver's  apparatuses  are  usually  subjected  to  a  com- 
pression of  from  one  to  four  atmospheres,  which  means  from  fifteen  to 
sixty  pounds  to  the  square  inch.  When  they  emerge  from  the  apparatus 
and  the  compression  is  withdrawn  the  symptoms  of  the  disease  make 
their  first  appearance.  .  Tlie  differences  in  individual  susceptibility  may 
explain  why,  under  the  same  conditions,  some  are  affected  while  others 
escape.  Every  indication  points  to  the  mechanical  pressure,  rather 
than  to  an}-  chemical  or  other  change  in  the  air,  as  the  primary  and 
essential  cause  of  the  disease. 

Pathology  and  Pathogexesis. — Not  many  post-mortem  exam- 
inations after  diver's  palsy  have  been  made  and  our  knowledge  of  its 
pathological  anatomy,  if  it  has  any,  is  meagre,  ^[ost  of  the  changes 
have  been  found  in  the  thoracic  part  of  the  cord.  They  have  consisted 
of  numerous  minute  foci  of  hemorrhage  and  small  patches  of  necro- 
biosis. Sometimes  signs  of  an  acute  myelitis,  disseminated  myelitis, 
were  noted.  There  were  also  slight  fissures  and  ruptures.  Changes  in 
the  brain  have  not  been  reported,  though  in  a  few  cases  the  symp- 
tomatology was  clearly  that  of  cerebral  apoplexy. 

On  account  of  the  scarcity  of  these  post-mortem  evidences,  all  ex- 
planations of  the  disease  are  to  be  taken  somewhat  tentatively. 

Perhaps  the  grossest  explanation  is  that  the  increased  pressure 
upon  the  surface  of  the  body  drives  the  blood  inward  and  that  whereas 
the  other  viscera  are  able  to  accommodate  themselves  to  the  congestion 
thus  caused,  the  brain  and  spinal  cord  being  encased  in  a  firm,  bony 
box,  are  not  able  to  accommodate  themselves  quickly  enough  to  the 
new  state  of  affairs.  A.  H.  Smith  is  the  leading  exponent  of  this  view. 
There  are  many  objections  to  it,  however.  The  first  is  that  the  symp- 
toms appear  not  when  the  congestion  is  produced,  but  when  it  is  re- 
lieved; not  when  the  man  is  under  the  increased  pressure,  but  when 
he  comes  out  from  it.  It  is  a  little  contradictory  to  declare  that  con- 
gestion and  minute  hemorrhages,  presumably  produced  while  the  man 
is  being  subjected  to  the  exalted  pressure,  should  produce  no  symptoms 
until  he  emerges  from  the  caisson  and  the  congestion  and  other  sup- 
posed circulatory  disturbances  are  relieved.  Symptoms  and  lesion 
must  be  synchronous  or  we  must  adopt  the  idea  that  the  evi- 
dences of  congestion  are  only  manifested  when  the  congestion  is 
undersroino-    reduction.     The  illogicalitv  of  this,  it  seems  to  me,  is  an 


572  THE  XOX-XEUROXIC  DISEASES 

argument  against  the  congestion  theory.  The  theory,  moreover,  upsets 
the  long-taught  physiological  fact  that  on  account  of  their  rich  anas- 
tomotic blood  supply,  both  the  brain  and  cord,  above  all  the  viscera, 
are  protected  from  sudden  and  external  circulator}"  disturbances  of 
a  purely  mechanical  nature.  And  finally,  it  does  not  harmonize  with 
the  localization  of  the  chief  center  of  the  trouble  in  the  dorsal  region 
of  the  cord.  Gowers  suggests  that  the  trouble  is  primarily  due  to  the 
revulsive  anaemia  following  the  congestion,  and  that  a  nutritional  dis- 
turbance, especially  in  that  part  of  the  cord  which  is  so  liable  to  nutri- 
tional disturbances,  the  dorsal  region,  is  the  immediate  source  of  the 
paraplegia. 

Snell's  hypothesis  that  it  is  due  to  the  bad  ventilation  of  the  caisson, 
and  the  escape  of  carbon  dioxide  and  oxygen  into  the  blood-vessels  and 
into  the  tissues,  needs  yet  to  be  confirmed. 

The  explanation  that  at  present  seems  to  have  the  strongest  ex- 
perimental and  pathological  support  is  one  in  which  it  is  affirmed  that 
there  is  a  sudden  effervescence  of  gas  in  the  blood  and  tissue  juices. 
In  this  way  the  peculiar  character  and  course  "of  the  symptoms,  and  the 
few  pathological  findings  that  have  been  noted,  such  as  the  spinal 
fissures  and  lacerations,  the  minute  hemorrliages  and  spots  of  necrobio- 
sis from  air  emboli,  are  thought  to  be  caused.  The  inflammatory 
changes  are  secondary  results.  Paul  Bert  was  the  first  to  suggest  this 
theory,  though  Hoppe,  Francois,  Rameau  and  Bacquay  had  previously 
surmised  it.  After  recently  experimenting  upon  animals.  Hill  and 
]\Iacleod  believe  they  have  confirmed  Bert's  conclusions.  In  their  sum- 
ming up,  these  investigators  say  that  the  circulation  is  not  affected 
mechanically  by  compressed  air.  The  cause  of  the  disease  is  the  escape 
of  gas  bubbles  in  the  blood-vessels  and  tissue  fluids  upon  the  withdrawal 
of  the  compression.  All  of  the  fluids  of  the  body  generally  effervesce 
somewhat  after  the  manner  of  an  opened  bottle  of  soda  water.  The 
symptoms  var\^  because  the  seats  of  the  air  emboli  vary. 

Symptoms. — After  a  pressure  of  three  or  more  atmospheres,  the 
symptoms  appear  in  those  aft'ected  usually  after  the  change  is  made 
from  the  hig'h  to  the  low  pressure,  especially  if  the  change  is  made 
quickly.  The  individual  must  have  been  subjected  to  the  pressure  for 
at  least  an  hour,  and  it  usually  is  noted  that  the  first  signs  of  the  dis- 
ease show  themselves  froin  half  an  hour  to  an  hour  after  he  returns  to 
the  lower  pressure.  He  may  not  have  reached  the  normal  atinosphere 
even  before  their  appearance. 

There  is  first  sudden  pain  in  the  limbs  and  joints,  quickly  followed 
by  powerlessness  and  complete  paraplegia.  Not  often  are  the  arms 
involved.  The  pain,  sharp  and  neuralgic  in  character,  may  appear  in 
the  epigastrium.  These  pains  are  often  paroxysmal  and  are  accom- 
panied by  nausea  and  vomiting.  Sometimes  the  legs  are  tender  to  the 
touch  and  the  gait,  when  not  completely  paraplegic,  is  stiff  and  awk- 
ward. Cephalalgia  and  dizziness  are  frequent.  In  the  severest  cases 
there  is  complete  paralysis  of  both  motion  and  sensation,  involving  legs,, 
arms  and  trunk.  In  a  few  rare  instances  there  have  been  seen  hemi- 
plegia, monoplegia  and  other  symptoms  suggestive  of  cerebral  apoplexy. 
Rapid  coma  and  death  have  taken  place  in  these  apoplectic  cases. 


THE  XOX-XEUROXIC  DISEASES  573 

The  sphincters  are  usually  involved,  and  there  may  be  retention  or 
involuntar}-  emission  of  urine,  constipation  and  erections  of  the  penis. 
Clonic  contractions  upon  movement  have  occurred  in  the  abdominal 
muscles.  In  the  paraple^c  cases  that  do  not  get  well  bedsores,  cystitis 
and  all  the  later  signs  of  a  transverse  myelitis  appear. 

Prognosis. — ^Nlild  cases  usually  get  well ;  severe  cases  usuallv  die. 
The  former  may  run  a  course  of  only  a  few  hours,  or  one  of  many 
weeks  and  months.  In  the  mildest  cases  the  recovery  is  generally  com- 
plete. In  other  cases  the  paraplegia  becomes  permanent.  ]\Iost  of 
these  cases  run  a  course  and  terminate  as  any  case  of  transverse 
myelitis  would.    Cases  ^\•ith  cerebral  symptoms  are  usually  fatal. 

Treatment. — Prophylaxis  is  obviously  most  important.  A  care- 
ful selection  should  be  made  as  to  the  general  age  and  physique  of  the 
mien  employed  in  caisson  work.  Only  strong,  young  men  should  be 
accepted  and  they  should  accustom  themselves  to  the  conditions  before 
fully  entering  upon  their  work.  It  is  imperative  that  they  be  total 
abstainers  and  tem^perate  in  all  their  habits.  It  is  weU  to  test  the  men 
with  low  pressures  first  before  engaging  them.  Hill  and  IMacleod  sug- 
gest  that  the  choice  men  for  the  work  are  those  who  are  small,  spare 
and  war}-,  and  from  twenty  to  twent}-five  years  of  age.  Emergence 
from  the  atmosphere  should  be  gradual  and  always  slower  than  en- 
trance. The  longer  the  shift  the  greater  will  be  the  saturation  of  the 
body  fluids  with  gas  and  the  slower  should  be  therefore  the  decom- 
pressing process.  The  higher  the  pressure  is,  the  shorter  should  be  the 
shift  and  the  slower  and  more  gradual  the  emergence.  Both  the  caisson 
and  the  decompression  chamber  should  be  thoroughly  ventilated  and 
maintained  at  a  temperature  of  about  60  degrees  F.  After  decompres- 
sion the  men  should  remain  quiet  for  an  hour  or  so  and  be  recompressed 
upon  the  slightest  sign  of  sickness.  By  observing  these  precautions 
Hill  and  ^lacleod  believe  that  work  of  this  character  can  be  carried  on 
without  loss  of  life  at  a  depth  even  of  two  hundred  feet  or  about  seven 
atmospheres  or  -|-ioo  pounds'  pressure. 

When  the  disease  has  appeared  its  treatment  is  entirely  symp- 
tomatic. The  intense  pains  will  demand  the  use  of  morphine.  A.  H. 
Smith  suggests  the  use  of  ergot.  Oxygen  inhalations  and  the  use  of 
compressed  air  have  been  recommended.  The  treatment  in  other  re- 
spects differs  in  nowise  from  that  of  myelitis. 

DISEASES  OF  THE  CAUDA  EQUIXA     AXD     FILU^I     TER- 

MIXALE. 

Some  authors  devote  a  special  section  to  these  diseases,  because  of 
the  multiplicity  of  the  nerve  roots  here  closely  grouped  together.  It 
seems  to  me  that  this  is  unnecessary,  as  any  disease  that  attacks  the 
cord  above  is  liable  to  attack  the  cauda  and  filum.  Hemorrhages, 
syphilitic  and  other  neoplasms,  inflammations  and  traumatisms  are 
among  the  lesions  found  in  this  lowermost  part  of  the  spinal  canal. 
In  the  absence  of  cord  segments,  the  symptomatology  will  correspond 
with  that  of  spinal  root  disease.    The  extent  and  character  of  the  lesion 


574 


THE  NON-NEURONIC  DISEASES 


will  determine  the  extent  and  character  of  the  symptoms.  All  of  this 
is  to  be  determined  by  a  rigid  comparison  oi  the  symptoms  with  what 
we  know  of  spinal  localization.  In  a  word,  the  diagnosis  of  diseases  in 
this  part  of  the  cord  is  a  localization  diagnosis,  plus  the  special  feature 
that  the  symptoms  will  be  of  the  root  variety,  but  of  very  wide  extent 
because  involving  so  many  roots.     Bilaterality  is  a  strong  characteristic 

FIGURE  125. 


Semidiagrammatic  illustration  to  show  the  topographical  relationship  between 
the  vertebrae,  the  cauda  and  the  conus.     (After  Raymond.) 


of  the  symptomatology,  though  not  absolutely  so.  There  are  small, 
focal  lesions  here  as  elsewhere. 

The  accompanying  diagrams  from  Raymond  and  Schultze  will 
assist  better  than  any  long  description  in  making  a  localization  diag- 
nosis. 

The  prognoisis  and  results  of  operative  treatment  in  this  part  of 
the  spine  are  rather  encouraging. 

Spinal  Concussion  is  a  term  used  by  some  writers  for  a  class  of 
spinal  symptoms  caused  by  a  fall,  a  blow  or  a  general  concussion,  such 


THE  NON-NEURONIC  DISEASES 


575 


as  occurs  in  railway  accidents,  and  supposed  to  be  withottt  any  ana- 
tomical foundation.  In  my  opinion,  the  statement  "without  any  ana- 
tomical foundation"  used  by  these  authors  in  this  connection  is  a  logical 
self-contradiction  and  at  once  wipes  out  spinal  concussion  as  a  special 
and  unique  disease.    The  term  is  misleading  and  had  better  be  dropped. 


FIGURE  126. 


jy^i 


^VLE 


A  schematic  representation  of  the  vertebral  column  with  the  lower  part  of 
the  cord  and  the  cauda.  A  lesion  at  A  and  one  at  B  will  produce  pretty  nearly 
the  same  set  of  symptoms.     (After  Schultze.) 

What  is  meant  by  it  is  a  traumatic  neurosis,  for  a  consideration  of 
which  the  reader  is  referred  to  another  chapter.  Under  it  the  cases  that 
are  not  of  the  nature  of  traumatic  neurosis  are  hemorrhages  and  other 
well-known  organic  troubles  that  need  no  further  discussion  than  what 
I  have  already  devoted  to  them. 


576  THE  NON-NEURONIC  DISEASES 

PART    11. 


Non -Neuronic  Diseases  of   the  Peripheral  Nerves. 


Anatomy  and  Physiology  of  the  Nerves. — We  have  already  seen  in 
our  studies  of  the  neurone  that  the  peripheral  nerves  are  nothing-  but 
the  processes  of  cells,  collected  together  into  bundles  and  supported  and 
protected  by  certain  non-neuronic  elements.  Therefore  literally  there 
are  no  such  things  as  peripheral  nerves  in  the  sense  of  being  a  special 
structure.  They  are  mere  outgrowths,  extensions,  branches,  arms,  as  it 
were,  from  the  central  cells.  We  must  get  rid  entirely  of  the  idea  that 
the  peripheral  nervous  system  is,  as  it  used  to  be  taught  in  the  older 
anatomy,  a  network  of  conducting  fibres,  or  wires,  so  to  speak,  to  con- 
duct impulses  from  one  point  to  another.  It  is  more  than  this.  It  is 
the  outlying  part  of  the  central  nervous  system  itself,  its  own  branches 
and  integral  structure.  This  newer  conception  of  the  nature  of  the 
peripheral  nerves  is  absolutely  necessary  to  grasp,  if  one  is  to  under- 
stand their  diseases.  Many  of  the  changes  in  the  peripheral  nerves, 
as  in  many  of  the  degenerative  forms  of  peripheral  neuritis,  so-called, 
are  but  the  expression  of  trouble  in  the  cells  Oif  the  anterior  horns  of 
the  cord  and  of  the  posterior  spinal  ganglia.  A  nerve  therefore  should 
always  be  regarded  as  a  mere  part  of  the  central  apparatus  and  not  in 
the  least  as  an  independent  structure.  As  the  nerves  are  intimately 
related  to,  or  are  parts  of,  the  spinal  cord  elements,  if  we  are  to  divide 
up  the  great,  uniform  and  harmonious  nervous  apparatus  into  such 
artificial  divisions  as  the  brain,  spinal  cord  and  nerves,  it  will  be  appro- 
priate to  discuss  the  diseases  of  the  nerves  immediately  after  the  dis- 
cussion of  the  diseases  of  the  spinal  cord. 

Anatomy  speaks  of  motor  and  sensory  nerves.  We  have  already 
noted  that  this  is  somewhat  of  an  artificial  distinction  so  far  as  the  con- 
stituent neurones  are  concerned ;  for  the  motility  and  sensation  depend 
not  upon  the  neurones  per  se,  but  upon  the  end-organs  with  which  they 
are  attached. 

The  motor  nerves  are  but  the  neuraxones  of  the  neurones  whose 
bodies  are  located  in  the  anterior  horns  of  the  cord  and  motor  cranial 
nuclei.    They  are  motor  because  they  stimulate  muscles. 

The  sensory  nerves  are  merely  the  peripheral  ends  of  the  neurones 
whose  bodies  lie  in  the  posterior  spinal  root-ganglia,  or  in  the  ganglia 
(petrosal,  jugular,  geniculate,  Gasserian,  etc.)  found  on  the  roots  of  the 
sensory  cranial  nerves,  and  whose  central  ends  project  into  the  cord  and 
miedulla.  They  carry  impulses  from  the  peripheral  parts  of  the  body 
to  the  central  ganglia  and  are  thus  sensory  in  function.  When  these 
motor  and  sensory  peripheral  processes  are  bound  together  by  con- 
nective tissue,  in  which  course  the  minute  nutrient  blood-vessels  and 
lymphatics,  we  have  what  is  termed  in  gross  anatomy  a  nerve. 

A  transverse  section  of  a  nerve  then  presents  an  easily  understood 
and  typical  picture.     It  is  a  bundle  of  smaller  bundles,  which  smaller 


THE  NOX-XEUROXIC  DISEASES 


577 


bundles  are  made  up  of  the  central  cell  processes.  The  smaller  bundles, 
called  funiculi,  are  embedded  in  the  perineurium  which  forms  itself  into 
concentric  rings  or  laminas  immediately  around  each  funiculus,  but 
whose  fibres  run  in  all  directions  between  them.  Around  the  outer 
edge  of  the  nerve,  where  it  is  named  the  epiiieurium,  it  again  assumes 
the  ring-like  arrangement. 

The  perineurium  is  a  connective  tissue  structure  and  contains  the 
arteries,  veins  and  lymphatics.  It  is  therefore  that  part  of  the  nerve 
that  is  capable  of  undergoing  inflammation,  hyperplastic  new  growths 
and  other  changes  common  to  the  vascular  and  connective-tissue  ele- 
ments. The  perineurium  immediately  around  each  funiculus  sends 
septa,  endoiieurium,  in  various  directions  into  it,  which  separate  and 


—Transverse  section  of  the  sciatic  nerve  of  a  cat  about  x  loo.— It  consists  of 
bundles  [funiculi)  of  nerve-fibres  ensheathed  in  a  fibrous  supporting  capsule,  epi- 
neuriuvi,  A  ,  each  bundle  has  a  special  sheath  (not  sufficiently  marked  out  from  the 
epineunum  in  the  figure)  or  penneuiium  B  ;  the  nerve-fibres  N/are  separated  from  one 
another  by  endonenrium  ;  L,  l)-mph  spaces  ;  Ar,  arterj- ;  V,  vein  ;  F,  fat.  Somewhat 
diagrammatic.    (V.  D.  Harris.) 

support  the  nerve-fibrils,  whose  cut  ends  we  can  recognize  in  the  little 
white  circles,  with  a  dot  in  the  middle  of  each  circle.  Blood-vessels  do 
not  seem  to  penetrate  the  funiculi,  but  the  endoneurium  as  well  as  the 
perineurium  contains  lymphatic  tracts  by  which  the  fibrils  are  nour- 
ished. When  a  nerve  sends  off  branches  to  unite  with  other  nerves  it 
is  a  funiculus  that  leaves  the  main  trunk.  The  funiculi  do  not  anasto- 
mose with  each  other  in  the  same  nerve  trunk,  nor  do  the  branching 
fibrils  emerge  from  the  funiculi  until  they  have  reached  their  destina- 
tion. 

In  its  last  analysis,  a  nerve  fibril  is  seen  to  consist  of  an  axis  cylin- 
der sitrronnded  by  the  nieduUary  zvhite  substance  of  Schnjann  and  the 
neurilemma.  The  axis  cylinder  consists  of  numerous  minute  strands 
running  along  side  by  side  and  representing  the  extension  of  the  intra- 
cellular fibrous  elements  of  the  neurone.  The  medullary  substance  is 
.seen  to  be  absent  or  almost  absent  at  various  regular  intervals  along  the 
-course  of  the  fibrils,  so  that  the  neurilemma  is  constricted  and  sinks 


D/ 


78 


THE  XOX-NEUROXIC   DISEASES 


down  close  to  the  axis-cylinder.     These  constrictions  in  the  fibril  are 
known  as  the  nodes  of  Ranvier.     It  is  supposed  that  the  nutrient  sub- 

FIGURE  129. 


FIGURE  128. 


— Anodeof  Ran- 
vier  in  a  medullated 
nerve  -  fibre,  \'iewed 
from  above.  The  me- 
dullary sheath  is  inter- 
rupted, and  the  primi- 
tive sheath  thickened. 
Copied  from  Axel  Key 
and  Retzius.  x  750. 
( Klein  &  Noble  Smith  ) 


-Nerve- 
flbre  stained 
■with  osmic 
acid.  &-,  node ; 
B,  nucleus. 
( Key  and  Ret- 
zius.) 


stance  enters  the  fibril  here.    At  all  events  it  is  always  at  tlie  nodes  that 
the  branches  are  eiven  ofit  bv  the  fibril.     In  the  white  medullary  sub- 


THE  NON-NLURONIC  DISEASES 


579 


stance  are  to  be  seen  numerous  minute  oblique  lines.  These  are  called 
Lanterniann's  incis^ires.  They  probably  represent  breaks  caused  by  the 
handling  of  the  nerve.  About  midway  in  each  inter-nodal  space,  and 
just  beneath  the  neurilemma,  is  a  nucleus.  Non-medullated  fibrils  are 
found  in  the  olfactory  and  sympathetic  nerves.  The  neurilemma  is  not 
found  on  the  neuraxones  making  up  the  white  substance  of  the  brain 
and  cord. 

There  is  nothing  to  be  said  of  rhe  physiology  of  the  nerves  beyond 
what  has  been  said  of  the  physiology  of  the  neurones. 

General  Pathology  of  the  Peripheral  Ner^'cs. — It  is  clear  from 
their  anatomical  structure  that  the  nerves,  like  all  Darts  of  the  nervous 


FIGURE  130. 


FIGURE  131. 


— Two  nerve-fibres  of 
sciatic  nerve,  a.  Node  of 
Ranvier.  b.  Axis-cylinder, 
c.  Sheath  of  Schwann,  with 
nuclei.  Medullary  sheath  is 
not  stained,  x  joo.  (Klein 
and  Noble  Smith  ) 


-Axis 
cylinder,  high- 
ly magnifled, 
showing  its 
component 
fibrils. 
(M.  Schultze.) 


system,  may  undergo  both  the  degenerative  and  the  inflavmnatory 
process.  The  former  used  to  be  called  parenchymatous  inflammation. 
In  our  previous  study  of  the  degeneration  and  regeneration  of  ■  the 
neurone  we  noted  that  it  was  not  an  inflammatory  process  at  all.  The 
latter  is  still  correctly  referred  to  as  an  interstitial  inflammation,  for  it 
is  a  true  inflammatory  process  and  involves  the  interstitial  connective 
tissue  and  its  vascular  contents.  When  this  interstitial  tissue  becomes- 
overgrown  the  nerve  fibrillse  are  compressed  and  more  or  less  degener- 
ated ;  the  nerve  becomes  hard ;  and  the  whole  condition  takes  the  name 
of  sclerosis.  The  degeneration  thus  caused  in  the  true  nerve-fibrils  is  a 
secondary  phenomenon. 

It  is  still  an  open  question  whether  a  primary  degeneration  ever 
takes  place  in  these  peripheral  nerve  fibrils  that  is  not  dependent  upon 
trouble  in  the  cell-bodies  and  their  nutrition.     In  certain   toxic  states 


580  THE  NON-NEURONIC  DISEASES 

we  often  find  the  peripheral  nerve  fibrils  wasted,  but  no  discoverable 
signs  of  inflammation  to  enable  us  to  say  the  degeneration  was  sec- 
ondary, nor  discoverable  changes  of  a  positive  character  in  the  related 
cell-bodies.  The  degeneration  under  such  circumstances  appears  to  be 
purely  primary.  Some  investigators  hold  that  the  toxin  has  directly 
damaged  the  peripheral  nerve-endings.  They  are  few,  however.  Oth- 
ers rnaintain  that  it  has  afitected  the  nutritive  function  of  the  central 
cells  and  so  caused  the  degeneration  in  these  remote  parts  of  the  neu- 
rones. When  the  damage  to  the  central  cells  is  obvious  and  mechanical, 
the  resulting  deterioration  in  the  peripheral  nerve  -filaments  is  not  a 
secondary  degeneration.  It  is  but  a  part  of  the  degenerative  process  in 
the  whole  neurone. 

In  primary  degeneration  I  assume  then  that  the  entire  neurone  is 
afifected ;  that  through  hereditary  or  other  influences  the  cell-body  has 
lost  its  power  of  keeping  up  the  nutrition  of  the  processes,  and  as  a 
result  the  latter  waste.  The  peripheral  degenerations  observed  in  many 
hereditary  diseases  and  in  many  toxic  and  infectious  states  are  un- 
doubtedly of  this  character.  Certain  cachectic  states  in  which  there  is 
especially  disturbed  nutrition,  thus  exhibit  peripheral  nerve  degenera- 
tion. Diabetes  is  an  example.  Defective  metabolism  associated  with 
lithsemic,  anaemic  and  autointoxic  conditions  may  be  accompanied  by 
the  parenchymatous  wasting  in  the  nerves. 

In  all  of  these  conditions  it  seems  to  me  very  essential  that  we 
should  regard  the  peripheral  degeneration  as  a  mere  expression  of 
a  disturbance  in  the  nutritive  function  of  the  central  cell-bodies,  and 
that  this  disturbance  is  the  result  of  a  much  larger  and  more  generalized 
disease  process.  In  this  sense  primary  degenerative  processes,  pure 
neuronic  disease,  in  the  peripheral  nerves,  is  never  any  thing  more  than 
a  collateral  exhibition  in  another  and  more  distinct  disease.  I  empha- 
size this  fact  because  upon  it  hang  the  prognosis  and  treatment  of  these 
peripheral  degenerative  manifestations  that  seem  to  be  primary.  I 
emphasize  it  also  because  it  will  serve  to  stimulate  the  practitioner  to 
always  look  further  than  the  nerves,  when  these  are  primarily  de- 
generated, for  a  more  profound  and  widespread  disease  involving  the 
entire  organism.  The  majority  of  the  cases  of  toxic  polyneuritis  serve 
as  apt  illustrations  of  my  point. 

The  secondary  degenerations,  similar  to  the  Wallerian  degenera- 
tion that  sometimes  occurs  in  the  peripheral  nerves,  result  from  trau- 
matic causes  that  compress,  lacerate  or  sever  the  neurones,  so  that 
parts  of  them  are  separated  from  their  nutritive  cell-bodies.  In  this 
condition  the  distal  or  severed  end  of  the  neurone  undergoes  complete 
disappearance;  the  proximal  end  passes  through  a  much  slower,  in- 
complete and  at  times  scarcely  noticeable  retroactive  degenerative 
process.  It  is  presumed  that  here  the  whole  neurone  has  been  put  out 
of  service  by  the  injur}  and  that  even  the  cellular  end  misses  the  normal 
stimulus  ncessary  to  keep  it  up  to  its  normal  nutritive  tone.  As  in  all 
of  these  traumatic  or  secondary  degenerations,  the  inflammatory  phe- 
nomenon sooner  or  later  makes  its  presence  known,  I  will  refer  to  them 
under  the  general  head  of  neuritis. 


THE  XON-NEURONIC  DISEASES  58i 

NEURITIS. 

An  inilammation  in  a  nerve  begins,  of  course,  in  the  interstitial  or 
non-neuronic  tissues.  The  nerve  fibrillse  are  damaged  secondarily.  It 
may  well  be  that  the  cause,  compression  for  instance,  may  be  just 
sufficient  to  initiate  the  degenerative  process  in  the  fibrillse  before  the 
inflammatory  process  in  the  interstitial  tissue  has  gotten  well  under 
way.  Under  such  circumstances  the  degeneration  would  be  regarded 
as  secondary,  but  not  due  to  an  associated  inflammatory  process.  The 
distinction  is  not  an  important  one,  however,  since  it  merely  means  that 
degeneration  is  quicker  to  occur  than  inflammation  in  the  presence  of 
the  same  active  cause. .  As  sooner  or  later  in  all  such  cases  inflamma- 
tion does  appear,  it  is  convenient  and  not  illogical  to  consider  the  two 
processes,  inflammation  and  secondary  degeneration,  together. 

When  the  inflammatory  process  originates  in  and  remains  con- 
fined to  the  perineurium,  the  disease  is  called  perineuritis.  If  the  in- 
terstitial tissue  is  the  seat  of  the  trouble,  it  is  known  as  interstitial 
neuritis.  The  parenchymatous  neuritis  of  the  older  writers  is  a  misno- 
mer, for,  as  I  have  shown,  it  is  not  inflammatory  at  all.  It  is  a  neural 
degeneration  and  exhibits  all  the  changes  seen  in  a  secondary  or  Wal- 
lerian  degeneration.  It  must  be  frankly  admitted  that  these  refinements 
of  classification  are  of  more  pathological  than  clinical  interest.  We 
very  rarely  have  a  pure  interstitial  neuritis  without  secondary  degenera- 
tion, or  a  secondary  traumatic  degeneration  without  an  accompanying 
inflammation.  Practically  all  cases  exhibit  the  same  symptoms.  It  is 
unfortunate  that  we  cannot  better  distinguish  the  degenerative  from 
the  inflammatory  trouble  by  the  respective  symptoms,  for  the  prognosis 
of  the  case  could  be  much  more  positively  affirmed  then.  According  to 
the  relative  amount  and  degree  of  the  degeneration  and  inflammation, 
so  would  the  outlook  of  the  case  be  bad  or  good. 

Etiology. — The  causes  of  inflammation  in  a  nerve  are  innumer- 
able. As  a  rule  they  can  be  classified  under  the  three  heads  trauma, 
intoxication  and  infection. 

The  traumatic  causes  include  all  factors  by  which  the  nerve  is 
compressed,  cut,  torn,  stretched  or  otherwise  mechanically  maltreated. 
Obviously  these  causes  may  be  severe  or  slight,  limited  or  of  wide 
extent,  mediate  or  immediate.  They  m.ay  be  rendered  more  destructive 
than  they  otherwise  would  be  by  a  predisposing  weakness  caused  by 
alcoholism,  infection  or  other  factor  in  the  patient.  To  mention  all  of 
the  ways  a  nerve  may  be  compressed  or  lacerated  would  require  a 
small-sized  volume  in  itself.  The  nerves  are  exposed  structures  and 
therefore  blows  and  contusions  can  easily  reach  them.  So-called  crutch- 
palsy,  craft-paralysis,  drunkard's  paralysis  caused  by  sleeping  with  the 
arm  in  a  strained  position  under  the  head,  are  all  due  to  pressure 
neuritis.  Cuts  and  knife  wounds  are  traumatic.  Mechanical  irritants 
like  excessive  electric  shocks,  violent  massage,  direct  blows  near  the 
nerve  may  easily  cause  it  to  become  inflamed,  especially  in  those  pre- 
disposed by  general  debility.  Inflamed  swollen  joints,  neighboring 
tumors,  exostoses,  dislocated  and  fractured  bones  are  not  infrequent 
causes.     Tight  bandages,  excessive  pressure  in  reducing  a  luxation, 


582  THE  KOX-XEUROXIC  DISEASES 

wrenches,  twists  and  nerve  stretching  of  all  sorts  are  to  be  reckoned 
with  etiologically.  Extremes  of  temperature  are  a  prolific  source,  es- 
peciall}'  when  there  is  an  underlying  diathesis.  In  this  way  cold  is  a 
common  cause  of  facial  neuritis.  Sometimes  two  or  more  causes  act 
together.  Sciatic  neuritis  may  be  due  to  the  cold  and  pressure  experi- 
enced in  going  to  stool  under  special  conditions.  Corroding  substances, 
acids,  burns,  scars  and  cicatricial  compression  are  of  the  nature  of 
traumata.  Strains  from  overuse  are  often  given  credit  for  lighting  up 
a  neuritis,  but  they  are  hardly  efficient  as  causes  without  the  presence 
of  an  infection  or  vitiated  state  of  the  constitution.  They  are  more  of 
the  nature  of  exciting  causes.  I  have  seen  a  neuritis  start  from  lifting  a 
child  suddenly  by  one  arm.  Birth  palsies,  especially  those  that  occur 
from  instrumental  delivery  and  abnormal  presentations,  are  usually 
neuritic.  Xon-purulent  ascending  neuritis  used  toi  be  much  talked  of 
by  the  elder  pathologists.  Nowadays  it  is  scarcely  believed  to  occur. 
Only  the  purulent  form  really  ascends  a  nerve.  Neuritis  may  be  caused 
by  puncture  of  the  nerve  with  a  hypodermic  needle,  or  the  introduction 
of  irritants  like  ether,  perosmic  acid,  chloroform,  etc.  This  explains 
undoubtedly  the  results  sometimes  obtained  by  the  injection  of  osmic 
acid  in  neuralgic  nerves  and  especially  in  tic  douloureux. 

These  traumatic  causes  are  especially  prolific  of  the  localized  forms 
of  neuritis.  Ofttimcs  they  are  never  anvthing  more  tha^n  mere  excit- 
ing causes. 

The  intoxiccDits  are  very  significant  factors  in  the  production  of 
neuritis.  These  and  the  infections  give  rise  to  generalized  rather  more 
frequently  than  localized  neuritis.  In  fact,  without  a  determining  local 
insult  of  some  sort  they  may  almost  be  said  to  never  produce  a  neuritis 
in  a  single  nerve.  An  infectious  process,  like  an  abscess  or  a  tuber- 
culous gland,  a  cancer  or  a  syphilitic  patch,  may  light  up  the  inflamma- 
tion in  a  neighboring  nerve.  xA.lcohol,  lead,  arsenic  and  other  metallic 
poisons,  carbonic  acid,  carbon  disulphide,  ptomaines,  nicotine,  are  all 
to  be  blamed  sometimes  for  neuritis. 

The  infections  that  have  preceded  the  malady  are  diphtheria,  vari- 
ola, typhoid,  tuberculosis,  influenza,  scarlet  fever,  etc.  I  have  seen 
syphilitic  peripheral  neuritis  of  the  multiple  type,  though  many  doubt 
its  ex;istence  and  attribute  it  to  the  use  of  mercury.  Syphilitic  neuritis 
of  the  spinal  and  cranial  nerve-roots  is  by  no  means  a  great  rarity. 
Puerperal  neuritis  is  infectious  in  origin.  Leprous  neuritis  and  the 
endemic  forms  known  as  beri-beri,  akatama,  etc..  are  to  be  mentioned 
here. 

In  many  cachectic  and  constitutional  states,  like  rheumatism,  gout, 
diabetes,  leukemia,  arteriosclerosis,  malnutrition  and  autointoxication 
undoubtedly  are  the  immediate,  noxious  factors.  Arteritis  obliterans 
acts  largely  in  the  same  way,  but  more  locally. 

It  is  hardly  necessary,  after  what  I  have  said  in  regard  to  the 
infections  and  their  importance  both  as  predisposing  and  exciting  causes 
of  neuritis,  to  mention  suppurative  processes,  nearby  or  remote  from 
the  nerve. 

Pathology  and  Pathogenesis. — The  whole  subject  of  the  pathol- 
ogy of  neuritis  has  been,  up  to  the  present  time,  in  a  sta/te  of  chaos. 


THE  XUX-XEUROXIC  DISEASES  583 

This  was  the  natural  resuh  of  the  clinical  study  of  these  diseases  pre- 
ceding the  pathological.  It  must  be  frankly  granted  that  clinically  all 
forms  of  ner\-e  inflammation  and  degeneration  are  practically  about 
the  same.  The  two  conditions  are  not  only  almost  always  found  to- 
gether, but  symptomatica!!}-  they  cannot  be  well  distinguished  apart. 
When,  however,  we  leave  the  clinical  side  of  the  question  and  take  up 
the  pathological,  the  distinctions  are  so  sharp  and  so  clean-cut  that  I 
believe  much  of  the  confusion  can  be  banished  by  attempting  a  positive 
classification  of  the  disease  on  a  purely  pathological  basis. 

Xeuronic  and  non-neuronic  processes  underlie  the  pathology  of 
neuritis.  The  former  are  degenerative,  the  latter  are  inflamynatory. 
In  some  conditions  the  former  may  appear  alone.  It  is  then  a  primarv 
degeneration  and  has  been  unfortunately  and  erroneously  called  paren- 
chymatous or  degenerative  neuritis.  As  I  have  shown,  it  is  not  a  neu- 
ritis at  all  and  should  be  banished  entirely  from,  consideration  under  this 
head.  It  is  a  rare  condition  and  is  merely  another  manifestation  of  a 
much  more  extensive  condition.     It  may  be  seen  in  locomotor  ataxia. 

The  much  more  common  form  of  neuritic  degeneration  is  the 
secondary.  A  consideration  of  this  is  strictly  in  place  here.  It  is  a  local 
trouble,  is  due  to  extra-neuronic  factors,  and  is  always  a  companion 
of  the  inflammatory  process,  though  it  mav  sometimes  precede,  some- 
times follow  the  latter. 

These  two,  inflammation  and  secondary  degeneration,  go  hand  in 
hand ;  sometimes  one,  sometimes  the  other  leading.  At  times  the  de- 
generation is  so  slight  or  the  cause  of  it  is  so  evanscent  that  the  neu- 
rones recover  before  the  interstitial  inflammatory  phenomena  have  got- 
ten a  fair  start.  Under  such  circumstances  recovery  takes  place,  and 
the  disease  has  all  the  appearance  of  having  been  a  temporary  form 
of  primar}-  degeneration.  Such  are  some  of  the  degenerative  poly- 
neuritides,  some  of  the  types  of  Landry's  paralysis,  some  of  the  severe 
infective  troubles  that  quickly  end  in  death  or  recovery  before  either 
degeneration  or  inflammation  has  gotten  sufficient  of  a  start  to  produce 
gross,  discoverable  changes.  Doubtless  the  character  of  the  infection 
and  the  neuropathic  state  of  the  patient  determine  to  a  large  extent 
the  predominence  of  the  degenerative  or  inflammatory  process  in  this 
tw4n-like  pathological  development.  In  many  cases  the  inflammatory 
process  is  so  violent,  the  disease  is  most  emphatically  a  neuritis  with 
all  the  symptoms  of  an  inflammation,  the  degeneration  coming  along  as 
a  later  and  slower  process. 

Thus  there  are  not  many  types  of  neuritis  as  authors  declare. 
There  is  only  one  neuritis  in  which  there  is  a  variable,  double  process 
going  on.  It  is  simply  confusing  to  talk  about  perineuritis,  interstitial 
neuritis,  parenchymatous  neuritis,  periaxile  segmentary  neuritis,  dis- 
seminated nodal  neuritis.  One  might  as  well  talk  about  motor  neuritis, 
sensory  neuritis,  neuritis  with  fever,  neuritis  without  fever,  cranial 
neuritis  and  podalic  neuritis.  Medicine  is  too  full  of  such  artificial  and 
useless  refinements  of  classification.  As  I  have  urged  before,  it  is  the 
aim  and  goal  of  science  to  combine  and  generalize  a  multiplicity  of  facts, 
not  to  break  what  is  already  plainly  combined,  into  a  multiplicitv  of 
fragments.      Primarv  degeneration  being  banished  entirelv  from   the 


584 


THE  NON-NEURONIC  DISEASES 


neuritides,  all  of  the  other  forms  are  but  phases  of  the  one  combined 
inflammatory  degenerative  pathological  process  which  for  want  of  a 
better  name  we  call  neuritis. 

The  ififlamuiatory  side  of  the  neuritic  picture  does  not  require  any- 
lengthy  description.  There  is  hypersemia,  proliferation  of  the  blood- 
vessels, extravasation  of  blood,  leucocytosis,  swelling,  oedema  and  all 
the  usual  signs  of  an  inflammation  anywhere.     The  swelling  does  not 

FIGURE  132. 


t 


—Degeneration  and  regeneration  of  nerve-fibres,  a^  nerve-fibre,  fifty  bours  after 
operation,  m  y,  medullary  sheath  breaking  up  into  myelin  drops,  p,  granular  proto- 
plasm replacing  myelin,  n,  nucleus,  j,  primitive  sheath,  b,  nerve-fibre  af tCT  f our 
days,  cy,  axis  cylinder  partly  broken  up  and  qnclosed  in  portions  of  myelin,  c,  a  more 
advanced  stagf  in  •which  the  medullary  sheath  has  almost  disapi)eared.  Numerous 
nuclei,  n"  are  seen,  d,  commencing.regeneration  ;  several  fibres  {tf,  i')  have  sprouted 
from  the  somewhat  bulbous  cut  end  (6)  of  the  nerve,  a,  an  axis  cylinder  which  has 
not  yet  acquired  its  medullary  sheath,  i,  «'. primitive  sheath  Qf  the  original  fibre. 
'Ranvier.) 

appear  uniformly  along  the  whole  course,  or  even  a  long  extent,  of  the 
nerve.  It  appears  more  prominently  in  foci  or  spots.  These  are  prob- 
ably the  explanation  of  the  tender  points  of  Valleix  seen  in  many  cases 
of  so-called  neuralgia.  Sometimes  in  these  spots  an  exudate  appears 
in  abundance  and  later  on  a  proliferation  of  the  connective  tissue,  af- 
fording ground  for  the  name  disseminated  nodal  neuritis. 

As  neurologists  we  are  more  interested  in  the  degenerative  side  of 
this  neuritic  process  than  we  are  in  the  inflammatory.  This  is  always 
of  the  secondary  or  Wallerian  type  of  degeneration.  It  means  that  the 
nerve  fibrils  have  been  more  or  less  severed  from  their  nutrient  centers. 


THE  XOX-XEUROXIC  DISEASES 


0°^ 


I  have  described  this  process  elsewhere.  The  medullary  white  substance 
of  Schwann  on  the  distal  side  of  the  lesion,  breaks  down  into  fat 
globules,  is  reabsorbed  and  leaves  nothing  but  the  axis-cylinder  and 
the  neurilemma.  The  neuclei  of  the  latter  proliferate.  The  axis-cylin- 
der swells  up,  liquifies  and  breaks  down  into  fragments.  Gradually 
these  are  absorbed  so  that  nothing  is  left  but  the  neurilemma  in  the 
shape  of  a  hollow  tube  filled  with  liquid  matter  and  nuclei.  Ranvier 
regards  the  nuclear  proliferation  as  the  primary  part  of  the  process,  and 
the  breaking  up  of  the  myelin -sheath  as  the  result  of  it.  Alterations 
take  place  simultaneously  in  the  epineurium  and  perineurium,  so  that 
the  nerve  becomes  smaller  and  harder,  in  fact  sclerosed.  The  termina- 
tions of  the  nerve  in  the  muscles  and  the  end-plates  ail  participate  in 
the  degeneration.  Forty-eight  hours  witnesses  these  changes  and  at 
the  end  of  a  couple  of  weeks  they  are  complete.  The  cut  end  of  the 
nerve  shows  the  absence  of  the  fibres  and  the  hyperplasia  of  the  con- 
nective tissue. 

The  muscles  innerv^ated  by  the  damaged  nerve  also  degenerate. 
The  fibres  diminish,  lose  their  striations,  become  granular  or  waxy. 
There  is  proliferation  of  the  sarcolemma  and  the  internal  perimysium. 
Finally  the  whole  muscle  atrophies  and  becomes  fibrous  or  cirrhotic. 

The  nerve  on  the  proximal  side  of  the  point  of  severance  or  lesion 
undergoes  the  change  known  as  the  reaction  a  distance.  This  is  a  de- 
generation of  a  slower  and  less  complete  type,  probably  due  to  the  ab- 
sence of  normal  stimuli. 

The  course  of  the  degeneration  follows  the  well-known  \A'allerian 
laws.  Thus  if  the  posterior  spinal  nerve  root  be  cut  between  the 
ganglion  and  the  cord,  the  degeneration  occurs  in  the  end  attached  to 
the  cord  and  passes  even  into  the  cord.  The  end  attached  to  the 
ganglion  remains  intact.  Motor  nerv^es  and  the  anterior  nerve  roots, 
when  cut,  degenerate  downward  in  their  distal  parts.  The  spinal  at- 
tachment does  not  degenerate. 

The  regeneration  of  a  nerve  is  a  most  interesting  and  important 
process.  It  can  only  take  place  when  the  degeneration  has  not  gone 
on  to  coiBpletion.  In  some  compression  neuritis  degeneration  of  a 
partial  character  and  regeneration  undoubtedly  take  place  with  great 
rapidity,  so  that  profound  symptoms  are  often  seen  to  quickly  appear 
and  disappear.  In  a  severed  nerve  that  has  been  sutured  the  process 
of  neurolization  takes  place,  though  it  is  denied  by  some.  It  consists  of 
a  growing  forward  of  the  axis  cylinder  from  the  central  stump  into  the 
severed  end.  If  the  nerve  fibrillae  are  given  a  bridge  of  decalcified 
osseous  matter  or  a  fine  bundle  of  catgut  over  the  lesion,  they  will  ad- 
vance all  the  more  rapidly  and  completely.  In  this  the}-  resemble  the 
advancing  branches  of  a  growing  vmt.  Months  and  years  are  some- 
times required  for  the  regenerative  process. 

Symptoms. — When  a  nerve  is  damaged  there  will  be  motor, 
sensory,  trophic,  reflex,  electrical,  vasomotor  and  secretory  disturbances. 
The  character  of  these  and  the  degree  of  their  severity  will  var}-  in 
accordance  with  the  complete  or  partial  character  of  the  damage  done. 
There  are  early  signs  of  irritation,  followed  by  those  of  more  or  less 
complete  paralysis.    It  cannot  be  too  strongly  impressed  upon  the  mem- 


586  THE  NON-NEURONIC  DISEASES 

orv  that  nen^e  lesions  show  signs  of  irritation  and  paralysis,  in  all 
functions,  in  the  areas  particularly  innervated  by  the  nerve  involved. 

The  motor  symptoms  are  spasms  and  tzvitchhigs  in  particular  mus- 
cles or  muscle  groups,  followed  by  a  flaccid  paralysis  more  or  less  pro- 
found. It  is  soon  followed  by  the  loss  of  reflex  response,  the  electrical 
reaction  of  degeneration  and  atrophy. 

The  early  symptoms  in  the  sensory  sphere  are  parccsthesice  of  vari- 
ous sorts.  There  are  numbness,  tingling,  pins-and-needles  sensation, 
sense  of  heat,  ants  crawling  on  the  skin  or  formication.  Soon  pains 
occur  both  along  the  course  O'f  the  nerve,  especially  ripon  pressure,  and 
in  its  peripheral  distribution.  On  account  of  the  pressure  on  the  nervi 
nervorum  the  pains  seem  to  shoot  here  and  there  along  the  course  of 
the  nerve.  The  skin  becomes  hypercesthetic.  Late  in  the  disease  it  be- 
comes hypcesthetic,  rarely  anaesthetic.  A  curious  and  almost  path- 
ognomic feature  about  the  sensations  is  that  they  are  in  spots  and  that 
hypsesthetic  areas  will  be  intermingled  with  hypersesthetic  areas.  The 
sensory  and  motor  disturbances  attack  correspoinding  parts,  showing 
thus  the  limitation  of  the  disease  process  to  particular  nerves.  In  neu- 
ralgias, so-called,  O'ften  the  neuritic  character  of  the  disease  is  shown 
by  the  local  tenderness,  the  painful  swellings  w'hich  can  be  felt  by 
palpation  and  which  are  probably  identical  with  Valleix's  tender  points, 
and  by  the  special  tenderness  of  the  nerve  where  it  passes  over  bony 
prominences. 

The  trophic  disorders  of  neuritis  include  a  glistening  of  the  skin, 
herpetiform  eruptions,  pemphigus,  gangrene,  formation  of  slow  healing 
sores,  changes  in  the  bone,  subcutaneous  tissues,  hair,  nails,  etc. 

The  vasomotor  and  secretory  troubles  are  local  hyperasmia  or 
cyanosis,  with  corresponding  change  of  temperature,  oedema,  hyperi- 
drosis. 

Fever  and  chills  sometimes  occur  early. 

Diagnosis. — The  chief  signs  of  neuritis,  whether  it  be  prominently 
degenerative  or  inflammatory,  is  the  gradual  break  in  all  functions  in 
the  parts  supplied  by  the  particular  nerves.  Especially  significant,  how- 
ever, are  the  early  irritative  signs,  such  as  spasms,  tonic  contraction.s. 
sharp  pains  and  parcrsthesia,  followed  by  flaccid,  atrophic  paralysis, 
with  loss  of  reflexes  and  reaction  of  degeneration.  One  can  hardly 
make  an  error  of  diagnosis  if  he  is  careful  to  get  all  of  these  sym.ptoms 
and  view  the  picture  formed  by  them  in  toto.  It  points  distinctly  to  a 
lesion  of  a  mixed  nerve. 

The  differential  diagnosis  of  neuritis  from  neuralgia  and  from  con- 
ditions in  which  it  occurs  as  a  side  issue,  will  be  taken  up  more  con- 
veniently in  the  discussion  of  these  other  diseases. 

Prognosis. — Except  in  the  mildest  cases  of  compression,  when 
recovery  may  take  place  in  a  few  days  or  weeks,  the  course  of  neuritis 
is  usually  a  prolonged  one,  six  months  or  a  year  at  least  being  its  aver- 
age duration.  The  prognosis  depends  upon  many  factors.  When  the 
disease  occurs  in  an  alcoholic  or  a  victim  of  lead  intoxication,  infection 
or  other  general  cachexia,  it  is  apt  to  be  severe  and  last  long,  though 
the  exciting  cause  may  seem  to  have  been  insignificant.  The  virulence 
and  character  of  the  toxin  in  the  toxico-infectious  cases  determines  the 


THE  XOX-XFUROXIC  DISEASES  587 

prognosis.  Some  toxins  seem  to  light  up  a  violent  inflammatory  condi- 
tion, which  soon  subsides  upon  the  removal  of  the  cause ;  other  toxins 
provoke  a  more  gradual  degenerative  state  with  a  mild  degree  of  asso- 
ciated inflammation,  which  becomes  chronic  and  even  leaves  a  perma- 
nent defect.  \\'hen  the  nerve  is  completely  severed  the  restitution  does 
not  occur  for  months  and  sometimes  not  at  all  vmless  the  stumips  are 
sutured  together. 

Cases  in  which  it  used  to  be  thought  that  the  neuritis  ascended  into 
the  cord  are  very  doubtful.  Most  of  them  have  been  toxic  cases  and 
the  degeneration  has  been  rather  of  the  primary  type  with  the  nutritive 
functions  of  the  central  cells  damaged  by  the  general  toxemia. 

The  prognosis  can  usually  be  based  upon  the  electrical  phenomena. 
If  the  reaction  of  degeneration  is  slight,  recovery  may  be  expected  early. 
If  the  reaction  of  degeneration  is  complete,  the  course  of  the  disease 
will  undoubtedly  be  prolonged,  and  perhaps  there  will  be  some  perma- 
nent defect  left  in  the  function  of  the  nerve.  Death  does  not  occur  from 
neuritis,  unless  the  nerves  involving  the  heart  and  respiration  are  af- 
fected. Pennanent  annoying  parsesthesiae,  pareses.  trophic  manifesta- 
tions need  not  cause  surprise,  though  they  cannot  be  said  to  be  common. 
Rheumatic  and  acute  infectious  cases  offer,  as  a  rule,  the  most  hopeful 
outlook. 

Treatment. — The  cause,  if  it  can  be  discovered,  must  be  removed 
promptly  and  thoroughly  before  any  treatment  is  instituted.  In  the 
majority  of  the  cases  practically  this,  and  putting  the  limb  at  rest,  are 
all  that  will  be  necessary.  In  removing  the  cause  both  medicinal  and 
surgical  resources  may  have  to  be  called  upon.  Diatheses,  such  as 
Theumatism,  tuberculosis,  malaria,  s\philis,  must  be  combated  in  the 
usual  way.  Abscesses  must  be  drained ;  cancerous  foci  must  be  re- 
moved ;  diseased  glands  must  be  cut  away.  It  hardly  needs  to  be  said 
that  alcohol,  lead,  arsenic  and  other  poisons  must  be  stopped  and  rapid- 
ly eliminated  from  the  system.  Luxations  and  subluxations,  fractures, 
■exostoses,  cicatrices,  compressing  tumors  may  all  have  to  be  removed 
before  anything  can  be  done  with  the  inflamed  nerve. 

If  the  nerve  has  been  severed  through  an  open  wound,  the  wound 
should  be  enlarged,  if  necessary,  and  the  ends  of  the  nerve  approximated 
promptly  by  sutures.  Primary  suturing  has  given  some  excellent  re- 
sults and  prevented  paralyses  and  other  troubles.  For  the  details  of 
ner\^e  suturing  works  upon  surgerv^  should  be  consulted. 

The  cause  having  been  attacked  as  completely  as  possible,  an  anti- 
phlogistic treatment  may  be  in  order.  Often,  however,  simple  rest  and 
quiet  is  all  that  is  necessary.  In  the  violently  inflamed  cases  cathartics, 
aconite,  general  diaphoresis  with  wet  packs,  and  hot  baths  may  all  be 
thought  of.  Locally  leeches,  hot  sand  bath,  hot  compresses  and  later  on 
inunctions  of  gray  ointment,  the  use  of  vesicants  and  light  touches  with 
the  Paquelin  cautery  are  valuable.  In  the  degenerative  cases  the  anti- 
phlogistic methods  need  not  be  so  vigorous.  Rest  and  antispecific  medi- 
cation is  about  all  they  require. 

There  is  probably  no  class  of  troubles  more  than  the  neuritides  in 
which  the  doctrine  of  laissez-faire  produces  its  happiest  results.  I  am 
convinced  that  had  electricity  never  been  introduced  into  therapeutics, 


588  THE  NON-NEURONIC  DISEASES 

more  cases  of  neuritis  would  have  gotten  well.  It  is  a  curious  fact  how 
electrical  treatment  is  at  once  thought  of  the  moment  the  diagnosis 
of  neuritis  is  made.  It  would  seem  that  some  have  the  idea  that  elec- 
tricity is  a  sort  of  a  beneficent  angel  for  all  diseased  nerves.  Only  let 
it  once  get  at  the  nerve  and  recovery  will  be  sure  to  take  place.  As  an 
actual  fact  electricity  has  been  the  bane  of  diseased  nerves,  for  in  being- 
used  too  early  and  in  all  cases  alike,  it  has  simply  rasped  and  irritated 
them  and  increased  the  trouble  tenfold.  I  have  frequently  seen  a  case 
of  neuritis  slowly  but  surely  recovering  suddenly  sent  into  a  severe 
relapse  because  the  attendant  labored  under  the  delusion  that  a  diseased 
nerve  was  the  golden  opportunity  for  him  to  flourish  forth  his  electrical 
paraphernalia.  The  more  my  observation  enlarges  the  more  I  am 
convinced  that  few  and  far  between  are  the  occasions  when  the  electrical 
treatment  of  neuritis  is  called  for.  If  it  can  be  absolutely  determined 
that  the  disease  is  prominently  of  the  degenerative  type,  and  that  there 
is  no  inflammatory  action  going  on — a  condition  which  it  is  almost  im- 
possible to  determine — electrical  treatment  with  galvanism  may  and 
does  prove  of  much  avail.  Such  a  condition  does  occur  very  late  in  the 
violently  inflamed  cases,  and  earlier  in  the  mildly  inflamed.  Hence  it  is 
absolutely  imperative  that  electrical  treatment  should  be  postponed  until 
all  signs  of  inflammation  are  gone.  In  this  stage  of  the  disease  elec- 
tricity and  massage  are  of  invaluable  service.  'Hie  kind  of  electricity  to 
be  employed  will  depend  upon  the  site  of  its  application  and  the  degree 
of  degenerative  reaction  present.  Galvanism  is  to  be  used  upon  the 
nerves,  faradism  upon  the  muscles.  If  there  is  much  degeneration  pres- 
ent, the  reaction  of  it  may  be  so  pronounced  that  neither  the  galvanic 
nor  faradic  current  will  awaken  a  response.  This  is,  however,  rarely 
the  case.  More  frequently  a  partial  reaction  is  present.  Under  such- 
circumstances  the  faradic  response  may  be  wanting  and  only  the  gal- 
vanic be  present.  In  using  the  galvanic  current  the  anode  may  be 
placed  upon  the  plexus  or  sternum,  and  the  cathode  upon  the  points- 
indicated  in  Erb's  diagrams  in  the  chapter  on  electrotherapeutics.  A 
stabile  current  is  to  be  used  and  its  strength  should  average  about  five^ 
ten  or  fifteen  milliamperes.  Labile  galvanic  stimulation  of  the  muscles 
may  be  added  to  the  treatment.  Faradic  stimulation  is  to  be  used  as 
soon  as  the  faradic  irritability  returns.  It  is  never  to  be  used  if  there  is- 
the  slightest  sign  of  inflammation  present.  It  is  positively  dangerous  in 
the  early  stages  of  the  disease.  Later  on  it  is  more  beneficial.  Even 
static  electrization  is  good  in  the  later  stages. 

Massage  must  not  be  employed  too  early  either.  As  a  restorative 
massage  is  second  only  to  electricity.  It  is  not  well  to  rub  directly  over 
the  nerve,  but  along  side  of  it.  The  manipulations  must  be  gentle  and. 
towards  the  body,  and  the  seances  should  be  daily. 

Invaluable  as  electricity  and  massage  are  in  the  treatment  of  the- 
degenerative  results  of  neuritis,  I  must  repeat  the  caution  not  to  use 
either  in  the  early  stage  of  acute  inflammation.  Atrophy,  contractures 
and  shortening  can  be  controlled  by  them  as  well  as  by  systematic 
active  and  passive  exercise. 

Recently  surgery  has  been  accomplishing  some  brilliant  feats  in 
old  neuritic  cases.     A  number  of  operations  in  the  way  of  secondary 


THE  XOX-NEUROXIC  DISEASES  589 

suturing,  transplanting  and  grafting  of  ner\' es  have  been  practiced  with 
great  success. 

The  distal  end  of  a  bisected  nerve  may  be  united  with  the  prox- 
imal end  of  another  that  has  been  uninjured.  The  facial  and  hvpo- 
:glossal  have  thus  been  united,  \^'here  there  has  been  a  break  in  a  nerve 
transplantation  of  nerves  from  animals  has  been  successfullv  performed. 
If  the  break  measures  more  than  about  four  centimetres,  the  results  are 
"not  so  promising.  Nerve  tumors  have  been  extirpated  and  the  ends  of 
the  stumps  thus  approximated.  Nerves  have  been  freed  from  tumors, 
cicatrices,  callus  and  exostoses,  even  after  sixteen  years'  standing,  and 
restoration  of  movement  and  sensation  obtained.  Ofttimes  splints  and 
bandages  have  to  be  worn  for  some  time  after  these  operations.  Elec- 
trical treatment  is  also  later  on  called  for  and  should  be  continued  for  a 
jear. 

MULTIPLE  NEURITIS. 

Paralysis  and  sensor}-  disturbance  was  observed  long  ago  to  fol- 
low the  ingestion  of  alcohol,  certain  febrile  exanthemata,  constitutional 
cachexia  and  poisons  of  various  sorts.  Such  paralyses  were  spoken  of 
as  alcoholic,  lead,  febrile,  diabetic  palsy,  etc.  Most  excellent  descrip- 
tions were  given  of  it  by  Jackson,  Huss,  Lancereaux,  Duchenne  and 
others.  ]\Iost  of  the  theories  propounded  to  explain  it  attributed  it  to 
■disease  of  the  brain  or  spinal  cord.  In  1864  Dumenil  made  the  first 
careful  post-mortem  examination  of  a  case  dead  from  alcoholic  paralysis 
a.nd  announced  that  the  peripheral  nerves  were  diseased  while  the  cord 
and  brain  seemed  to  be  perfectly  normal.  Though  at  first  neglected, 
Dumenil's  observation  soon  began  to  be  confirmed  by  the  observations 
■of  others,  notably  Eichhorst,  Joftroy  and  Leyden.  The  last  observer 
finally  established  the  disease,  in  1880,  as  a  distinct  entity.  Since  the 
work  of  Leyden,  our  knowledge  of  the  malady  has  been  steadily  ad- 
vanced by  the  investigations  of  Eisenlohr,  Striimpell,  Ross,  Buzzard, 
Hun,  Mills,  Cole  and  many  others.  That  there  is  such  a  disease  as  a 
pure,  uncomplicated  polyneuritis  is  undeniable;  that  it  is  rare  is  being 
more  and  more  recognized.  As  an  associated  trouble  with  general  con- 
stitutional intoxication  and  disease  of  the  central  nervous  system  it  is 
very  frequent.  Many  problems  still  await  a  solution  in  regard  to  its 
pathogenesis,  its  extent  and  distribution,  its  complications  and  accidents 
and  associated  troubles,  the  essential  nature  of  its  disease-process,  the 
differential  diagnosis  and  pathology  of  its  various  forms,  its  course  and 
prognosis  and  its  proper  management. 

Etiology. — The  causes  of  multiple  neuritis  are  numerous.  Lender 
the  head  of  pathology  will  be  discussed  the  various  types  of  the  disease 
with  mention  of  the  etiological  factors  that  play  the  principal  role  in 
each  type.  In  the  vast  majority  of  cases  intoxication  and  infection  are 
the  causes.  This  is  so  overwhelmingly  the  case  that  it  is  beginning  to 
be  believed  that  all  other  causes  than  intoxication  and  infection  serve 
merely  as  excitants  and  not  as  essential  etiological  factors.  Alcohol 
is  the  supreme  toxic  cause,  especially  when  taken  steadily,  though  mod- 
erately, for  a  long  period  of  time.  It  matters  but  little  wliether  it  is 
imbibed  in  the  form  of  whisky,  beer  or  wine,  so  long  as  it  sets  up  a 


590  THE  NON-NEURONIC  DISEASES 

State  of  chronic  alcoholism.  After  alcohol  we  find  that  the  disease  is 
caused  by  ether  intoxication,  bisulphide  of  carbon,  carbon  dioxide, 
naphtha,  lead,  arsenic,  coffee,  mercury,  anilin,  ptomaine  and  leucomaine 
poisoning.  It  has  been  attributed  to  sulphonal  and  other  drugs  and 
medicinal  preparations.  Among  the  infectious  antecedents  we  note 
leprosy,  typhoid  fever,  variola,  scarlatina,  influenza,  diphtheria,  erysipe- 
las, purulent  pleuritis,  acute  articular  rheumatism,  mumps,  gonorrhoea 
and  dysentery.  To  these  must  be  added  tuberculosis,  syphilis,  malaria, 
diabetes  mellitus,  severe  an?emia,  carcinoma  and  marasmus  from  any 
cause.  Septicaemia  and  puerperal  fever  have  preceded  its  outbreak. 
It  has  been  charged  to  alimentary  autointoxication,  constipation  and 
putrid  bronchitis,  icterus  and  hepatic  cirrhosis. 

Akatama,  kakke  and  beriberi  are  endcuiic  forms  of  the  disease 
doubtless  due  to  an  infection. 

The  senile  form  of  the  disease  has  been  attributed  by  Oppenheim, 
Joffroy,  Gombault,  Schlesinger  and  others  to  arterio-sclerosis  and 
arteritis  obliterans. 

Exposure  to  cold,  overexertion,  mental  and  nervous  strain  are 
provocative  only  in  the  presence  of  other  conditions,  such  as  those 
mentioned  above,  and  hence  are  to  be  regarded  more  in  the  light  of 
mere  exciting  or  initiatory  causes. 

The  middle  period  of  life,  when  the  above  causes  are  most  in 
evidence,  is  the  time  when  multiple  neuritis  is  most  frequently  met  with. 
In  children  the  diphtheritic  form  is  the  most  common  as  well  as  those 
forms  that  are  due  to  scarlatina  and  other  infantile  infections.  In  old 
age  the  cachectic  ^orms  of  the  disease  predominate.  Women  are  the 
victims  of  the  alcoholic  type  far  oftener  than  men.  Other  etiological 
factors  of  the  disease  depend  upon  the  etiology  of  the  underlying  con- 
stitutional intoxication  and  infection. 

Pathology  and  Pathogenesis. — The  characteristic  pathological 
finding  of  multiple  neuritis  is  a  parenchymatous  degeneration  of  the 
peripheral  nerve  ends.  By  the  older  writers  this  was  supposed  to  be  a 
secondary  result  of  an  interstitial  inflammation  of  the  nerve  trtmk  or  of 
a  primary  parenchymatous  inflammation.  Hence  the  name  neuritis, 
and  its  division  into  mterstitial  and  parenchymatous  neuritis.  No 
pathologist  of  repute  nowadays  speaks  of  the  latter  as  an  inflammation. 
As  a  result  of  the  direct  action  of  the  alcohol  and  ether  poisons  upon 
the  nerve  fibre  or  its  cell,  a  degenerative  process  occurs.  Therefore 
we  speak  at  present  of  two  great  classes  of  neuritides,  namely,  those  of 
inflammatory  (interstitial  or  periaxial)  and  those  of  degenerative 
(parenchymatous,  axial)  origin.  They  are  the  same  disease,  however. 
As  I  have  explained  under  the  head  of  neuritis,  this  is  a  degenerative 
trouble,  not  of  the  purely  primary  type,  but  of  the  combined  degenera- 
tive and  inflammatory  type.  Both  processes  are  dependent  upon  the 
same  cause  and  are  mutually  to  a  certain  extent  dependent  upon  each 
other.  Sometimes  one,  sometimes  the  other  is  the  more  prominent 
feature  of  the  disease,  but  both  go  together.  Under  thi^  conception  we 
find  that  polyneuritis  can  be  conveniently  subdivided  into  three  general 
classes,  all  of  which  differ  slightly  from  one  another  in  regard  to 
etiology,  symptomatology,  pathology,  prognosis  and  treatment. 


THE  NON-NEURONIC  DISEASES  59T 

In  the  first  class,  perhaps  the  most  typical,  certainly  the  largest 
class,  we  include  the  neuritides  of  the  degenerative  type,  whether  the 
primary  cause  be  toxic  (alcohol,  arsenic,  mercury,  etc.)  or  infectious 
(typhoid,  variola,  puerperal  fever,  tuberculosis,  syphilis,  etc.)  or 
cachectic  (diabetes,  carcinoma,  marasmus).  Some  of  these  are  primary- 
degenerations  and,  as  1  have  noted  elsewhere,  are  but  side  issues,  as  it 
were,  of  other  diseases.  They  are  not  special  any  more  than  tubercu- 
lous glands  would  be  special  diseases  apart  from  general  tuberculosis. 

In  the  second  class  may  be  conveniently  grouped  the  neuritides, 
neuritis  of  the  inflammatory  type,  in  which  the  parenchymatous  degen- 
eration is  entirely  secondary.  These  cases  include  the  endemic,  infec- 
tious types  such  as  leprosy,  beriberi  and  certain  forms  of  unknown 
origin. 

In  the  third  class  both  inflammation  and  degeneration  play  a  role 
in  their  origin.  They  are  the  neuritis  of  diphtheria  and  some  primary 
forms  of  unknown  origin.  The  second  and  third  class  are  the  true 
types  of  neuritis. 

In  all  forms  of  multiple  neuritis  the  inflammatory  signs  are  never 
as  prominent  as  are  the  degenerative.  There  may  be  in  some  of  them 
redness  and  swelling  of  the  nerve  tnmk  and  hyperjemia  of  the  sheath. 
Even  minute  hemorrhagic  extravasations  with  all  the  usual  manifesta- 
tions of  a  severe  local  inflammation  may  be  seen  here  and  there  along 
the  course  of  the  nerve.  This  is  not  common,  however.  More  fre- 
quently there  are  no  discoverable  interstitial  changes ;  only  more  or  less 
atrophy  of  the  individual  nerve-fibres.  The  myelin  substance  is  broken 
into  clumps ;  the  contour  of  the  fibre  is  irregular  in  outline ;  and  the 
fibres  are  reduced  in  size  and  diminished  in  number.  Among  this  mass 
of  wasted  and  diminished  fibres  some  are  seen  to  be  regenerating,  while 
others  retain  their  normal,  healthy  appearance.  The  disease  process 
in  many  cases  seems  to  grow  less,  both  in  severity  and  extent,  as  we 
ascend  the  nerve  trunk.  The  point  of  transition  from  diseased  to 
healthy  nerve  tissue  varies  in  different  cases  and  in  different  nerves 
even  in  the  same  case. 

In  some  of  the  cases  the  lesion  is  limited  to  the  peripheral  nerve- 
fibres.  This  is  especially  true  of  the  diphtheritic  cases,  wherein  the 
poison  acts  directly  upon  the  nerves  in  the  immediate  neighborhood  of 
the  infected  focus.  Nevertheless,  in  the  diphtheritic  cases  and  much 
more  so  in  the  other  toxic  and  infectious  cases,  foci  of  disease  are  found 
in  the  spinal  nerve  roots,  the  spinal  cord  and  its  membranes.  In  alco- 
holic, lead  and  other  cases,  the  myelitic  and  encepJiaUc  evidences  of  dis- 
ease are  being  discovered  post-mortem  more  and  more  frequently. 
These  partake  of  the  nature  of  poliomyelitic  and  encephalitic  processes 
with  atrophy  of  the  cells.  On  account  of  this  the  view  is  growing  that 
in  these  cases  the  toxin  affects  the  entire  nervous  system,  of  w^hich 
the  polyneuritis  is  but  one  of  many  local  expressions.  In  this  w'ay  its 
great  variety  of  symptoms  is  explained.  Some  attribute  the  neuritis 
even  to  the  functional  damage  done  to  the  cells  in  the  cord  by  the  poison. 
Cole  and  others  among  the  most  recent  investigators  frankly  affirm  that 
multiple  neuritis,  especially  of  the  alcoholic  type,  is  a  widespread  affec- 
tion of  the  nervous  svstem  ;  that  the  central  changes  are  not  attributable 


592  THE  XOX-NEURONIC  DISEASES 

to  the  peripheral  trouble ;  that  the  lesion  of  the  peripheral 
neurones  is  only  one  of  many  manifestations  of  the  disease 
and  is  accompanied  by  lesions  identical  in  nature,  affecting  many 
groups  of  neurones  situated  entirely  within  the  central  nervous  system  ; 
that  though  in  some  cases  the  peripheral  neurones  are  mainly  affected, 
in  others  the  morbid  process  implicates  chiefly  the  central  neurones, 
two  groups  of  cases  which  do  not  appear,  however,  to  be  sharply  divided. 
The  same  is  true,  though  not  to  the  same  marked  degree,  in  regard  to 
the  other  forms  of  polyneuritis,  especially  those  due  to  lead  and  arsenic 
and  in  which  mild  delirium  occurs  with  febrile  phenomena.  As  the 
bacterial  products  and  not  the  bacteria  themselves  are  credited  with  the 
production  of  the  disease,  it  is  not  surprising  that  the  infectious  cases, 
like  the  toxic,  should  show  the  same  general  characteristics  in  regard 
to  the  entire  nervous  apparatus. 

Symptomatology. — Charcot  used  to  contend  that  peripheral  neu- 
ritis is  not  a  distinct  disease,  but  a  substratum  underlying  the  symptoms 
of  several  very  different  affections.  His  contention  was  supported  by 
the  dissimilarity  in  the  clinical  pictures  presented  by  the  different  forms 
of  multiple  neuritis.  Even  to-day  we  are  obliged  to  discuss  the  symp- 
tomatology of  alcoholic,  lead,  arsenic,  diphtheritic  paralysis,  etc.,  under 
their  own  respective  heads.  Unlike  as  they  are  in  many  respects,  these 
various  forms  of  multiple  neuritis  present  a  sufficiently  constant  and 
uniform  set  of  symptoms  to  base  a  clinical  description  upon.  As  the 
alcoholic  type  of  the  disease  is  the  most  common  and  uniform,  it  will 
be  described  first  as  a  sort  of  symptomatic  model. 

I.  Toxic  Forms;  (a)  Alcoholic  Type. — The  first  symptom 
noticed  by  the  patient  is  a  paresthesia  in  the  feet  and  hands.  It  comes 
on  more  or  less  suddenly  and  consists  of  numbness,  "pins-and-needles"' 
sensation  and  a  feeling  of  pricking.  There  may  be  actual  pain  in  the 
limbs,  sharp  and  shooting  or  dull  and  rheumatoid  in  character.  These 
early  sensations  may  occur  in  the  course  of  chronic  alcoholism  or  after 
an  attack  of  delirium  tremens.  Occasionally  the  temperature  may  be  ele- 
vated, but  as  a  rule  there  are  no  febrile  manifestations.  The  paraesthe- 
sia  is  bilateral  in  distribution.  It  attacks  all  four  limbs  about  in  the 
same  way  and  gradually  ascends  toward  the  hips  and  shoulders.  The 
pains  are  irritating,  may  be  sharp  or  dull,  may  come  and  go  in  the 
course  of  particular  nerves,  and  gradually  lessen  in  severity  as  the 
disease  advances.  A  feeling  of  weakness  appears  in  the  limbs  in  a  few 
days  and  the  muscles  and  tendons  begin  to  feel  like  stiff  parchment  to 
the  patient,  or  as  if  they  were  tense  and  just  a  little  too  short.  Between 
the  numbness,  weakness  and  slight  rigidity,  the  patient  cannot  coordi- 
nate his  movements  and  so  finds  difficulty  in  walking  and  using  the 
hands.  In  a  little  while  the  weakness  passes  into  an  actual  paralysis. 
This  seems  to  involve  the  extensor  more  than  the  flexor  muscles,  caus- 
ing wrist-drop  and  ankle-drop.  All  the  nei^es  of  the  extremities  may 
be  involved,  but  the  musculo-spiral  and  the  anterior  tibial  seem  to  be 
especially  affected.  The  muscles  of  the  trunk  and  head  as  a  rule  escape 
and  the  mind  is  affected  in  a  particular  way  only  in  certain  cases.  The 
reflexes  are  lost,  both  deep  and  superficial.  The  muscles  are  noticeably 
wasted  and  if  tested  electrically  exhibit  more  or  less  completely  the 


THE  NON-NFURONIC  DISEASES  593 

reaction  of  degeneration.  There  is  some  ancesthesia,  distributed  gener- 
ally or  in  spots  over  the  limbs.  Hyperalgesia  is  often  a  valuable  symp- 
tom and  the  local  tenderness  in  the  muscles  and  nerve  trunks  is  so 
characteristic  a  sign  that  it  helps  to  differentiate  the  disease  from  other 
affections  with  similar  disturbances  of  sensation  and  motion.  Hyper- 
<Bsthesia  may  be  discovered  in  areas  of  the  skin  alongside  of  areas  of 
hypgesthesia.  As  a  result  of  the  sensory  disturbances  ataxia  may  be 
present.  Hyperidrosis,  oedema,  szvelling  in  and  about  the  joints  and 
even  certain  skin  eruptions  and  ulcers  may  be  expected  among  the  later 
vasomotor,  secretory  and  trophic  manifestations.  The  rectal  and  vesical 
functions  as  a  rule  are  unaffected.  Such  in  outline  is  the  clinical  pic- 
ture of  a  typical  multiple  neuritis.  Such  a  pure  type,  however,  is  rare 
and  it  is  therefore  necessary  to  consider  some  of  the  symptoms  a  little 
more  in  detail. 

The  more  prominent  of  the  sensory  symptoms,  being  subjective  in 
character,  are  less  valuable  as  symptoms  than  some  other  signs  on  that 
account.  They  are  indicative  only  of  the  disease  when  studied  as  a 
part  of  the  clinical  picture  in  toto.  If  taken  by  themselves  they  may  be 
mistaken  for  hysterical  and  other  psychoneurotic  manifestations. 
Though  the  sensory  phenomena  are  rarely  absent,  they  assume  the 
most  varied  and  bizarre  characteristics.  For  instance,  in  the  soles  of 
-the  feet  all  qualities  of  sensation  may  be  decreased  or  lost ;  or  there 
may  be  anaesthesia  with  hyperalgesia  or  hypersesthesia  with  analgesia. 
A  very  common  combination  which  I  have  seen  often  is  anaesthesia  with 
hypersesthesia  in  adjoining  areas.  The  touch  and  muscular  senses  may 
be  diminished,  while  the  pain  sense  is  highly  exaggerated,  or  vice  versa. 
Instead  of  being  diminished  the  sensations  may  only  be  delayed.  In 
the  trunk  a  rare  girdle  sensation  is  sometimes  found,  but  it  belongs  to 
the  other  symptoms  of  central  disease  usually  accompanying  alcoholic 
neuritis.  It  is  to  be  noted  carefully  that  these  sensory  manifestations 
are  symmetrical  in  distribution,  that  they  are  more  extensive  than  the 
corresponding  paralysis,  that  they  are  partly  subjective  and  objective 
in  character  and  that  they  exhibit  the  variability  and  irregularity  that 
one  would  expect  from  a  variable  lesion  involving  a  large  number  of 
separate  and  unrelated  peripheral  nerve  fibres.  Such  an  incongruous  set 
of  phenomena  could  only  be  imitated  by  a  pure  psychosis,  but  a  psycho- 
sis can  easily  be  distinguished  from  a  polyneuritis  by  other  symptoms. 

Much  more  striking  than  the  sensory  symptoms  is  the  motor 
paralysis.  In  some  forms  of  multiple  neuritis  this  is  almost  the  only 
symptom.  It  is  of  course  of  the  flaccid,  degenerative  type  of  paralysis, 
since  the  lesion  involves  the  lower  or  peripheral  motor  neurones.  It  is 
always  accompanied  by  distinct  muscular  atrophy  and  alterations  in  the 
electrical  reactions.  It  is  usually  more  profound  in  the  legs  than  in  the 
arms,  though  great  variations  are  possible  as  to  the  areas  of  its  distribu- 
tion. In  some  respects  it  resembles  marvelously  the  paralysis  of  an- 
terior acute  poliomyelitis,  for  it  may  involve  one  leg  or  certain  muscles 
only  in  that  leg,  or  only  certain  muscles  in  all  four  limbs  or  even  all  the 
muscles  of  all  the  limbs.  Curiously  where  a  nerve  innervates  more  than 
one  muscle,  it  sometimes  happens  that  one  muscle  will  be  paralyzed 
while  the  others  escape.     The  nerves  may  show  the  electrical  reactions 


594  THE   XOX-XEURONIC  DISEASES 

of  degeneration  and  yet  their  corresponding  muscles  not  be  paralyzed. 
The  peculiar  character  of  this  paralysis  has  even  led  some  to  think  that 
the  disease  is  primarily  a  toxic  injury  of  the  cells  of  the  anterior  horns 
of  the  cord  with  a  mere  secondary  degeneration  in  the  peripheral 
axones.  Though  this  is  not  entirely  acceptable,  it  is  undoubtedly  true 
that  in  some  cases,  at  least,  the  pathological  process  and  its  resulting 
paralysis  is  partly  poliomyelitic  as  well  as  neuritic. 

In  some  cases  ataxia  rather  than  paralysis  is  the  chief  motor  mani- 
festation. It  is  rare,  however,  and  is  the  symptomatic  basis  of  the 
peripheral  pseudo-tabes  of  Dejerine.  It  is  often  associated  with  anaes- 
thesia, and  implicates  the  legs  much  more  often  than  the  arms.  Of 
course,  it  changes  the  gait  and  active  movements  and  may  lead' to  an 
erroneous  diagnosis  of  locomotor  ataxia.  Involuntary  muscular  twitch- 
ings  sometimes  accompany  it. 

The  atrophy  and  tenderness  of  the  muscles  are  two  characteristic 
symptoms  of  this  disease.  They  are  most  always  present  and  when 
found  together  in  the  same  patient  are  pathognomonic.  The  wasting  of 
the  limbs  is  marked  and  rapid.  It  is  not  as  severe  and  rapid  perhaps, 
nor  does  it  pick  out  individual  muscles  so  strikingly,  as  does  the  atrophy 
of  infantile  palsy.  It  may  for  a  time  be  obscured  by  oedema  or  fatty 
deposits.  The  muscles  feel  soft  and  flabby,  are  cold  and  somewhat  pale 
in  color.  Pressure  and  passive  movement  often  cause  such  intense  pain 
that  it  is  impossible  to  make  a  complete  examination. 

Abolition  of  the  deep  reflexes  is  the  characteristic  of  polyneuritis. 
Usually  this  is  complete  and  early  in  appearing.  Sometimes,  however, 
it  is  for  a  brief  time  preceded  by  an  exaggeration.  Occasionally  it  is 
incomplete  and  capable  of  being  partially  elicited  by  reinforcement.  The 
paralysis  in  such  cases  is  a  partial  one. 

The  cranial  nerves  are  frequently  involved,  though  their  implica- 
tion is  in  no  way  pathognomonic.  The  same  may  be  said  of  the  brain. 
And  yet  it  is  not  to  be  wondered  at  in  view  of  the  frequency  with  which 
disturbances  of  the  brain  and  cranial  nerves  are  met  with  that  many 
are  beginning  to  look  upon  them  as  essential  manifestations  of  the  dis- 
ease and  not  as  mere  complications  and  accidents.  In  other  words,  the 
view  is  spreading  that  the  polyneuritis  is  but  one  manifestation  of  a 
much  more  extensive  disease  process,  namely,  a  toxic  degeneration  of 
the  entire  ner\'Ous  system  (Buzzard,  Cole  and  others). 

Among  the  cranial  nerves  the  third  is  most  often  affected ;  next  the 
sixth.  Reflex  pupillar\-  rigidity  is  rare,  but  nystagmus,  diplopia  and 
ptosis  may  all  be  looked  for.  \'ery  seldom  is  the  optic  nerve  involved, 
tliougli  optic  neuritis  and  even  partial  optic  atrophy  have  been  observed 
several  times.  There  may  be  a  central  scotoma,  especially  for  colors. 
Among  the  other  cranial  nerves  that  may  be  involved  are  the  facial,  the 
vagus  and  phrenic  and  the  nerves  of  mastication  and  deglutition. 
Striimpell  saw  the  auditory  nerve  involved.  A  polyneuritis  limited  to 
the  cranial  nerves  would  be  a  curiosity,  and  yet  such  has  been  referred 
to  by  Hosslin  and  Mannaberg. 

The  mental  symptoms  of  alcoholic  neuritis  are  deserving  of  special 
consideration.  They  consist  of  failure  of  memor}^,  confusion  and  loss 
of  the  proper  conceptions  of  time  and  space.     Korsakoff  was  the  first 


THE  NON-NEURONIC  DISEASES  595 

to  name  and  systematize  this  polyneuritic  psychosis,  though  others  had 
observed  and  described  it  before  him.  Amnesia,  disorientation,  pseudo-- 
reminiscence  and  confabulation  are  its  chief  characteristics.  Events  oi 
the  past  are  spoken  of  as  about  to  occur  in  the  future  a.rA  vice  versa. 
Hallucinations  and  mild  delusions  are  sometimes  present.  They  are 
easily  repressed.  Occasionally  they  are  determined  by  the  sensory 
symptoms.  One  of  my  cases  spoke  of  having  just  been  out  in  the  gar- 
den picking  flowers  and  getting  covered  with  burrs,  when,  as  a  matter 
of  fact,  it  was  a  cold,  midwinter  day  and  she  had  not  been  out  of  bed  for 
ten  days.  By  many  this  confusional  type  of  psychosis  is  regarded 
merely  as  an  alcoholic  complication  of  the  polyneuritis.  Others  attribute 
it  to  a  mild  toxic  encephalitis,  which,  like  the  peripheral  neuritis,  is  one 
of  the  outward  expressions  of  the  underlying  chronic  toxaemia  or  alco- 
holism. The  hypothesis  has  even  been  set  up  (Turner)  that  it  is  the 
result  of  the  isolation  of  the  patient's  mind  by  the  shutting  off  oi  his 
normal  affenent  impulses  through  the  widespread  neuritis.  If  alcoholic 
polyneuritis  is  a  distinct  disease  in  itself,  then  these  mental  manifesta- 
tions are  of  the  nature  of  pure  complications  or  accidents.  If,  hoiwever, 
the  real  disease  is  an  alcoholic  degeneration  of  the  entire  nervous  sys- 
tem, with  peripheral  neuritis  as  one  of  its  outward  expressions,  the 
central  symptoms  will  then  have  to  be  regarded  in  the  light  of  another 
set  of  outward  manifestations. 

Alcoholic  polyneuritis  in  the  majority  of  instances  runs  an  acute 
or  subacute  course  and  its  prognosis  is  in  the  main  favorable.  It.  ap- 
pears rather  abruptly,  rises  to  its  climax  in  a  few  weeks  or  months, 
remains  stationary  for  about  the  same  time  and  then  gradually  recedes. 
There  are  violent  cases  that  run  a  rapid  course  and  terminate  in  death 
in  a  few  days.  In  such  cases  the  cranial  nerves,  especially  the  vagus 
and  phrenic,  are  likely  to  be  involved.  The  general  condition  of  the 
patient,  the  implication  of  the  cranial  nerves,  the  extent  of  the  paralysis, 
and  the  degree  of  muscular  atrophy  are  all  factors  that  influence  the 
prognosis.  Rarely  the  disease  runs  a  progressive  or  even  remittent 
chronic  course.  Occasionally  recovery  is  complete ;  more  frequently  it 
occurs  with  some  more  or  less  permanent  defect.  This  is  especially  true 
of  the  cases  with  mental  symptoms.  Convalescence  is  always  slow  and 
tedious.  Irritative  symptoms,  like  pain,  disappear  first ;  then  the 
angesthesia  gradually  clears  up  or  is  replaced  by  pargesthesia ;  and 
finally  after  a  long  time  the  hypersesthesia  diminishes  to  normal.  Some- 
times two  years  have  to  elapse  before  all  signs  of  paralysis  have  van- 
ished. Relapses  are  not  uncommon.  Permanent  paralysis  in  particular 
muscles,  and  contractures  and  deformities  from  overaction  of  antag- 
onistic muscles,  are  unfortunately  possible. 

(b)  Lead  Type. — Lead  intoxication  produces  a  polyneuritis  strik- 
ingly unlike  the  other  forms  of  the  disease  in  some  respects.  It  was, 
this  fact  that  led  Charcot  to  contend  that  multiple  neuritis  is  not  a  dis- 
tinct, uniform  disease.  Motor  paralysis  confined  to  a  certain  area, 
without  distinct  sensory  disturbances,  constitutes  the  predominant  fea- 
ture in  its  clinical  exhibition.  That  the  disease,  however,  is  an  intoxica- 
tion of  the  entire  nervous  system  is  shown  by  the  brain  symptoms  and 
the  arthritic  pains.     The  ingestion  of  lead  is  the  cause  of  the  disease ; 


596  THE  NON-NEURONIC  DISEASES 

though  it  has  been  seen  as  an  inheritance  in  children  whose  parents  have 
been  lead  workers.  There  are  man)'  sources  from  which  the  lead  enters 
the  system.  Painters,  type-setters,  pipe-layers  and  other  workers  in 
lead ;  potters  using  lead  glazes ;  weavers  handling  leaden  weights ; 
users  of  cosmetics  containing  lead ;  washers  oi  bottles  employing  lead 
shot;  and  drinkers  of  water  drawn  through  lead  pipes  are  all  exposed 
to  the  disease.  So  extensive  is  the  use  of  the  metal  in  modern  industry 
and  so  insidious  at  times  is  the  onset  of  the  paralysis  tliat  only  a  most 
painstaking  search  will  reveal  the  source  of  the  intO'xication. 

In  many  cases  the  motor  paralysis  is  the  only  symptom ;  in  all 
cases  it  is  the  characteristic  symptom.  When  it  is  preceded  or  accom- 
panied, as  it  is  usually,  by  lead  colic  with  its  griping  pains  in  the  abdo- 
men, by  arthralgia  with  its  pains  and  soreness  in  and  about  the  joints 
and  muscles  and  especially  by  encephalopathia  saturnina  with  its  mental 
mmifestations,  the  diagnosis  cannot  be  mistaken.  The  blackish  streak 
or  blue-black  coloration  of  the  gums  along  the  edge  of  the  teeth,  the 
anaemia,  the  cachectic  state,  the  disease  of  the  kidneys  and  the  arterio- 
sclerosis all  indicate  the  wide  extent  of  the  intoxication  and  help  to 
confirm  the  true  origin  of  the  palsy. 

As  I  have  said,  this  palsy  is  striking  and  pathogno^monic  almost, 
for  it  is  never,  or  rarely,  accompanied  by  sensory  phenomena,  is  limited 
practically  to  the  arms  and  preferably  to  certain  muscles.  It  is  a 
degenerative  paralysis  as  shown  by  the  loss  of  reflex  action,  the  marked 
atrophy  of  the  muscles  and  the  electrical  reaction  of  degeneration.  It 
involves  the  peripheral  muscles  of  the  limbs  symmetrically,  showing  a 
remarkable  selective  action.  Occasionally  certain  muscles  individually 
are  picked  out  as  in  infantile  palsy.  At  other  times  the  disease  is  Hmited 
to  one  arm.  This  is  usually  determined  by  the  patient's  occupation,  the 
arm  or  muscles  most  employed  being  the  first  to  succumb.  The  ex- 
tensors of  the  hand  and  fingers  are  particularly  liable  to  the  paralysis, 
resulting  in  the  easily  recognized  "■wrist-drop"  and  flexion  of  the  fin- 
gers. If  the  feet  are  involved,  as  rarely  they  are,  the  peroneal  nerve 
■distribution  is  the  one  mostly  diseased.  The  tibialis  anticus  muscle 
usually  escapes  under  such  circumstances.  There  is  no  uniformity  with 
which  the  muscles  of  the  arms  are  involved,  but  in  typical  cases  the 
supinators,  especially  the  supinator  longus  and  the  triceps,  are  spared. 
The  extensior  carpi  ulnaris  and  the  abductor  longus  poUicis  are  also  un- 
affected as  a  rule.  In  other  words,  the  radial  nerve,  and  its  distribution 
is  in  the  more  typical  cases  the  focus  of  the  disease.  In  other  cases  the 
smaller  muscles  of  the  hand  and  thumb  under  the  control  of  the  ulnar 
and  median  nerves  are  also  paralyzed.  Still  more  rarely  the  interossei 
muscles  and  the  deltoid  are  paralyzed  along  with  the  extensors.  In 
Remak's  upper-arm  type  of  the  disease,  which,  however,  is  atypical,  the 
biceps  brachialis  internus  and  deltoid  are  implicated. 

Associated  with  the  paralysis  there  is  generally  a  certain  degree  of 
Hhrillary  tremor,  swelling  about  the  wrist-joint  and  rarely  thickening 
of  the  metacarpal  bones. 

A  generalized  form  of  the  disease  beginning  acutely  with  fever 
and  following  a  saturnine  encephalopathy  involves  all  the  muscles  of 
the  arms,  legs  and  trunk.  ■ 


THE  NON- NEURONIC  DISEASES  597 

The  cerebral  disturbances  that  often  accompany  saturnine  poly- 
neuritis are  numerous  and  miportant.  They  may  be  general  or  focal, 
organic  in  origin  or  functional.  In  this  way  hemiplegia  and  hemi- 
anaesthesia,  temporary  or  permanent,  may  be  occasionally  observed. 
Convulsions,  delirium  and  coma  may  be  preceded  by  vertigo,  tinnitus 
aurium,  restlessness  and  insomnia.  There  may  be  distinct  hallucina: 
tions  of  sight  and  hearing  and  all  the  manifestations  of  acute  deliriun:. 
The  cranial  nen^es  may  all  be  affected,  optic  neuritis  and  implication 
of  the  pneumogastric  and  phrenic  being  particularly  ominous.  The 
oculomotorius  involvement  is  shown  in  mild  mydriasis,  as  I  recently 
saw  in  a  ver}-  obscure  chronic  case  of  general  lead  intoxication.  In 
chronic  encephalopathia  melancholia  with  delusions  is  the  more  common 
manifestation.  The  mental  power  fails  or  there  are  exalted  delusions 
as  there  are  in  dementia  paralytica.  A  degenerative  meningoencephal- 
itis is  the  patholog}^  in  these  cases.  Hemorrhages,  local  encphalomala- 
cia  with  arteritis  may  occur  here  as  in  any  form  of  severe  intoxication 
or  infection. 

The  prognosis  of  this  form  of  multiple  neuritis  is  favorable  in  the 
earlier  stages  of  the  disease  and  before  grave  paralyses  have  occurred 
or  such  serious  complications  as  saturnine  cachexia,  nephritis,  optic 
neuritis  and  other  organic  destruction  of  the  tissues  of  the  brain  and 
cranial  nerves.  Recovery  may  be  hoped  for  even  after  the  appearance 
of  the  reaction  of  degeneration.  Several  attacks  in  succession  of  the 
paralysis  add  to  the  gravity  of  the  outlook. 

(c)  Arsenical  Type. — Intoxication  may  result  from  the  use  of 
arsenical  coloring  matters  in  pigments,  wall  papers,  book  covers,  etc. 
Attempted  suicide  with  arsenic  or  Paris  green  may  terminate  in  a  multi- 
ple neuritis.  Most  of  the  cases  of  arsenical  paralysis  are  due,  however, 
to  the  excessive  m.edicinal  use  of  the  metal  in  the  form  of  arsenious 
acid  or  Fowler's  solution. 

Symptomatically  arsenical  paralysis  resembles  most  strikingly  the 
alcoholic  type  and  both  forms  of  the  disease  differ  from  the  saturnine 
and  diphtheritic  types  in  the  greater  prominence  of  the  sensory  mani- 
festations. There  seem  to  be  two  classes  of  arsenical  palsy.  In  one 
the  muscles  are  decidedly  paralyzed,  especially  the  extensors  of  the 
hands  and  feet.  In  the  other  the  sensibility  is  especially  affected  giving 
rise  to  a  condition  of  ataxia  or  pseudo-tabes.  These  symptoms  follow 
either  acute  or  chronic  poisoning  and  make  their  appearance  in  from 
a  few  days  to  a  few  weeks. 

The  paralysis  in  the  arms,  flaccid  and  degenerative  in  character, 
involves  usually  the  same  muscles  and  causes  the  same  characteristic 
attitude  as  lead  palsy.  The  same  is  true  in  the  legs.  The  deep  reflexes 
are  diminished  or  abolished  and  the  usual  electrical  reaction  of  degen- 
eration is  present.    Muscular  atrophy  occurs  very  rapidly. 

Unlike  lead,  arsenic  poisoning  provokes  a  greater  degree  of  sensory 
disturbance.  The  sensitiveness  of  the  nerves  and  muscles  to  pressure 
is  exceedingly  acute.  There  are  initial  parcesthesice  of  various  sorts  on 
the  back  of  the  forearms  and  front  of  the  legs.  Severe  darting  pains  are 
complained  of.  Ancesthesia  or  hypercesthesia  may  be  general  or  scat- 
tered about  in  patches.    Sensation  m  general  is  almost  always  decreased, 


598  THE  NON-NEURONIC  DISEASES 

especially  in  the  feet,  hands  and  fingers.  In  these  pronounced  sensory 
cases  there  is  incoordination  of  such  a  character  that  they  closely  re- 
semble ordinary  tabes.  The  differentiation  between  the  two  diseases  is 
made  largely  upon  the  presence  of  a  true  palsy  in  the  arsenical  neuritis. 
Though  we  speak  of  a  motor  and  ataxic  form  of  arsenical  polyneuritis, 
the  motor  symptoms  are  more  or  less  present  always  in  both.  In  these 
ataxic  cases  the  knee  reflexes  are  practically  always  absent,  pains  are 
present,  and  the  sensations  are  diminished  in  regard  to  touch,  increased 
in  regard  to  pain.  Dana,  to  whom  we  owe  much  of  our  knowledge  of 
this  pseudo-tabes,  saw  optic  neuritis  in  one  of  his  cases.  In  Seelig- 
miiller's  case  the  patella  refiex  was  not  lost. 

Psychic  disturbances  are  present  in  cases  of  arsenical  polyneuritis, 
though  they  are  not  so  prominent  as  in  some  other  forms  of  intoxication. 
The  weakness  of  the  memory,  the  mental  confusion,  and  the  dis- 
orientation bear  a  resemblance  to  the  mental  manifestations  of  alcoholic 
neuritis.    Epilepsy  and  amaurosis  have  been  recorded. 

Among  the  trophic  symptoms,  especially  in  the  prolonged  and  se- 
vere cases,  are  to  be  noted  herpetiform  eruptions  on  the  skin,  true 
herpes  zoster,  pemphigus,  erythematous  and  bullous  outbreaks,  glossi- 
ness of  the  skin,  alopecia,  falling  otT  of  the  nails  and  other  indications 
of  a  profound  state  of  cachexia. 

The  initial  conjunctivitis  and  gastric  irritation  are  not  unfre- 
quently  seen  in  cases  in  which  medicinal  arsenic  has  been  administered 
to  the  limit  of  tolerance.  In  many  cases  the  temperature  is  slightly 
increased  and  in  nearly  all  of  them  the  pulse  is  more  or  less  accelerated. 

Recovery  is  the  rule  in  this  form  of  polyneuritis,  though  the  con- 
valescence may  last  for  months  or  years.  As  the  bulbar  nerves  are 
scarcely  ever  implicated  life  is  rarely  jeopardized.  Fatalities  usually 
result  from  respiratory  or  cardiac  failure  when  they  do  occur. 

(d)  Argentic  Type.  Argyria. — This  is  an  exceedingly  rare 
form  of  polyneuritis.  Gowers  has  reported  a  remarkable  case  in  which  the 
symptoms  corresponded  almost  identically  with  those  of  lead  poisoning, 
namely,  paralysis  in  both  arms  of  the  long  extensor  of  the  fingers  and 
of  the  extensors  of  the  phalanges  of  the  thumb  without  involvement  of 
the  extensor  of  the  metacarpal  bone  of  the  thumb,  atrophy  of  the 
muscles  and  reaction  of  degeneration.  The  legs  were  not  affected  and 
there  seem  to  have  been  no  sensory  phenomena.  The  well-known  bronz- 
ing of  the  skin  and  blue-black  line  on  the  gums  were  present.  The 
source  of  the  silver,  in  this  case  as  well  as  in  the  non-neuritic  cases  of 
argyria  generally,  was  its  prolonged  medical  administration.  As  sil- 
ver is  not  employed  now  as  it  used  to  be  in  the  treatment  of  such 
chronic  diseases  as  epilepsy  and  spinal  sclerosis,  argentic  intoxication 
is  less  frequently  heard  of.  Scarcely  any  cases  of  multiple  neuritis 
from  this  cause  have  been  reported. 

(e)  Mercurial  Type. — It  has  been  asserted  that  there  is  a  mercu- 
rial multiple  neuritis.  If  so  we  know  very  little  about  it.  In  most  of 
the  cases  so  reported  there  has  been  a  history  of  syphilis  treated  with 
mercury.  It  is  an  open  question  whether  the  polyneuritis  was  of 
syphilo-toxic  or  mercurial  origin.  Schultze,  Buzzard  and  Oppenheim 
have  described  syphilitic  polyneuritis ;  others  doubt  its  existence.    There 


THE  NOX-XEUROXIC  DISEASES  599 

is  no  question  but  that  a  polyneuritis  in  a  syphilitic  may  be  made  worse 
by  the  administration  of  mercury.  I  have  lately  seen  this  most  forcibly 
exemplified  and  it  has  been  confirmed  by  ^linkowski,  Engel  and  Op- 
penheim.  The  symptoms  of  hydrargyria  point  to  lesions  of  the  brain 
and  cord  rather  than  of  the  peripheral  nerves.  They  consist  of  a 
peculiar  tremor  not  wholly  unlike  that  of  paralysis  agitans.  slight  loss 
of  muscular  power  in  one  limb  more  than  the  other,  pains  in  the  region 
of  the  fifth  nerve  and  aroimd  the  joints,  formication  in  the  limbs  and 
local  analgesia,  mental  irritability,  loss  of  the  power  of  attention,  dis- 
tress, insomnia,  hallucinations  and  even  maniacal  outbreaks.  There 
may  even  be  considerable  hemiplegic  weakness,  aphasia  and  deafness. 
AVith  all  this  there  is  no  typical  paralysis  of  neurotic  origin  though 
these  cases  are  ofttimes  of  great  severity  and  acquire  their  mercury 
from  gross  sources  as  manufactures,  mines  and  the  industrial  use  of 
the  metal.  The  stomatitis,  ulceration  of  the  mucous  membrane  of  the 
mouth,  fetor,  bone  necrosis,  gastric  and  intestinal  catarrh  and  other 
symptoms  of  profound  mercurial  intoxication  are  never  accompanied 
by  the  typical  signs  of  a  peripheral  multiple  neuritis.  It  seems  to  me 
therefore  that  the  existence  of  mercurial  polyneuritis  may  be  legiti- 
mately doubted  and  that  the  reported  cases  in  which  there  has  been  a 
history  of  syphilis  are  to  be  attributed  to  the  specific  infection. 

II.  Infectious  Forms. — The  infectious  forms  of  polyneuritis  do 
not  differ  symptomatically  from  the  toxic  forms  though  they  are  de- 
pendent upon  such  a  multiplicity  of  infective  processes.  In  the  main 
they  are  all  alike,  differing  from  one  another,  as  in  the  toxic  cases,  in 
some  minor  details.  As  the  infection  is  general  the  lesions  of  the 
nervous  system  are  of  wide  extent  with  a  predommance  of  parenchy- 
matous degeneration.  The  symptoms  are  therefore  cerebral,  spinal  and 
neuritic  in  origin.  In  some,  as  in  typhoid  and  scarlatina,  they  are 
largely  cerebral ;  in  others,  as  in  variola,  dysentery  and  measles,  they 
are  apt  to  be  spinal ;  in  still  others,  as  in  diphtheria,  acute  rheumatism, 
er\-sipelas  and  puerperal  sepsis,  they  are  mostly  neuritic.  There  are 
no  fixed  rules  in  this  respect,  but  as  the  peripheral  neuritis  is  of  a  varia- 
ble degree  and  extent  common  to  all  of  these  infective  conditions,  I  refer 
to  them  under  this  head,  using  one  or  two  of  the  more  striking  ones, 
like  diphtheria,  rheumatism  and  puerperal  sepsis,  as  more  or  less  illus- 
trative of  all  of  them. 

The  universal  character  and  wide  extent  of  the  intoxication  is 
shown  by  the  multiplicity  and  variety  of  the  symptoms  and  especially 
by  the  uncertainty  among  pathologists  as  to  whether  the  peripheral 
neuritic  degenerations  are  due  to  the  primary  damage  of  the  central 
cells  or  to  a  mere  simultaneous  degeneration  in  both  central  cells  and 
peripheral  processes.  Perhaps  the  larger  number  of  investigators  are 
ready  to  accept  both  explanations.  None  of  the  more  recent  patholo- 
gists believe,  however,  but  what  the  interstitial  changes  sometimes 
found  in  these  cases,  and  suggestive  of  true  inllammation  of  the  nerves, 
are  but  late  and  secondar}-  results  of  the  degeneration. 

(a)  Diphtheritic  Type. — In  about  one-quarter  of  the  cases  that 
recover  from  diphtheria  a  remarkable  form  of  motor  paralysis  occurs, 
usually  appearing  from  two  to  three  weeks  after  the  subsidence  of  the 


600  THE  NON-NEURONIC  DISEASES 

throat  trouble,  rising  to  its  maximum  in  two  or  three  weeks  more  and 
finally  disappearing  in  from  two  to  three  months  to  a  year  later.  The 
lesions  of  the  nervous  system  seem  to  be  the  result  of  both  a  local  and 
general  infection.  For  this  reason  some  authorities  speak  of  two  forms 
of  diphtheritic  neuritis,  the  local  and  the  generalized.  A  true  inflam- 
mation of  the  nerves  near  the  site  of  the  primary  infection  is  believed 
to  characterize  the  local  form,  while  a  general  specific  toxic  degenera- 
tion is  thought  to  represent  the  latter.  This  may  in  part  be  true,  but 
I  am  inclined  to  think  that  in  the  main  the  process  is  a  generalized 
intoxication  which  in  some  cases  afifects  only  the  nerves  round  about 
the  original  focus  of  infection  where  the  poison  would  naturally  be  the 
most  abundant  and  virulent,  but  not  sufficiently  so  to  involve  the  more 
distant  nervous  tissues,  and  in  other  cases  affects  both  the  local  and 
more  distant  nerves.  This  is  shown  in  the  accidental  and  experimental 
infection  of  other  parts  of  the  body  with  diphtheria  wherein  the  local 
nerves  are  again  the  ones  first  to  be  affected,  and  in  the  fact  that  in 
nearly  all  the  cases  of  generalized  and  distant  neuritis  there  is  or  has 
been  more  or  less  local  neuritis  near  the  primary  disease. 

Motor  paralysis,  flaccid  and  degenerative,  is  the  predominant 
symptom  of  this  type  of  polyneuritis.  All  the  usual  characteristics  of 
disease  of  the  lower  motor  neurone,  such  as  loss  of  reflex  action,  mus- 
cular atrophy  and  the  electrical  reaction  of  degeneration  accompany  this 
paralysis.  Sensory  manifestations  are  insignificant  or  entirely  absent. 
They  are  always  more  or  less  present  when  the  paralysis  is  severe,  and 
consist  of  parsesthesiae,  such  as  numbness,  tingling,  formication  or 
anaesthesia,  sometimes  hypersesthesia  or,  what  is  more  common,  hypses- 
thesia.  All  forms  of  sensation  may  be  altered  so  that  incoordination 
obtains.  Aubertin  doubts,  however,  the  occurrence  of  true  ataxia. 
Rarely  the  bladder  and  rectum  are  affected  and  there  is  a  remarkable 
absence  of  vasomotor,  secretory  and  trophic  symptoms.  Alhuniinnria 
is  common  and  in  fatal  cases  almost  constant. 

It  is  to  the  distribution  of  the  motor  paralysis  that  diphtheritic 
polyneuritis  owes  its  distinction.  In  the  larger  number  of  cases  it  is 
more  or  less  confined  to  the  muscles  of  the  soft  palate.  By  reason  of 
this  fluids  regurgitate  through  the  nose  and  the  speech  is  embarrassed 
with  a  nasal  twang.  Deglutition  is  therefore  difficult  and  gargling  is 
quite  impossible.  Puffing  of  the  cheeks  and  the  blowing  out  of  a 
candle  can  only  be  accomplished  when  the  nares  are  compressed.  Upon 
inspection  the  palate  is  seen  to  be  lower  than  normal,  perhaps  on  one 
side  a  little  more  than  on  the  other,  and  it  does  not  draw  up  as  it 
should  when  the  patient  utters  the  sound  "ah."  Its  sensibility  is  dimin- 
ished or  lost  and  no  reflex  response  can  be  obtained  through  it.  If  the 
disease  is  prolonged  the  palatal  muscles  will  be  seen  to  be  distinctly 
atrophied.    The  majority  of  these  cases  get  well  within  a  few  weeks. 

Next  to  the  paralysis  of  the  palate,  both  in  the  time  of  its  appear- 
ance and  the  frequency  of  its  occurrence,  is  the  paralysis  of  the  mus- 
cles of  accommodation.  In  many  cases,  with  or  without  the  implica- 
tion of  the  palate,  the  patient  complains  of  diminution  of  vision  for 
near  objects  while  it  may  be  normal  or  even  increased  for  far  objects. 
In  the  fact  that  this  cycloplegia  often  precedes  the  palsy  of  the  palate 


THE  NON-NEURONIC  DISEASES  6oi 

and  is  in  all  probability  due  to  nuclear  degeneration,  the  generalized 
nature  of  the  intoxication  receives  support.  The  reactions  of  the  pu- 
pil are  generally  normal.  It  may  be  sluggish  to  light,  but  is  scarcely 
ever  lost.  It  may  contract  when  an  effort  is  made  to  accommodate 
even  though  the  accommodation  is  absent.  Sometimes  the  external 
ocular  muscles  are  involved.  Any  of  the  remaining  cranial  nerves  may 
be  affected.  Immobility  of  the  epiglottis  from  implication  of  the  su- 
perior laryngeal  nerves  makes  swallowing  a  difilicult  and  dangerous 
task  for  fear  of  food  getting  into  the  trachea.  Paralysis  of  the  vocal 
cords  through  the  involvement  of  the  inferior  laryngeal  nerve  causes 
hoarseness  of  the  voice  and  even  aphonia.  Disturbances  of  the  respira- 
tory and  cardiac  functions  are  particularly  to  be  dreaded.  These  are 
not  rare  and  often  are  the  cause  of  death.  Though  the  ophthalmoscope 
reveals  no  morbid  changes,  a  concentric  contraction  of  the  fields  of 
vision,  marked,  of  course,  by  the  effect  of  the  cycloplegia,  has  been  occa- 
sionally seen.  Hearing  seems  never  to  have  been  affected,  but  taste  and 
smell  have.     The  tongue  and  face  are  rarely  ever  paralyzed. 

In  many  patients  paralysis  in  the  limbs  follows  the  above  manifes- 
tations. It  may  come  on  while  the  cranial  palsies  are  still  existent  or 
after  they  have  begun  to  clear  up.  Weakness,  paraesthesise  and  pains 
are  first  complained  of  in  all  four  extremities.  This  quadriplegia  is 
the  indication  of  the  polyneuritic  character  of  the  trouble.  The  legs 
more  often  suffer  before  the  arms.  The  muscles  are  soft  and  flabby. 
The  reflexes  are  diminished  or  lost.  The  electrical  reaction  of  degen- 
eration is  present  and  there  is  some  atrophy.  In  a  word,  the  paralysis 
is  of  the  typical  flaccid,  progressive,  degenerative  type.  As  it  involves 
the  extensors  and  flexors  of  the  limbs  about  equally,  there  are  no  de- 
formities. Walking  is  impaired  or  rendered  impossible.  The  sensory 
manifestations  with  an  ataxic  gait  may  lead  to  a  mistaken  diagnosis 
of  locomotor  ataxia  if  the  history  and  entire  course  of  the  disease  are 
not  given  careful  consideration. 

Not  often  are  the  trunk  muscles  involved,  and  yet  they  may  be  so 
weak  that  the  patient  cannot  turn  over  in  bed,  or  the  respirations  may 
be  embarrassed,  or  it  may  be  impossible  to  hold  up  the  head.  The 
diaphragm  may  cease  to  act. 

The  prognosis  of  diphtheritic  paralysis  is  particularly  favorable 
if  deglutition  is  not  too  much  interfered  with  and  the  respiratory  and 
cardiac  functions  continue  intact.  The  local  forms  of  the  disease  usu- 
ally get  well  in  a  few  weeks ;  the  generalized  forms  attain  their  maxi- 
mum in  about  two  or  three  months  and  then  rapidly  decline,  the  aver- 
age length  of  time  being  three  months.  Recovery,  as  a  rule,  is  com- 
plete, though  in  exceptional  cases  certain  muscles  may  remain  par- 
tially paralyzed.  Dangerous  symptoms  are  paralysis  of  the  vagus  nerve 
and  of  the  respiratory  muscles,  particularly  the  phrenic. 

Myocarditis  and  cardiac  paralysis  are  not  unfrequent  and  fatal 
occurrences.  Death  by  inanition  has  occurred  in  deglutitory  paralysis. 
Severe  cases  when  fatal  die  early ;  others  run  an  irregular  course  with 
what  seems  like  a  series  of  relapses  and  then  die  of  cardiac  or  respira- 
tory paralysis.  In  every  case  the  prognosis  is  uncertain  and  especially 
so  if  there  is  involvement  of  the  trunkal  musculature. 


602  THE  NON-NEURON IC  DISEASES 

Antitoxin  treatment  of  diphtheria  does  not  seem  to  have  lessened 
the  relative  frequency  and  severity  of  the  subsequent  paralysis  ;  though 
it  is  claimed  by  Lublinski  and  some  others  that  the  generalized  form 
is  seen  more  frequently  without  the  preceding  localized  form. 

(b)  Rheumatic  Type. — Polyneuritis  sometimes  occurs  in  con- 
nection with  rheumatism.  It  is  rare,  but  such  cases  have  been  reported 
by  Putnam,  Dana,  Gowers,  Remak  and  others.  I  have  under  observa- 
tion now  an  ataxic  case  due  solely  to  rheumatic  polyneuritis.  Paralysis 
of  neuritic  origin  not  uncommonly  occurs  in  the  joints  that  are  in- 
flamed and  swollen,  especially  the  ankle  joint.  The  exact  relationship 
of  the  arthritis  to  the  neuritis  is  not  clear.  Some  hold  that  it  is  infec- 
tious, others  that  it  is  purely  mechanical  and  irritative.  The  symptoms 
of  the  neuritis  are  typical.  Thus  in  a  patient  reported  by  Gowers  and 
seen  by  Remak  there  was  subacute  articular  rheumatism  of  both  ankle 
joints  with  considerable  pain  and  later  on  incomplete  palsy  of  all  four 
limbs,  partial  atrophy  of  the  muscles  with  the  reaction  of  degenera- 
tion, absence  of  knee-jerk,  tremors  and  involuntary  twitchings  and 
disturbances  of  sensibility.  The  generalized  nature  of  the  trouble  was 
still  further  emphasized  by  the  implication  of  the  face  and  facial 
nerves  and  the  existence  of  some  optic  neuritis.  This  picture  is  dupli- 
cated by  my  case.  The  modern  view  that  acute  articular  rheumatism  is 
primarily  a  general  infection  would  seem  to  receive  some  support  from 
the  occasional  occurrences  thus  of  polyneuritis  with  it. 

(c)  Puerperal  Type. — This  has  only  been  recognized  the  last 
few  years.  It  may  occur  during  pregnancy,  especially  in  those  who 
suffer  from  excessive  vomiting.  It  is  due  to  septic  infection  and  ap- 
pears in  both  the  localized  and  generalized  forms.  In  the  former  the 
ulnar  and  median  nerves  are  the  affected  nerves  of  choice.  Some- 
times particular  nerves  in  the  lower  limbs  are  similarly  affected.  In 
the  generalized  form  of  the  trouble  all  of  the  peripheral  nerves  of  the 
limbs,  and  any  of  the  cranial  nerves,  are  affected.  Optic  neuritis  has 
several  times  been  seen.  In  some  cases  the  clinical  picture  corresponds 
quite  a  little  to  Landry's  paralysis. 

(d)  Other  Types. — Almost  any  form  of  general  infection  seems 
capable  of  setting  up  a  general  neuritis.  As  the  bacilli  themselves  do 
not  provoke  the  lesion,  but  rather  their  poisonous  products,  these  post- 
febrile cases  correspond  with  those  that  result  from  alcohol  and  the 
metallic  poisons.  The  lesion  is  toxic  in  origin,  of  wide  distribution  and 
degenerative  in  character.  Owing  to  some  obscure  influence,  the  differ- 
ent infections  give  rise  to  some  slight  differences  in  symptomatic  de- 
tails, justifying  somewhat  the  use  of  the  term  types  of  polyneu- 
ritis in  connection  with  them.  For  example,  typhoid  infection  of  the 
nervous  systern  shows  itself  more  prominently  in  brain  symptoms  and 
paraplegic  weakness.  The  same  is  true  of  typhus  fever,  though  the 
paraplegic  weakness  and  the  more  pronounced  signs  of  poliomyelitis 
are  less  common.  Variola  is  characterized  more  particularly  by  spinal 
manifestations  along  with  the  neuritic.  Spinal  symptoms  are  rare 
after  scarlet  fever,  whereas  cerebral  trouble  with  non-nephritic  neuro- 
retinitis  is  not  uncommon.  r\Iany  of  the  symptoms  of  influenza  are 
undoubtedly  due  to  a  mild  generalized  polyneuritis  which  in  some  re- 


THE  XOX-XEUKOXIC  DISEASES  603 

3]jccts  resembles  post-diphtheritic  neuritis.  ]\lumps,  dysentery,  erysip- 
elas, pneumonia,  malaria,  gonorrhoea  and  purulent  pleuritis  have  ail 
been  followed  by  neuritis  of  a  more  or  less  disseminated  and  degener- 
-ative  type.  Pure  peripheral  neuritis,  especially  of  the  lower  limbs,  has 
heen  observed  symptomatically  during  life  and  microscopically  after 
death  in  tuberculous  patients.  The  rarit}'  of  true  syphilitic  polyneu- 
ritis has  caused  some  to  doubt  its  existence.  I  have  seen  it,  however, 
though  I  am  inclined  to  question  whether  it  ever  occurs  without  some 
implication  of  the  brain  and  cord.  If  it  be  true,  as  Savage  and  others 
contend,  that  syphilis  never  attacks  the  neurones  themselves,  then  we 
jnust  look  to  the  nutritive  disturbances  of  the  cells  in  the  cord  through 
the  specific  arteritis  or  to  the  compression  of  the  spinal  roots  by  the 
specific  meningitis  to  explain  the  degeneration  of  the  peripheral  nerves 
in  tabes,  in  pseudo-tabes  and  specific  polyneuritis  generally.  Diabetic 
^polyneuritis  is  characterized  by  an  atrophic  paralysis,  but  especially 
by  the  severity  of  its  sensory  symptoms.  The  weakness  complained  of 
in  the  lower  extremities  is  mostly  due  to  implication  of  the  crural, 
•obturator  and  peroneal  nerves.  The  eye  symptoms  and  visual  dis- 
turbances in  diabetics  have  long  been  recognized.  I  have  a  diabetic 
under  observation  in  whom  paresis  of  the  lower  extremities,  optic 
neuritis,  unilateral  facial  numbness,  pains  and  parjesthesise  in  various 
parts  of  the  body,  especially  about  the  lips  and  herpetic  eruptions  upon 
the  skin  of  the  forehead,  have  all  appeared  in  a  remittent  sort  of  a 
way.  On  account  of  the  prominence  of  the  sensor}-  disturbances  in 
these  cases  a  pseudo-tabes  may  appear  and  be  confused  with  locomotor 
ataxia.     The  prognosis  of  this  form  of  neuritis  is  usually  favorable. 

Of  great  interest,  especially  to  tropical  practitioners,  are  the  en- 
demic forms  of  polyneuritis.  We  do  not  know  much  about  these 
though  it  is  generaJlv  accepted  that  they  are  due  to  an  infective  agent 
"belonging  to  certain  localities.  They  occur  endemically  and  epidem- 
ically. Beriberi,  sometimes  called  kakke  and  found  especialh^  in  Japan 
-and  along  the  east  coast  of  Africa,  is  a  form  of  infectious  polyneuritis 
in  which  the  heart  and  blood-vessels  seem  to  be  particularly  involved. 
The  cranial  ner\"es  usually  escape,  except  the  pneumogastric.  The  in- 
tellectual and  emotional  centers  remain  untouched.  Trophic  skin  symp- 
toms are  exceedingly  rare  or  entirely  absent.  Dropsy  is  a  constant 
manifestation.  In  the  early  stages  of  the  disease  the  specific  gravity 
•of  the  urine  is  always  low,  then  it  rises,  and  finally  ends  by  going  above 
the  normal.  There  are  'no  particularly  abnormal  elements  in  the  urine. 
The  mortality  rate  under  certain  conditions  is  ver\-  high.  The  general 
infectious  character  of  the  trouble  is  shown  by  the  indication  of  spinal 
-cord  lesions  in  the  zone-like  distribution  of  the  anaesthesia  along  with 
the  polyneuritis  symptoms.  The  old  view  that  the  eating  of  rice  con- 
stituted the  most  important  etiological  factor  in  the  disease  has  been 
seriously  shaken  by  some  recent  careful  observations  and  experiments. 
Some  authorities  believe  that  a  form  of  malarial  poisoning  is  the  real 
agent  in  the  production  of  the  disease.  Glogner  and  ethers  claim  that 
they  have  found  in  the  blood  of  these  patients  malarial  plasmodia  or 
similar  organisms. 

Akatama  is  a  form  of  endemic  peripheral  neuritis  found  in  West 


604  THE  XOX-XEUROXIC  DISEASES 

Central  Africa,  of  obscure  origin  and  characterized  by  numbness,  prick- 
ling and  burning  sensations  in  the  presence  of  cold  or  damp.  It  is 
found  in  all  ages  and  both  sexes,  but  more  often  in  men  than  in  women, 
in  the  young  and  middle  aged  than  in  the  old,  and  never  in  children  or 
Europeans.  The  symptoms  are  all  indicative  of  a  mild  generalized 
neuritis.  Prognosis  is  good  as  to  life,  but  uncertain  as  to  relief.  After 
years  of  suffering  the  trouble  sometimes  ceases  spontaneously. 

Leprous  polyneuritis  is  an  endemic,  specific  form  of  the  disease. 
The  cause  of  the  disease  is  the  bacillus  of  leprpsy  and  the  pathogenesis. 
of  the  nerv'ous  manifestations  is  a  toxic  peripheral  neuritis.  The  bacil- 
lus is  abundantly  found,  as  I  have  seen,  in  the  diseased  nerv^es.  The 
neuritis  seems  to  be  of  the  primary  interstitial  type,  though  it  is  an 
open  question  whether  the  parenchymatous  degeneration  is  due  sec- 
ondarily to  mechanical  compression  b}'  the  inflamed  interstitial  tissue 
or  primarily  to  the  poisonous  products  of  the  bacilli.  The  symptoms,, 
motor,  sensor}-  and  trophic,  with  the  sensory  predominating,  are  all 
typical  of  a  peripheral  multiple  neuritis. 

DiAGXOSis. — Generally  the  diagnosis  of  multiple  neuritis  is  not; 
difificult.  A  careful  consideration  of  the  etiological  factors  in  the  case,, 
the  mode  of  origin  and  general  course  of  the  disease,  the  character  and 
distribution  of  the  symptoms  goes  far  in  establishing  it.  The  entire 
clinical  picture  exhibited  by  the  patient  and  not  one  or  two  symptoms 
alone  must  be  studied  if  mistakes  are  to  be  avoided.  There  are  two 
features  in  the  clinical  picture  which,  when  taken  in  conjunction,  will 
make  the  diagnosis  absolutely  positive.  In  the  first  place,  one  must 
discover  the  cardinal  indications  of  a  peripheral  neuritis  or  degenera- 
tion, disease  of  the  lower  neurones.  These  consist  of  flaccid  motor 
paralysis,  loss  of  deep  reflexes,  muscular  atrophy,  certain  trophic  mani- 
festations, electrical  reaction  of  degeneration  and  sensory  phenomena 
of  a  variable  character.  The  details  in  regard  to  these  symptoms  have 
been  considered  in  the  symptomatology.  In  the  second  place,  the  wide- 
distribution  of  these  symptoms  must  be  noted  and  their  relatively  irreg- 
ular severity  within  this  wide  area  of  distribution.  A  progressive  quad- 
riplegia,  involving  more  or  less  symmetrically  first  the  ends  of  the  lower 
limbs  and  then  the  upper,  with  cutaneous  patches  of  hypersesthesia, 
anaesthesia,  hyperalgesia  and  analgesia,  is  pathognomonic. 

If  the  above  facts  are  kept  well  in  mind,  the  ditterential  diagnosis 
between  polyneuritis  and  acute  anterior  poliomyelitis,  ascending- 
myelitis,  tabes  dorsalis,  spinal  meningitis  and  hemorrh.age  is  not  diffi- 
cult. 

In  acute  anterior  poliomyelitis  the  age  of  the  patient,  the  initial  feb- 
rile disturbance  and  the  course  of  the  disease  are  quite  different.  In 
infantile  palsy  there  is  apt  to  be  a  recession  of  the  symptoms  from  an 
initial  wide  extent  of  them ;  in  polyneuritis,  the  trouble  usually  begins- 
in  a  limited  area  and  rapidly  extends.  In  the  former,  especially  after 
the  symptoms  have  begun  to  recede,  there  is  a  remarkable  limitation  of 
the  paralysis  to  individual  muscles  and  muscle  groups,  whereas  in  the 
latter  much  larger  groups  or  even  the  whole  limb  is  gradually  involved 
in  the  paralysis.  In  poliomyelitis  the  atrophy  is  somewhat  more  rapid 
and  severe,  especially  in  particular  muscles.     Aloreover,  the  damage  is 


THE  NON-NEURON IC  DISEASES  605 

more  permanent  than  it  is  in  multiple  neuritis.  There  are  no  sensory 
phenomena  as  in  the  latter  disease,  nor  are  the  cranial  nerves  ever  im- 
plicated. The  symmetrical  distribution  of  the  symptoms,  their  pro- 
gressive character,  the  presence  of  sensory  phenomena,  and  the  impli- 
cation of  the  cranial  nerves  establish  the  diagnosis  of  neuritis  posi- 
iively  in  contradistinction  to  poliomyelitis.  It  does  not  follow,  however, 
that  there  may  not  be  some  poliomyelitic  manifestations  along-  with  the 
neuritic.  As  I  have  pointed  out  in  connection  with  the  toxic  and  in- 
fectious cases,  the  disease  process  is  an  extensive  one  and  it  is  probable 
that  some  of  the  peripheral  degeneration  is  due  to  damage  to  the  cells 
in  the  gray  matter  of  the  cord.  In  these  cases,  however,  there  is  always 
.some  primary  disease  of  the  peripheral  nerves  also,  and  on  account  of 
this  the  local  tenderness  of  the  nerves  and  muscles  proves  the  presence 
of  the  polyneuritis.  If  inflammatory  alterations  of  the  optic  nerve  can 
'J>e  detected,  the  case  is  positively  one  of  peripheral  neuritis. 

In  myelitis  the  symptoms  are  more  distinctly  paraplegic  in  char- 
acter, with  involvement  of  the  rectal  and  vesical  sphincters.  There  is 
present  a  girdle-pain  and  the  sensory  phenomena  generally  tend  to- 
wards anaesthesia.  In  myelitis  high  up  in  the  cord  the  reflexes  are 
•exaggerated,  the  muscles  more  or  less  rigid  and  later  on  contractured. 
The  muscular  atrophy  is  not  so  distinct,  whereas  the  cutaneous  trophic 
.symptoms  are  more  pronounced.  The  electrical  responses  are  not  much 
altered. 

In  spinal  hemorrhage  and  meningitis  the  character  of  the  pains 
and  their  distribution  about  the  trunk,  as  well  as  the  limbs,  the  local 
tenderness  in  the  spine,  the  inclination  towards  opisthotonos,  the  in- 
volvement of  the  sphincters  and  the  absence  of  cranial  symptoms, 
make  the  diagnosis  clear. 

The  sensory  types  of  multiple  neuritis  may  easily  be  mistaken  for 
tabes  dorsalis,  for  the  ataxia,  the  pains,  the  absence  of  the  reflexes  and 
•even  some  of  the  trophic  symptoms  are  the  same  in  both.  Pseudo-tabes 
is  an  excellent  name  for  these  neuritic  cases  on  account  of  this  close 
similarity.  The  differential  diagnosis  in  a  few  exceptional  cases  is 
absolutely  impossible.  The  followmg  points,  if  carefully  noted,  will 
Tielp  to  distinguish  one  disease  from  the  other  in  most  of  the  cases :  A 
Iristory  of  syphilis  is  obtained  in  most  of  the  cases  of  locomotor  ataxia. 
The  existence  of  a  true  syphilitic  polyneuritis  is  open  to  question.  In 
the  history  of  multiple  neuritis  toxins  play  the  greatest  role,  and  after 
them  the  infections  of  a  severe  and  acute  character.  In  tabes  dorsalis 
the  symptoms  approach  gradually  and  several  years  after  the  primary 
infection ;  in  pseudo-tabes  the  onset  of  the  symptoms  is  rather  abrupt, 
their  extension  is  rapid,  and  their  distribution  includes  generally  all 
four  extremities  early  and  equally.  The  ataxia  in  polyneuritis  is  not 
so  distinctly  sensory  as  it  is  in  tabes ;  it  is  a  little  more  paralytic  in 
character.  The  Argyll-Robertson  pupil  is  not  a  symptom  of  multiple 
neuritis  and  the  early  bladder  troubles  of  tabes  are  rarely  complained 
of  in  polyneurites.  Local  tenderness  upon  pressure  is  not  found  in 
tabes,  Whereas  it  is  all  but  pathognomonic  in  multiple  neuritis.  The 
crises,  especially  the  gastric  crises,  are  not  symptoms  of  the  latter. 
The  trunkal  anaesthesia  of  tabes  is  practically  unknown  in  polyneuritis. 


6o6  THE  NON-NEURONIC  DISEASES 

The  progressive  and  incurable  character  of  tabes  is  to  be  contrasted 
with  the  curabihty  of  polyneuritis  and  its  tendency  after  a  short  time  to 
get  well. 

Treatment. — The  results  of  the  proper  treatment  of  multiple 
neuritis  are  among  the  happiest  that  are  to  be  attained  in  neurology. 
A  clear  recognition  of  the  origin,  nature  and  stage  of  the  disease  is  a 
sine  qua  non,  however,  of  its  successful  management.  The  diagnosis 
having  been  positively  established,  the  first  thing  to  do.  is  to  secure  the 
patient's  entire  confidence  and  co-operation  and  to  impress  upon  him  the 
favorable  character  of  the  prognosis  if  he  is  hopeful  and  submissive. 
It  is  well  to  explain  very  clearly  to  him  that  the  greatest  danger  of  a 
fatal  issue  lies  in  the  possible  implication  of  the  cardiac  and  respiratory 
nerves,  and  that  this  is  to  be  avoided  by  perfect  serenity  of  mind  and 
quietude  of  body.  It  is  also  well  to  prepare  his  mind  by  telling  him  that 
the  disease  usually  increases  in  severity,  though  not  necessarily  in  ex- 
tent, for  the  first  four  or  five  weeks,  then  remains  stationary  with  now 
and  then  a  possible  slight  relapse  for  a  month  or  two  longer,  and 
finally  disappears  in  the  course  of  several  months  more  or  a  year.  The 
avoidance  of  surprises,  disappointments  and  rebellious  opposition  as  a 
result  of  this  forewarning  is  to  me  a  desideratum  of  much  more  con- 
sideration than  is  the  momentary  chagrin  and  depression  on  the  part 
of  the  patient  when  he  learns  of  the  prolonged  course  of  his  disease. 
Most  patients  when  thus  reasonably  appealed  to,  respond  heartily  to 
all  that  is  about  to  be  done  for  their  restoration  to-  health.  If,  however,, 
they  revolt  against  the  physician's  advice,  decline  his  further  ministra- 
tions and  undertake  a  line  of  treatment  and  a  mode  of  life  which  may 
hasten  a  fatal  termination,  the  physician  will  escape  all  blame  in  the 
matter. 

The  two  cardinal  factors  in  the  management  of  multiple  neuritis 
are  to  remove  the  cause  and  to  put  the  patient  at  absolute  rest.  No 
compromise  can  be  allowed  in  regard  to  these. 

In  the  removal  of  the  cause  both  passive  and  active  therapy  may 
be  necessary.  Unless  the  heart  is  too  weak,  all  alcoholics  should  be  at 
once  discontinued.  In  some  cases  the  alcohol  can  only  be  diminished. 
The  amount  of  the  diminution  can  vonly  be  determined  and  regulated  by 
a  careful  observation  of  the  pulse  in  each  individual  case.  It  is  not 
well  therefore  ever  to  suddenly  deprive  a  patient  v/ith  alcoholic  poly- 
neuritis of  all  stimulus.  A  much  safer  way  would  be  to  gradually  re- 
duce the  alcohol,  rapidly  in  some  cases  and  more  slowly  in  others,  but 
always  as  promptly  and  completely  as  possible,  and  to  gradually  in- 
crease the  administration,  pari  passu,  of  some  other  form  of  stimulant, 
like  strychnia,  ammonium  salts,  etc. 

If  the  disease  is  due  to  lead,  arsenic,  copper,  mercury  or  other 
toxic  agent,  of  course  the  source  of  the  poisoning  must  be  sought  for 
and  eliminated  at  once.  The  iodide  of  potassium  will  help  to  remove 
the  lead  from  the  body.  Whatever  the  toxic  substance  may  be  its 
elimination  from  the  organism  should  be  hastened  by  free  purgation, 
diuresis  and  diaphoresis.  Free  bathing  is  excellent  for  this  purpose, 
but  it  must  not  cause  too  much  exertion  on  the  part  of  the  patient. 

The  infection  that  may  lurk  behind  the  multiple  neuritis  calls  for 


THE  XON-XEUROXIC  DISEASES  607 

its  own  appropriate  therapy.  Quinine  must  be  given  when  there  is 
maJaria  present.  Antistreptococcic  serum  may  be  tried  in  scarlatinal, 
puerperal  and  other  forms  of  septic  polyneuritis.  The  salicylates  are 
indicated  in  rheumatic  neuritis.  Autointoxication  with  treatment  di- 
rected to  the  alimentary  canal  must  be  thought  of.  Endemic  cases  of 
the  disease,  like  beriberi,  must  be  removed  from  the  infected  locality 
and  the  latter  cleaned  up  as  far  as  possible  with  bactericides.  Severe 
anaemia,  cachexia  and  senility  with  arterio-sclerosis,  with  which  poly- 
neuritis is  sometimes  associated,  call  for  their  own  special  treatment. 

If  there  is  a  histor}^  of  syphilis  preceding  the  neuritis,  one  natural- 
ly thinks  of  the  administration  of  mercury.  It  is  well  to  try  the 
remedy,  but  it  must  be  done  very  cautiously.  It  is  not  positively  set- 
tled yet  w'hether  the  polyneuritis  that  sometimes  occurs  in  syphilitics  is 
due  to  the  infection  or  to  the  heroic  use  of  mercury,  which  in  most 
of  these  cases  will  be  found  to  have  just  preceded  the  onset  of  the 
paralysis.  In  my  own  opinion  the  polyneuritis  is  due  to  the  syphilis 
and  not  to  the  mercury,  reasons  for  which  belief  I  will  not  stop  here 
to  elaborate.  Nevertheless  I  am  convinced  from  personal  observation 
that  the  administration  of  mercury  may  render  the  multiple  neuritis 
decidedly  worse.  Therefore,  if  there  is  no  improvement,  and  especially 
if  the  symptoms  are  increased  by  the  cautious  use  of  mercury  in  poly- 
neuritis in  a  syphilitic  patient,  it  had  better  be  promptly  discontinued 
and  the  iodide  of  potash  used  instead. 

If  the  case  is  a  severe  one,  absolute  quiet,  both  of  mind  and  body, 
is  imperative.  The  paralysis  will  usually  effect  the  physical  rest;  the 
mental  calmness  must  be  secured  by  seclusion  and  appropriate  diver- 
sion. Hence  in  the  early  stage  of  the  disease  these  patients  had  better 
be  placed  in  a  hospital  where  they  can  be  kept  apart  from  all  domestic 
and  business  intrusion,  or  if  they  must  remain  at  home,  they  should 
be  given  a  firm  and  tactful  nurse  and  isolated  in  some  remote  apartment. 
It  is  more  difficult  to  manage  in  this  respect  the  milder  cases,  for  they 
will  insist  upon  moving  about  some  in  their  partially  paralyzed  condi- 
tion. They  must  be  enjoined  to  keep  their  bed  and  only  move  for  the 
sake  of  change  from  the  bed  to  the  couch  or  rolling  chair.  In  a  word, 
all  active  functioning  of  the  nervous  system  must  be  prohibited  during 
the  first  two  or  three  weeks  of  the  disease.  Nor  must  there  be  any 
passive  activity,  such  as  massage,  hauling  of  the  patient  about,  etc., 
during  this  same  period.  If  immobility  and  mental  rest  are  accom- 
plished in  the  beginning  of  the  disease  and  the  cause  promptly  removed, 
it  will  cease  that  much  sooner  to  extend  and  the  stationary  and  con- 
valescent period  will  be  that  much  earlier  secured.  It  must  never  for  a 
moment  be  forgotten  that  the  cardiac  and  respiratory  functions  are 
liable  to  be  affected  in  any  case  and  to  avoid  this  danger  the  rest 
must  be  almost  absolute.  The  patient  must  not  move  about  in  bed 
hastily,  or  sit  up,  until  all  acute  symptoms  show  signs  of  abating.  Even 
then  caution  must  be  observed. 

In  the  first  stage  diaphoretic  measures,  if  used  carefully,  may  be 
highly  advantageous.  Hot  baths,  hot  packs  fostering  perspiration  for 
an  hour  or  two  daily  or  every  other  day,  may  be  employed.  The  heart 
action  must  be  closely  watched.    Hot  drinks  may  be  of  some  benefit  in 


6o8  THE  NOX-NEURONIC  DISEASES 

provoking  diaphoresis  and  diuresis,  with  or  without  the  hot  baths.  In 
one  or  two  instances  I  have  seen  the  disease  increased  and  extended 
by  the  too  vigorous  use  of  heat  in  this  way.  Cold  is  always  contra- 
indicated,  hence  the  room  must  be  kept  warm  and  free  from  draughts. 

The  weakness  and  pains  are  two  of  the  most  prominent  symptoms 
calling  for  special  attention.  The  former  is  to  be  combated  by  a 
strengthening  and  nutritious  diet  and  by  the  appropriate  use  of  stimu- 
lants. Milk  in  abundance,  egg-nog,  meat  juices,  tender  beef,  fats  and 
cod-liver  oil  are  to  be  given  as  freely  as  the  digestive  organs  will  dis- 
pose of  them.  Diphtheritic  patients  may  have  to  be  fed  through  a  tube. 
For  the  weakness  it  may  be  necessary  to  resort  to  wine,  strychnia, 
camphor,  aromatic  spirits  of  ammonia,  etc.  The  shooting  pains  and 
muscular  tenderness  are  often  so  marked  that  relief,  however  slight, 
must  be  attempted.  For  this  purpose  the  salicylate  of  soda,  in  twenty- 
grain  doses  every  two  or  three  hours,  is  sometimes  useful.  Dana  says 
that  a  dram  or  two  of  the  fluid  extract  of  ergot  repeated  in  three  hours 
sometimes  relieves  the  pain.  The  coal-tar  preparations  have  not  been 
very  effective  in  my  hands  and  T  am  loath  to  push  them  on  account 
of  their  depressing  action  upon  the  Jieart.  I  prefer  the  use  of  warmth, 
such  as  swathing  the  limibs  in  hot  flannels  and  in  cloths  wrung  out  in 
hot  water.  Painting  the  limbs  with  menthol  and  enveloping  them  in 
cotton  batting  is  sometimes  soothing.  As  a  last  resort  morphine  may 
be  used. 

When  the  diminution  of  the  pains  indicates  that  the  disease  has 
entered  upon  its  stationary  or  convalescent  stage,  in-assage,  electricity 
and  measures  to  counteract  late  contractures  and  deformity  are  to  be 
instituted.  If  there  are  any  signs  of  irritation  remaining,  galvanism  in 
the  form  of  a  stabile  current  is  the  only  form  of  electricity  permissible. 
Later  on  the  labile  current,  in  strength  of  five  to  eight  milliamperes, 
may  be  administered  daily  for  about  five  minutes.  The  faradic  current 
to  stimulate  the  muscles  should  only  be  em.ployed  when  convalescence 
has  gotten  well  under  way.  Much  more  effective  than  electricity  in 
my  experience  has  been  massage.  The  muscles  should  be  gently  rubbed 
and  kneaded  and  stroked  once  or  twice  a  day  for  a  short  time.  The 
use  of  olive  oil  or  cocoanut  oil  in  the  hand  of  the  masseur  is  agreeable 
to  the  patient.  The  stroking  should  be  gentle,  towards  the  body  and  in 
the  vicinity  of  the  principal  nen^es  affected.  It  may  be  increased  in 
vigor  as  the  case  continues  to  improve.  Passive  exercises  and  mild 
gymnastics  may  later  on  take  the  place  of  the  massage.  Exhaustiorf 
must  be  carefully  guarded  against  in  all  these  mechanical  measures  and 
the  patient  should  be  urged  to  lie  down  and  rest  frequently.  Tonics, 
such  as  strychnia,  arsenic,  iron,  quinine  and  the  hypophosphites,  are  to 
be  administered.  In  obstinate  paralysis  Oppenheim  recommends  the 
subcutaneous  administration  of  strychnia,  one-sixtieth  to  one-twentieth 
grain  several  times  daily.  Iodide  of  potassium,  two  per  cent,  carbolic 
acid  and  carbolmorphine,  the  latter  two  hypodermically  in  the  neighbor- 
hood of  the  affected  nerves,  have  received  high  endorsement.  In  ad- 
vanced convalescence  general  tonic  and  hygienic  measures,  including 
baths,  change  of  climate,  abundance  of  fresh  air,  good  food  and  judi- 
ciously guarded  exercise  are  to  be  recommended. 


THE  NON-NEURONIC  DISEASES  609 

Deformities,  particularly  in  young  persons,  are  to  be  prevented  by 
watching  the  attitude  of  the  limbs  during  the  course  of  the  disease. 
When  late  contractures  begin  to  manifest  themselves  they  are  to  be 
combated  by  massage,  passive  motion,  forcible  replacement  with  the 
appropriate  use  of  splints  and  other  apparatus.  Tenotomy  is  not  de- 
manded here,  as  it  often  is  in  poliomyelitis,  for  the  disease  being  more 
generalized  opposing  sets  of  muscles  are  apt  to  be  more  equally  af- 
fected. 

Relapses  are  to  be  warned  against  and  prevented  by  a  strict  ad- 
herence to  the  directions  of  the  medical  adviser. 

TUMORS  OP   THE  NERVES.     NEUROMATA. 

A  neuroma  in  the  modern  sense  is  a  nerve  tumor,  but  not  all  nerve 
tumors  are  neuromata.  Since  the  discovery  of  Virchow  that  there  are 
specific  nerve  newgrowths,  and  newgrowths  in  the  nervous  system  that 
are  not  specifically  neural,  neuromata  have  been  divided  into  the  true 
and  the  false.  It  is  but  fair  to  say  that  some  pathologists  do  not  accept 
the  distinction  thus  made  by  Virchow. 

The  true  neuroma  is  very  rare  and  consists  of  true  nervous  ele- 
ments. Virchow  speaks  of  the  "myelinic"  and  "amyelinic''  forms,  those 
that  contain  respectively  medullated  and  non-medullated  fibres.  Ziegler 
is  among  those  who  doubt  the  propriety  of  separating  the  neuromata 
into  a  special  class  and  believe  that  the  nerve-fibres  are  not  implicated 
in  the  neoplasm.  He  thinks  the  growths  are  merely  neurofibromata,  neu- 
rosarcomata,  neurolipomata,  etc.,  arising  in  the  epineurium  and  peri- 
neurium. 

The  false  neuromata  are  heterologous  growths  and  are  given  the 
same  names  that  they  would  have  were  they  in  other  parts  of  the  body. 
They  include  the  fibromata,  sarcomata,  myxomata,  syphilomata,  etc. 
The  first  are  the  most  common  and  are  the  basis  probably  of  the 
majority  of  the  true  neuromata.  There  is  nothing  distinctive  about 
these  false  neuromata  that  need  special  notice  because  they  happen  to 
occur  in  the  nervous  system. 

Neurone  cell-bodies  have  scarcely  ever  been  discovered  in  the  true 
neuromata.  Between  the  nerve  fibres  there  is  connective  tissue  which 
renders  the  growth  hard  and  firm  and  which  is  ofttimes  so  abundant 
that  the  neoplasm  stands  midway  between  the  true  and  false  neuro- 
mata. These  tumors  are  multiple  or  single.  They  occur  mostly  on 
the  spinal  nerves  and  are  usually  small,  varying  in  size  from  a  pea  to  a 
pigeon's  egg  (i  cm.  to  6  cm.).  They  are  prone  to  appear  as  multiple 
growths  in  particular  nerve  areas.  For  example,  the  brachial  plexus, 
the  Cauda  equina  or  the  nerves  of  the  pelvis  may  be  the  seat  of  them. 
Sometimes  they  are  strung  along  the  nerve  trunks  like  beads. 

Multiple  neuromata  are  of  the  neuro-fibromatous  variety.  They 
are  exceedingly  numerous  sometimes,  as  many  as  a  thousand  or  more 
having  been  counted  in  one  individual. 

Fibroma  molluscum  multiplex,  a  general  neuro-fibromatosis,  is  the 
condition  in  which  multiple  neuromata  are  found  upon  the  trunks  of  the 


6io 


THE  NON-NEURONIC  DISEASES 


subcutaneous   nerves.      Naevi   are   generally    associated    with    it,    thus 
indicating  the  congenital  nature  of  the  trouble. 

Plexifonn  neurouia,  or  congenital  elephantiasis,  is  where  there 
is  a  great  interlacing  of  cords,  nodular  and  tortuous.  The  fibres  of  the 
nerves  as  for  example,  the  trigeminal,  the  lumbar,  the  brachial  and 
solar  plexuses,  the  nerves  of  the  penis  and  mammse,  thicken,  break  up 
and  recombine  in  a  twisted  sort  of  a  way.     They  can  be  felt  plainly 

FIGURE  133- 


Geueral  ueurofi- 
bromata.  Rosary-like 
arrangement  of  the 
neuroma  along  the 
peripheral  nerves  of 
the  right  arm ;  the 
small  knots  areplainly 
visible  beneath  the 
skin.  (After  Robert 
Smith,  reproduced  by 
Marie.) 

under  the  skin.  The  nerve-fibres  are  united  by  the  hyperplastic  con- 
nective tissue.  The  disease  begins  in  foetal  life  and  is  related  to 
pachydermatocele  and  elephantiasis  mollis.  The  growth  of  this  condi- 
tion is  extremely  slow.  It  exerts  pressure  upon  the  neighboring  struc- 
tures. 

Sometimes  multiple  neuromata  are  malignant.  Trauma  and  hered- 
ity are  behind  them  and  the  greater  nerve  trunks  are  the  seat  of  them, 
especially  the  perineurium.  They  are  spindle-shape  and  sometimes  are 
very  large  in  size.    Sarcomatous  cells  are  often  found  in  them. 


THE   XOX-XEUROXIC  DISEASES  6ll 

Tuhercula  dolorosa  are  small  multiple  tumors,  mostly  of  the  fibro- 
niatous  variety,  that  occur  in  great  profusion  on  the  subcutaneous 
sensory  nerves.     They  are  painful  and  can  easily  be  felt. 

Gliomata  are  not  frequently  seen  in  the  peripheral  nerves.  Thev 
occur  in  the  auditory  ner\^e. 

Carcinoma  usually  occurs  as  a  secondary  condition  in  the  form  of  a 
diffuse  or  nodular  infiltration  of  the  nei^^e  from  a  neighboring  growth. 
Rarely  it  is  seen  as  an  isolated  neoplasm. 

Syphilomata  occur  mostly  on  the  cranial  and  spinal  nen.-e  roots ; 
not  so  often  on  the  peripheral  nerves. 

In  lepra  ancssthctica  the  nerves  are  often  infiltrated,  to  a  ver}-  great 
degree,  causing  netiro-fibromatous  swellings  upon  them.  The  condi- 
tion is  of  the  nature  of  a  cirrhotic  inflammation  rather  than  a  nodular 
development. 

Nerve  tumors  are  practically  ahvavs  within  the  ner\-e  sheath.  If 
they  are  on  one  side,  the  nerve  itself  may  pass  intact  around  them. 
Frequently,  however,  the  nerve  is  involved  and  infi.ltrated,  with  its 
fibres  spread  out  ever  the  surface  of  the  gro\\th.  Even  under  these 
circumstances  the  nerve  may  not  be  much  damaged,  which  explains  the 
frequent  absence  of  symptoms.  False  neuromata  are  more  damaging 
to  the  nen'e  fibres  and  are  therefore  accompanied  by  more  pronounced 
symptoms  tlian  are  the  true  neuromata. 

Etiology. — The  etiology  of  tumors  has  not  been  brought  to  com- 
pletion yet.  Heredity  and  a  neuropathic  constitution  are  undoubtedly 
responsible  for  certain  types  of  them,  and  to  some  degree  for  all  of 
them.  This  is  shown  in  their  familial  characteristics  and  their  frequent 
association,  especially  the  multiple  neuromata,  with  idiocy  and  cretin- 
ism. The  phthisical  and  scrofulous  condition  were  thought  by  \Trchow 
to  be  blameable  for  them.  Curiously  the  multiple  variety  of  the  disease 
seems  to  belong  to  men,  the  isolated  to  women.  Age  exercises  no  in- 
fluence upon  their  appearance.  Even  the  hereditary  form  of  the  dis- 
ease may  not  appear  till  middle  age. 

The  cachexicc  give  rise  to,  and  determine,  the  character  of  the 
neoplasms.  Whatever  underlies  in  the  patient's  constitution  the  forma- 
tion of  the  fibrous  growths,  sarcoma,  carcinoma,  myxoma,  lipoma,  tuber- 
cle, is  responsible  for  the  same  conditions  in  the  nervous  system. 
Traumata  and  chronic  neuritis  may  initiate  the  neuromata.  Amputa- 
tion neuromata,  or  so-called  bulbous  nerves,  belong  here.  As  the  nerve 
fibrillae,  when  cut,  grow  out  from  the  proximal  end  like  the  twigs  of  a 
vine,  it  is  easy  to  understand  how  by  mechanical  obstruction  and  other- 
wise they  may  become  twisted  and  agglutinated  together  and  held  by 
the  connective  tissue  in  a  mass. 

Symptoms. — I  have  already  remarked  that  as  the  nerve  often 
courses  intact  around  the  tumor,  there  are  no  neural  symptoms  of  its 
presence.  On  the  other  hand,  the  symptoms  may  be  most  severe  and 
even  dangerous,  the  latter  when  the  growth  are  in  such  nen-es  as  the 
pneumogastric,  phrenic  or  ether  splanchnic  nerve.  The  symptoms  are 
of  an  irritative  or  paralytic  character  and  involve  all  neural  functions, 
motor,  sensory,  trophic,  vasomotor  and  secretorv.  In  a  word,  they  are 
the  symptoms  of  neuralgia  and  neuritis. 


6l2  THE  NON-NEURONIC  DISEASES 

Pain  is  a  particularly  common  symptom.  It  may  be  a  local  tender- 
ness or  a  peripheral  sharp,  shooting  pain.  Often  it  is  acute,  burning, 
boring  and  darting.  It  follows  the  co'urse  of  the  nerve  or  appears  in 
the  area  of  its  distribution.  In  the  Siime  area  parcBSthesice  occur  and 
more  or  less  hypcesthesia.  The  topographical  correspondence  of  these 
sensory  phenomena  with  the  motor  manifestations  is  a  particularly 
characteristic  feature. 

The  motor  phenomena  include  twitchings,  jerkings,  spasms  and 
tonic  contractions  in  the  muscles  innervated  by  the  diseased  nerve. 
Paralysis  and  atrophy  are  very  rare.  General  convulsions  and  reflex 
epilepsy  have  been  seen ;  also  hysteria,  neurasthenia  and  hypochondria- 
sis. The  pain  is  the  most  disturbing  feature,  often  completely  wearing 
the  patient  out  and  reducing  him  physically. 

In  general  neurofibromatosis  Marie  has  noted  the  occurrence  of 
psychosis,  sensory  disorders  and  convulsions. 

Paraplegia  and  vesical  paralysis  sometimes  are  the  result  of  neuro- 
mata of  the  Cauda. 

Plexiform  neuroma  rarely  produces  any  other  symptom  than  a 
hypaesthesia. 

Prognosis. — Neuromata  are  progresssive,  though  they  may  be- 
come stationary  or  regress.  Multiple  neuromata  offer  a  better  general 
prognosis  than  do  the  isolated  neoplasms.  The  reason  is  obvious. 
Multiple  neuromata  are  usually  fibrous.  Among  the  isolated  tumors 
occur  the  heterologous  growths,  such  as  sarcoma,  cancer,  etc.  The 
presence  and  the  severity  of  the  symptoms  add  to  the  gravity  of  the 
prognosis. 

Treatment. — Except  in  syphilomata,  when,  of  course,  mercury 
and  the  iodides  are  called  for,  medicines  are  useless  in  tumor  of  the 
nerves.  The  condition  is  essentially  a  surgical  one.  Of  course,  this 
applies  to  isolated  tumors  that  can  be  reached  and  that  reveal  symptoms. 
After  extirpation  of  a  neuroma,  the  possibility  of  complete  paralysis 
is  great.  This  can  be  obviated  sometimes  by  an  immediate  suturing, 
transplanting  or  other  form  of  operation  upon  the  nerve  stumps.  Some 
tumors  can  be  peeled  off,  as  it  were,  from  the  nerve  and  when  thus  re- 
moved there  will  be  a  restoration  oi  the  neural  functions.  This  has 
happily  occurred  several  times. 

In  cases  of  multiple  tumors  some  of  the  growths  with  marked  symp- 
toms can  be  operated  upon.    Return  of  them  is  the  rule,  however. 

Electrolysis  and  caustics  are  inadvisable.  There  is  danger  of 
setting  up  neuritis  and  making  what  is  bad  worse.  Strong  galvanic 
currents  applied  percutaneously,  mercury  and  large  doses  of  iodides 
have  been  recommended  for  true  neuromata  and  neurofibromata.  The 
results  of  the  treatment,  however,  are  not  very  encouraging. 

The  terminal  neuromata  of  tubercula  dolorosa  may  be  cut  out 
without  danger;  otherwise  these  and  all  painful  tumors  must  needs 
be  quieted  with  analgesics. 

There  is  no  treatment  for  plexiform  neuroma.     Excision  is  inad 
visable. 


THE  XOX-XEUROXIC  DISEASES  613 

DISEASES  OF  THE  SPINAL  NERVES. 
PHRENIC  NER\'E. 

Diaphragmatic  paralysis  is  usually  due  to  spinal  cord  disease.  Dis- 
ease that  involves  the  third  and  fourth  cer\dcal  roots  implicates  the 
phrenic  nerve.  It  need  hardly  be  mentioned  that  such  diseases  include 
spinal  meningitis,  particularly  pachymeningitis,  caries  of  the  spine, 
fractures,  dislocations,  exostoses,  tumors,  hemorrhage  and  especially 
gummatous  meningitis.  Direct  traumata  do  not  often  reach  the  nerve, 
because  it  is  very  deep  in  the  neck.  Wounds  in  the  neck  and  tumors 
and  aneurisms  in  the  thorax  may  implicate  it.  Duchenne  has  met 
with  disease  of  the  nerve  in  lead  poisoning.  It  has  been  affected 
bilaterally  in  alcoholic  intoxication.  Diphtheria  has  infected  it.  The 
influence  of  cold  in  setting  up  a  phrenic  neuritis  should  be  regarded 
with  skepticism. 

Paralysis  of  the  diaphragm  is,  of  course,  the  symptom  of  phrenic 
nerve  disease.  If  one  nerve  is  iinplicated,  one  side  of  the  diaphragm 
only  is  paralyzed.  The  continued  activity  of  the  other  side,  however, 
causes  the  whole  muscle  to  move  so  that  it  is  often  difficult  to  discover 
the  unilateral  paresis. 

In  a  state  of  quietude  on  the  part  of  the  patient,  the  loss  of 
diaphragmatic  stimulation  does  not  materially  lower  the  breathing  ca- 
pacity. Exertion,  however,  causes  quick  breathing  and  a  weakening 
of  the  voice.  This  dyspnoea  may  become  very  pronounced  and  dis- 
tressing. Both  inspiration  and  expiration  are  affected.  The  movements 
of  the  thorax  are  usually  increased,  the  upper  part  of  the  abdominal 
wall  being  so  much  drawn  forward  as  to  simulate  the  eft'ect  of  the 
descent  of  the  diaphragm. 

Paralysis  of  the  diaphragm  proditces  trouble  in  diagnosis  only 
when  it  is  unilateral.  In  most  forms  of  phrenic  neuritis  it  is  unilateral. 
It  is  bilateral  generally  in  spinal  cord  diseases  and  diseases  of  the  spine. 
Careful  examination  will  enable  one  to  detect  a  unilateral  paralysis. 
The  breathing  sounds  at  the  base  of  the  lung  upon  that  side  will  be 
diminished.  The  electrical  responses  will  be  diminished.  The  objective 
diaphragmatic  phenomenon  will  be  absent.  And  there  may  be  a  painful 
spot  to  pressure  on  the  scaleni  muscles  near  the  sterno-mastoid  muscle. 

Sometimes  the  diaphragm  is  paralyzed  from  myositis.  This  may 
lead  to  an  erroneous  diagnosis  of  phrenic  neuritis.  It  is  usually  a 
secondary-  trouble  from  peritonitis  or  pleuritis,  on  account  of  which 
it  can  usually  be  readily  differentiated.  Thie  characteristic  pains  of 
these  latter  diseases  are  also  distinguishing. 

It  is  very  doubtful  if  there  is  a  true  hysterical  diaphraginatic 
paralysis.  Superior  costal  breathing  is  more  common  in  women  than 
in  men  and  it  is  the  type  of  respiration  in  ner\-ous  people  and  hysterics. 
It  is  easy,  therefore,  for  a  hysteric  to  simulate  diaphragmatic  paralysis. 
Mental  distraction  will  cause  the  epigastrium  to  advance  and  thus  show 
the  absence,  when  a  deep  inspiration  is  unguardedly  taken,  of  a  true 
organic  paralysis.     Dyspnoea  does  not  occur  in  hysterics.     Ether  nar- 


6l4  THE  A'ON-NEURONIC  DISEASES 

cosis  would  confirm  tlie  diagnosis.  According-  to  Wernicke,  there  is  a 
hysterical  insufficiency  of  the  phrenic  nerve  which  is  associated  with 
fear  and  inspiratory  dyspncea. 

Callender  has  described  a  primary  and  isolated  degeneration  of 
the  diaphragm  after  death.  Whether  it  ever  produces  inaction  of  the 
ni'uscle  during  life  we  do  not  know.  In  spinal  cord  disease  that  causes 
diaphragmatic  paralysis,  other  muscles  are  symptomatically  affected 
also. 

The  prognosis  is  generally  favorable,  though  it  is  dependent  upon 
the  cause.  Multiple  neuritis  as  a  cause  offers  a  rather  unfavorable 
prognosis.  I  have  seen  dyspncea  and  death  occur  in  this  disease  in  this 
way. 

Tlie  treatment  involves  first  the  removal  of  the  cause.  Counter- 
irritation  over  the  anterior  triangle  of  the  neck  and  electrical  stimula- 
tion of  the  nerve  when  inflamanation  has  subsided,  about  sums  up  the 
therapy.  Strychnia  has  been  especially  commended  in  the  diphtheriti; 
paralysis. 

THE  BRACHIAL  PLEXUS. 

Anatomy. — The  brachial  plexus  is  formed  by  the  union  of  the  an- 
terior trunks  of  the  four  lower  cervical  and  the  greater  part  of  the  first 
dorsal  nerves.  It  reaches  from  the  lower  part  oi  the  neck  to  the  axil- 
lary space.  Opposite  the  coracoid  process  it  ends  in  the  large  nerves 
that  go  to  supply  the  upper  extremity. 

The  fifth  and  sixth  cervical  nerves  join  together  at  the  outer  bor- 
der of  the  scalenus  medius  to  form  an  upper  trunk.  The  eighth  cervical 
and  first  dorsal  form  in  the  same  way  a  lower  trunk.  The  seventh 
forms  the  middle  trunk  between  these  two.  Just  outside  of  the  scaleni 
muscles,  each  primary  trunk  divides  into  an  anterior  and  a  posterior 
branch.  The  anterior  branches  of  the  upper  and  middle  trunks  unite 
and  form  the  upper  or  outer  cord  of  the  plexus.  The  anterior  branch 
of  the  lower  trunk  alone  forms  the  lozver  or  inner  cord  of  the  plexus. 
The  posterior  branches  of  all  the  three  trunks  unite  to^  form  the  middle 
or  posterior  cord. 

The  branches  that  come  olf  from  the  brachial  plexus  are  very 
numerous.  Those  that  originate  above  the  clavicle  are  the  posterior 
thoracic  and  the  suprascapular  nerves,  a  nerve  for  the  rhomboid  mus- 
cle, another  for  the  snbclnznus,  branches  for  the  scaleni  and  long  us  colli 
muscles  and  sometimes  a  branch  to  the  phrenic  nerve.  Those  that 
originate  from  the  plexus  below  the  clavicle  may  be  arranged  as  fol- 
lows, according  to  Quain,  whom  I  follow  in  these  anatomical  facts : 

From  the  upper  or  outer  cord — the  external  of  the  two  anterior 
thoracic  nerves,  the  musculo-cntancotis,  and  the  outer  head 'of  the 
fnedian. 

From  the  lower  or  inner  cord — the  inner  of  the  two  anterior 
thoracics,  the  nerve  of  Wrisberg  or  small  internal  cutaneous,  the  in- 
ternal cutaneous,  the  ulnar  and  the  inner  head  of  the  median. 

From  the  posterior  cord — the  subscapular  nerves,  the  circumflex 
and  the  musculo-spiral. 


THE  NON-NEURONIC  DISEASES 


615 


For  the  spinal  segmental  origin  and  the  ultimate  distribution  of 
the  branches  of  the  brachial  plexus,  the  reader  is  referred  to  the  admira- 
ble tables  compiled  from  Starr,  Mills,  Sachs,  Dana  and  Thorburn  at 


FIGURE  134. 

Diagrammatic 
outline  of  the  cervical 
and  brachial  plexuses. 
^      (A.  T.)     ^ 

The  nerves  are  separated 
from  the  spinal  cord  at  their 
origin  and  are  supposed  to 
be  viewed  from  before  :  CI, 
the  first  cervical  or  sub- 
occipital nerve,  and  the 
IJoman  numbers  in  succes- 
sion from  II,  to  V III,  the cor- 
res^jonding  cervical  nerves  ; 
DI,  the  first,  and  II,  and 
III,  the  second  and  third 
dorsal  nerves  ;  the  origin  of 
the  posterior  primary  branch 
is  shown  in  all  the  nerves  ; 
of  these  p  2,  indicates  the 
great  occipital  from  the 
second,  and/*  3,  the  smallest 
occipital  nerve  from  the 
third.  Cervical  plexus :  1, 
anterior  primary  branch  of 
the  first  cervical  nerve  and 
loop  of  union  with  the  second 
nerve ;  2,  small  occipital 
nerve ;  3,  great  auricular 
nerve ;  3',  superficial  cervical 
nerve ;  3  n,  communicating 
branches  to  the  descendens 
noui  from  the  second  and 
third  ;  3  s,  communicating 
to  the  spinal  accessory  from 
the  third  and  fourth  nerves ; 
4,  supraclavicular  nerves  ; 
the  loops  or  arches  of  com- 
munication between  the  foux' 
upper  cervical  nerves,  and 
between  the  fourth  and 
fifth,  are  shown ;  4',  phrenic 
aerve.  BracMal  plexusr  V,  to  VIII',  and  D',  the  five  roots  of  the  brachial  plexus  ; 
5,  the  rhomboid  nerve  ;  5',  suprascapular ;  5",  posterior  thoracic  ;  6,  nerve  to  the 
snbclavius  muscle  ;  7,  7,  inner  and  outer  anterior  thoracic  nerves ;  8,  8',  8",  sub- 
scapular nerves.  In  the  larger  nerves  proceeding  to  the  shoulder  and  arm  from  the 
plexus,  those  of  the  anterior  divisions  are  represented  of  a  lighter  shade,  those  belong- 
ing to  the  posterior  division  darker  ;  ec,  external  cutaneous  or  musculo-cutaneous  ;  m, 
median  ;  u,  ulnar  ;  ic,  internal  cutaneous  ;  iv,  nerve  of  Wrisberg ;  r^  musculo-spiral  ;  c, 
circumflex  ;  i,i,  intercostal  nerves  ;  i',  lateral  branch  of  the  same  ;  ih,  intercosto-humeral 
nerve. 

(From    Quain.) 


the  end  of  the  chapter.     In  localizing  the  lesion  in  the  spinal  nerve 
palsies,  the  table  should  be  constantly  consulted. 

Individual  trunks,  as  well  as  the  whole  plexus,  may  be  attacked 
by  disease.     It  is  practically  impossible  to  make  a  clinical  differentia- 


6l6  THE  NON-NEUROXIC  DISEASES 

tion  between  diseases  of  the  trunks  of  the  plexus  and  the  roots  out  of 
which  they  are  formed. 

Traumatic  J  toxic  and  infectious  causes  are  here  as  usual  the  source 
of  the  trouble.  The  first  far  outnumber  the  other  two.  Dislocations, 
fractures,  contusions,  blows  about  the  shoulder  are  especially  impor- 
tant as  causes. 

Compressing  tumors,  exostoses,  aneurism,  arteriosclerotic  dilata- 
tions are  of  the  nature  of  mechanical  traumata.  An  arthritis  of  the 
joint  may  set  up  a  neuritis  in  the  neighboring  nerves.  Tight  bandages, 
handcuiTs,  lying  on  the  arm  may  produce  local  trouble  in  the  nerves. 

I  will  now  take  up  in  detail  some  of  the  special  paralyses  of  the 
brachial  plexus  and  its  branches. 

Erb's  Palsy. — This  is  a  combined  palsy  of  the  shoulder  and  arm 
and  is  due  to  a  lesion  of  the  trunk  of  the  brachial  plexus  formed  by  the 
fifth  and  sixth  cervical  roots.  The  muscles  that  are  paralyzed  are  the 
deltoid,  the  biceps,  the  brachialis  intemus,  supinator  longus  and  some- 
times the  supinator  hrevis,  infraspinatus  and  subscapular.  It  is  a  fifth 
and  sixth  cervical  root  or  primary  trunk  palsy.  The  central  parts  and 
upper  cords  of  the  plexus  are  damaged.  It  is  often  spoken  of  as  the 
upper  arm  palsy.  Traumata  are  the  chief  cause  of  it,  though  it  has 
been  seen  as  an  isolated  paralysis  in  toxic  and  infectious  maladies.  The 
position  of  the  arm  in  which  the  plexus  is  made  to  compress  for  a  long 
time  the  clavicle  may  cause  it.  Thus  it  occurs  as  an  obstetrical  palsy, 
as  a  result  of  prolonged  narcosis  with  the  arm  forcibly  elevated  out- 
ward and  backward.  Carrying  of  heavy  burdens  on  the  shoulder  has 
produced  it.  It  has  been  seen  to  occur  bilaterally.  The  arm  hangs 
by  the  side  of  the  body  and  the  forearm  cannot  be  flexed. 

As  an  obstetrical  palsy  Erb's  type  is  slow  to  recover  and  when  due 
to  injury  in  adults  it  is  apt  to  be  severe.  It  has  all  the  characteristics 
of  a  peripheral  palsy,  such  as  the  flaccidity  of  the  paralysis,  the  atrophy, 
the  loss  of  reflex  and  the  reaction  of  degeneration. 

Klumpke's  Palsy. — This  is  a  brachial  plexus  paralysis  due  to  dis- 
ease of  the  eighth  cervical  and  first  dorsal  branches.  As  it  involves  the 
triceps,  the  wrist  flexors  and  pronators,  and  the  flexors  and  extensors 
of  the  hand,  it  is  often  called  the  lozcer  arm  palsy.  Elevation  of  the 
arm  can  take  place  and  the  forearm  can  be  flexed  and  supinated,  but 
extension  of  the  forearm  is  impossible  and  the  hand  is  entirelv 
paralyzed. 

Tumors,  exostoses  on  the  first  rib,  cervical  rib,  operative  traumata, 
syphilitic  meningitis  and  simple  neuritis  may  cause  this  lower  brachial 
paralysis.  A  total  brachial  paralysis  may  recede  and  leave  this  form  as 
a  residuum.  In  some  cases  ulnar  sensory  disturbances  are  present  and 
even  median  nerve  ansesthesia.  If  the  lesion  is  close  to  the  cord,  involv- 
ing the  rami  communicantes  to  the  sympathetic  nerve,  vasomotor  and 
oculo pupillary  phenomena  may  be  observed. 

The  usual  treatmient  and  nerve  suture  apply  to  these  palsies. 

Total  Plexus  Palsy. — This  is  usually  of  traumatic,  rarely  of 
infectious  neuritic  origin.  It  occurs  sometimes  in  obstetrical  operations. 
All  or  parts  of  the  nerves  may  be  involved.  Sensor}'  as  well  as  motor 
phenomena  are  in   evidence.     As  the  intercosto-humeral   nerve  often 


THE  NON-NEURONIC  DISEASES  617 

innervates  the  inner  side  of  the  upper  arm,  sensation  is  sometimes  pre- 
served here.  Regeneration  in  these  cases  takes  place,  but  it  is  slow 
and  prolonged  and  usually  is  incomplete,  thus  leaving  some  paralysis 
and  atrophy.  The  treatment  is  based  upon  general  principles  and  along 
the  lines  indicated  under  the  head  of  neuritis.  Tlie  disease  cannot  be 
confounded  with  progressive  muscular  atrophy,  because  the  sensory 
phenomena  and  reaction  of  degeneration  are  so  prominent.  Arthritic 
palsy  is  accompanied  by  the  joint  manifestations. 

Obstetrical  Palsy. — This  form'  of  paralysis  is  of  the  brachial 
plexus  type.  It  is  due  to  unusual  presentations  and  the  use  of  the  fin- 
ger and  instruments  in  the  axilla,  directly  pressing  the  nerves  or  forc- 
ing the  shoulder  and  clavicle  upward  and  backward  against  them.  Vari- 
ous manoeuvres  have  been  the  cause  of  it  and  even  the  wrapping  of 
the  cord  around  the  child's  neck  has  resulted  in  the  palsy.  Duchenne 
was  the  first  to  describe  typical  obstetrical  palsy.  It  rarely  if  ever 
occurs  in  normal  deliveries. 

The  whole  brachial  plexus,  or  a  part  of  it,  may  be  involved.  Usu- 
ally the  muscles  implicated  are  the  deltoid,  biceps,  brachialis  internus, 
supinator  longiis  and  brevis  and  infraspinatus.  The  paralysis  is  of  the 
usual  peripheral,  neuritic  type  with  flaccidity,  atrophy,  loss  of  reflex 
and  reaction  of  degeneration. 

Sensory  disturbances  are  prominent,  though  they  are,  of  course, 
hard  to  discover  in  infants.  The  reflex  response  is  the  means  that  we 
must  depend  upon  to  indicate  their  presence  or  absence. 

Many  of  the  obstetrical  palsies  belong  to  the  Erb  type  previously 
described. 

Rarely  the  trouble  is  bilateral,  though  practically  it  is  a  local  and 
unilateral  palsy. 

The  disease  usually  disappears  slowly  after  many  weeks  or  months. 
Permanent  damage  of  some  sort  usually  remains,  though  complete  re- 
coveries have  been  seen.  If  there  is  no  inflammation,  early  electrical 
treatment  along  lines  already  indicated  under  the  head  of  neuritis  should 
be  employed  and  persisted  in. 

SPECIAL  NERVE  PALSIES  OF  THE  UPPER  LIMB. 
POSTERIOR  OR  LONG  THORACIC  NERVE. 

This  is  not  a  common  trouble  and  it  occurs  mostly  in  yonng  male 
adults.  The  nerve  may  be  damaged  in  the  suprascapular  region  or 
in  the  axilla.  Blows,  heavy  weights,  wounds  in  the  axilla  may  injure 
the  nerve.  As  a  rule  strains  and  over-exertion  with  the  arms  raised 
above  the  head  are  the  most  prolific  cause  of  it.  Young  gymnasts, 
trapeze  performers  and  those  who  use  their  arms  in  this  way  and  swing 
the  heavy  weight  of  the  body  from  them  are  the  sufferers.  The  right 
nerve  is  more  frequently  affected  than  the  left.  It  has  been  seen  to 
follow  infection  (diphtheria,  typhoid  and  influenza),  rheumatism  and 
the  puerperium.  Verhaagen  thinks  it  may  occur  as  a  hysterical  phe- 
nomenon. 

The  serratus  magnus  is  the  muscle  that  is  paralyzed.  The  arm 
cannot  be  raised  above  the  horizontal  and  the  shoulder  is  weakened. 


6l8  THE  NON-NEURONIC  DISEASES 

If  the  arm  is  held  out  horizontally,  the  lower  angle  of  the  scapula  stands 
outward  from  the  thoracic  wall.  If  the  arm  is  elevated  and  carried  for-  • 
ward  the  scapula  swings  away  from  the  thoracic  wall  in  such  a  way 
as  to  produce  a  deep  groove  between  the  latter  and  its  posterior  or 
inner  edge,  thus  giving  a  wing-like  appearance  tO'  it.  When  the  arm 
hangs  limp  beside  the  body,  the  lower  point  of  the  scapula  is  a  little 
closer  to  the  spinal  column  than  it  normally  should  be. 

Pains  occur,  but  typical  sensory  disturbances  do  not  accompany 
serratus  palsy. 

Prognosis  is  fair.  Course  slow.  Treatment  follows  the  usual  lines. 

CIRCUMFLEX  NERVE. 

Circumflex  palsy  is  a  common  trouble.  It  is  usually  due  to  trauma 
or  prolonged  pressure  from  crutches,  or  the  wearing  of  apparatuses 
for  shoulder  joint  and  humeral  injuries.  Infection,  intoxication,  with 
lead  especially,  and  cachectic  states  such  as  diabetes  may  all  provoke 
a  circumflex  neuritis.  I  saw  it  follow  a  fracture  of  the  head  of  the 
humerus.  It  has  followed  knife  wounds  in  the  axilla.  Continued  ele- 
vation of  the  arms  in  sleep  has  been  reported  as  a  cause  of  it  by  Ray- 
mond. 

The  muscles  supplied  by  this  nerve  are  the  deltoid,  teres  minor  and 
third  head  of  the  triceps.  It  is  believed  to  carry  the  trophic  nerves 
to  the  shoulder  joint.  It  receives  the  sensation  of  the  entire  upper  sur- 
face of  the  shoulder  and  down  the  outer  side  of  the  arm  as  far  nearly 
as  the  middle.  When  this  nerve  is  paralyzed  the  arm  cannot  be  abduct- 
ed, much  less  raised  to  a  horizontal  position.  Sometimes  a  little  power 
of  movemient  is  shown  in  the  deltoid  from  the  supply  of  its  anterior 
portion  from  the  anterior  thoracic  nerves.  Rotation  of  the  ami  outward 
is  impossible. 

Hypcesthcsia  and  anccsthesia  occur  on  top  of  the  shoulder  and  down 
the  outer  side  of  the  arm  as  far  as  the  middle.  Changes  of  a  trophic 
nature,  with  late  ankylosis  even,  may  take  place  in  the  shoulder  joint. 

The  fixation  of  the  joint  caused  by  rheumatism  or  arthritis  must  be 
distinguished  from  deltoid  paralysis.  In  the  former  the  scapula  moves 
with  the  humerus  ;  there  is  no  true  paralysis  in  the  muscles  ;  the  sensa- 
tions are  not  typically  disordered  ;  and  there  is  no  reaction  of  degen- 
eration. 

MUSCULO-CUTANEOUS  NERVE. 

Rarely  has  isolated  paralysis  of  this  nerve  been  observed.  It  has 
occurred  after  dislocation,  extirpation  of  a  tumor  and  pressure.  The 
resulting  paralysis  was  in  the  flexors  of  the  forearm,  excepting  the 
supinator  longus.  There  was  anccsthesia  of  the  external  surface  of  the 
forearm.  The  paralysis  of  the  biceps  and  hrachialis  is  particularly  con- 
spicuous when  the  arm  is  supinated  and  the  supinator  longus  cannot 
flex  the  elbow. 

SUPRASCAPULAR  NERVE. 

This  is  very  rarely  damaged  alone.  It  usually  accompanies  circum- 
flex paralysis  from  falls,  blows  and  dislocations  of  the  humerus.     The 


THE  NON-NEURONIC  DISEASES  6ig 

supra-  and  infraspinatus  muscles  are  paralyzed  ;  also  the  teres  minor. 
The  arm  cannot  be  rotated  outward  and  extra  work  is  thus  thrown  on 
the  deltoid.  This  is  due  to  the  paral}'sis  of  the  infraspinatus.  When 
the  supraspinatus  and  teres  minor  are  paralyzed,  it  is  only  important 
in  connection  with  circumflex  paralysis.  The  supraspinatus  rotates  the 
.shoulder  inward.     This  nerve  also  supplies  the  joint. 

MUSCULO-SPIRAL  NERVE.    WRIST  DROP.     LEAD  PALSY. 
COMPRESSION  PARALYSIS. 

In  the  toxic  and  infectious  polyneuritides  this  nerve  is  affected 
along  with  the  others.  It  is  preeminently  involved  in  lead  intoxication, 
as  has  been  noted  under  the  head  of  multiple  neuritis.  Of  all  the 
nerves  of  the  extremities  it  is  the  nerve  most  frequently  diseased.  This 
is  because  of  its  particularly  exposed  position  and  proximity  to  bone  in 
its  course  around  the  upper  arm  in  the  musculo-spiral  groove  of  the 
humerus. 

Etiology. — Traumata,  especially  compression  by  the  head  when 
the  arm  is  elevated  during  sleep  in  driuikards,  is  the  chief  cause  of 
the  paralysis.  Alcoholic,  lead  and  senile  cachexia  predispose  to  it.  It 
is  thus  often  a  toxico-tranuiatic  paralysis.  It  has  occurred  in  sudden 
and  severe  muscular  action,  as  in  the  sudden  extension  of  the  arm  in 
.grasping  a  support  when  falling,  or  in  violently  throwing  a  ball.  Stabs, 
blows,  fractures  and  other  traumata  have  provoked  it.  In  crutch 
palsy  and  dislocations  it  is  involved  more  often  with  other  nerves.  It 
is  said  to  have  followed  over-exertion.  It  has  been  observed  during 
typhoid  fever,  rheumatism  and  the  puerperium.  Once  it  occurred  in 
the  beginning  of  locomotor  ataxia.  Arsenic,  silver  and  opium  intoxica- 
tion have  shown  themselves  in  musculo-spiral  palsy. 

As  a  result  of  chemical  alteration,  not  puncture  or  direct  injury,  it 
has  followed  the  hypodermic  injection  near  it  of  ether,  chloroform, 
alcohol  and  osmic  acid. 

Thus  many  are  the  conditions  in  which  this  nerve,  along  with 
others,  may  be  diseased.  Trauma  and  tdxasmia,  however,  are  the  great 
leading  causes  and  especially  so  in  the  isolated  types  of  the  trouble. 

Symptoms. — This  nerve  supplies  the  extensor  muscles  and  skin  of 
the  hand  and  forearm.  It  extends  and  supinates  the  forearm,  extends 
the  wrist  and  fingers  and  slightly  adducts  and  abducts  the  latter.  When 
it  is  paralyzed  therefore  the  great  prominent  SA-mptonij  is  ivrist-drop. 
The  hand  hangs  limp  at  a  rig"ht  angle  to  the  arm  when  the  latter  is  held 
horizontally.  There  is  a  spastic  flexion  of  the  hand  at  the  wrist,  for 
when  it  is  brought  out  of  the  position  it  immediately  resumes  it  again. 
The  fingers  at  the  metacarpo-phalangeal  joints  are  flexed.  The  thumb 
is  pressed  inward  and  opposed  to  the  fingers.  The  patient  is  absolutely 
incapable  of  extending  the  hand.  There  is  a  slight  power  of  extension 
in  the  first  and  second  phalanges  of  the  fingers  on  account  of  the  action 
of  the  intact  interossei  and  lumbricales  muscles.  The  third  phalanges 
are  paralyzed  like  the  wrist. 

If  the  hand  and  fingers  are  rested  upon  a  support,  a  slight  abunv- 


620  THE  NON-NEURONIC  DISEASES 

Hon  and  adduction  in  the  fingers  may  be  observed.     Abduction  and 
hyperextension  of  the  thumb  are  lost. 

The  arm  generally  rests  in  a  position  of  pronation.  It  cannot  be- 
supinated.  If  the  forearm  is  flexed,  supination  may  be  accomplished 
by  the  biceps  or  by  the  outward  rotation  of  the  upper  arm  with  the 
infraspinatus. 

The  paralysis  is  of  the  ordinary  neuritic,  flaccid,  atrophic  type,  with, 
absence  of  the  reflexes  and  electrical  reactions. 

ParcESthesicE  conslitute  the  chief  sensory  disorders,  though  these 
are  not  prominent.  In  fact,  they  are  usually  absent  in  the  cases  due  tO' 
compression.  Numbness  and  formication  are  the  chief  manifestations.. 
Hypccsthesia  often  occurs ;  rarely  ancesthesia.  There  may  be  no  anaes- 
thesia even  when  the  nerve  is  completely  severed. 

The  sensory  phenomena  are  in  the  radial  distribution.  This  in- 
cludes the  radial  half  of  tfie  back  of  the  hand  and  thimib,  the  back  of 
the  first  three  fingers,  excepting  the  dorsal  surface  of  the  last,  or  both 
distal  phalanges,  which  areas  are  innervated  by  the  median  nerve,  and 
the  forearm  along  a  narrow  strip  upon  the  radial  side  innervated  by 
the  posterior  inferior  cutaneous  nerve. 

There  are  some  slight  variations  in  this  clinical  picture.  For  in- 
stance, in  a  high  lesion,  as  in  enitch  palsy,  the  anaesthesia  is  slight  and 
is  found  chiefly  on  the  front  of  the  arm  in  the  area  oi  distribution  of 
the  external  and  internal  cutaneous  nerves.  A  considerable  variety  of 
anaesthetic  areas  may  be  observed.  In  crutch  palsy  and  in  dislocation 
paralysis  the  triceps  is  involved.  Even  an  isolated  paralysis  of  this- 
muscle  has  been  observed. 

In  lead  paralysis  the  supinators  and  sometimes  the  abductor  longus 
pollicis  are  spared.  Forearm  lesions  may  involve  the  branches  of  the 
musculo-spiral  in  such  a  way  individually  or  collectively  as  to  give 
quite  a  variety  of  clinical  presentations.  It  is  rare  for  the  nerves  below 
the  point  where  the  branches  for  the  supinator  are  given  off  tO'  be  com- 
pressed. 

In  compression  paralysis  the  electrical  reactions  are  not  marked,^ 
if  noticeable  at  all.  In  severer  lesions,  such  as  wounds,  lacerations^ 
crushes,  the  reaction  of  degeneration  is  generally  well  developed. 

Later  in  the  disease  the  tendon  sheaths  are  swollen  and  there  is 
often  hyperostosis  of  the  metacarpal  bones. 

Prognosis. — Most  cases  recover.  Mild  cases  run  a  few  weeks. 
Severe  cases  last  man)'  months  or  a  year  or  more.  The  degree  of  the 
reaction  of  degeneration  will  foretell  somewhat  whether  the  case  will 
be  a  long  or  short  one.  Most  compression  cases  recover  in  four  or  six 
weeks ;  rarely  in  a  few  da}'s.  Recently  I  saw  a  compression  case 
(hanging  the  arm  over  the  back  of  a  chair)  in  a  rheumatic  with 
peripheral  neuritis,  recover  almost  completely  in  three  or  four  days. 
Cases  due  to  knife  wounds,  pvmctures  and  dislocations  of  the  head  of 
the  humerus  are  not  so  promising.  They  usually  exhibit  signs  of 
severe  degeneration  and  therefore  require  many  months  to  recover.  A 
completely  severed  nerve  offers  a  bad  outlook  imless  it  is  immediately 
sutured,  and  then  it  requires  many  months  for  the  restoration  of  its 
function.    Ether  paralysis  runs  several  months. 


THE  NON-NEUROi\IC  DISEASES  62 1 

Treatment. — The  general  lines  of  this  have  already  been  laid 
down  under  the  head  of  Neuritis.  Remove  and  avoid  the  cause.  Nerve 
suturing  has  accomplished  some  very  encouraging  results  upon  the 
musculo-spiral  nerve.  In  freeing  the  nerve  from  a  tumor,  the  danger 
of  paralysis  must  always  be  thought  of.  Transplantation  has  been  suc- 
•cessfuUy  performed  upon  this  nerve. 

After  irritative  symptoms  have  subsided  there  is  no  treatment  so 
available  as  that  with  electricity  and  massage.  Rubber  muscles  and  the 
fixation  of  the  hand  in  hyper-extension  with  splints  and  bandages  may 
"be  necessary  in  old  and  severe  cases. 

The  only  medicinal  treatment  that  will  be  called  for  will_be  that  to 
■combat  the  underlying  intoxication  or  infection.  Salicylates  may  be 
needed  for  rheumatism,  iodides  for  saturnism,  quinine  for  malaria. 
Hypodermics  of  strychnine  are  at  times  efficacious. 

MEDIAN  NERVE. 

An  isolated  paralysis  of  this  nerve  is  very  rare  and  is  practically 
always  due  to  trauma.  The  nerve  supplies  cutaneous  branches  to  the 
■entire  palm  and  to  three  and  a  half  Angers.  It  stimulates  the  pronator 
muscles,  the  flexors  of  the  carpus  and  the  long  flexors  of  the  fingers 
(except  the  ulnar  flexor  of  the  carpus  and  part  of  the  deep  flexor  of  the 
iingers).  The  outer  set  of  the  short  thumb  muscles  and  two  lumbricales 
are  also  excited  by  it. 

The  median  is  frequently  involved  with  other  nerves  and  it  is  then 
due  to  luxations,  strangulation,  as  with  tight  bandage,  fractures  of  the 
Ixmes  of  the  forearm  and  callus.  Forcible  muscular  contraction  of  the 
pronator  teres,  a  severe  distortion  of  the  wrist,  compression  of  the 
cervical  ribs  and  embolism  of  the  axillary  artery  have  been  charged 
with  median  palsy. 

The  median  is  usually  involved  in  the  craft-palsies^  which  must 
not  be  confounded  with  the  occupation  neuroses.  Milkers,  drummers, 
cigar-makers,  carpet-beaters,  dentists,  locksmiths  and  all  those  who 
have  to  use  monotonously  and  for  prolonged  periods  certain  muscles  of 
the  arms.  The  median  and  ulnar  nerves  are  the  most  frequent  seat  of 
puerperal  toxic  neuritis. 

Disease  of  this  nerve  is  revealed  in  a  weakened  grip  of  the  hand 
and  impairment  of  flexion  and  abduction  of  the  thumb  and  flexion  of 
the  first  and  second  fingers.  There  is  not  much  change  in  the  attitude 
of  the  hand  except  a  slight  deviation  toward  the  ulnar  side.  The 
flexion  of  the  basal  phalanges  is  not  involved.  Pronation  of  the  hand 
is  lost. 

Median  injuries  are  usually  severe  ones  with  the  typical  atrophy 
and  reaction  of  degeneration  manifestations. 

The  sensory  symptoms  are  particularly  prominent.  They  consist 
of  pains,  hypercesihesia  and  particularly  hypcesthesia  in  the  area  of 
distribution  of  the  nerve.  The  entire  area  may  be  involved,  including 
thus  the  volar  part  of  the  palm  as  far  as  the  fourth  metacarpal  bone, 
the  volar  surface  of  the  first  three,  and  the  radial  side  of  the  fourth 
finger  and  the  dorsal  surface  of  the  index  and  middle  fingers.     Oc- 


622  THE  NON-NEURONIC  DISEASES 

casionally  aiiiesthesia  is  absent.  It  has  even  not  been  pronounced  itr 
complete  section  of  the  nerve.  Anomalous  anastomoses,  or  rather 
anomalous  innervations  from  the  ulnar,  have  upset  both  the  motor  and 
sensory  appearances  of  miedian  disease. 

The  trophic  and  ■z'asoiiwtor  symptoms  are  prominent  in  disease  of 
this  nerve.  Herpes,  pemphig-us-vesicks,  sluggish  ulcers,  glossing  of 
the  skin,  falling  of  the  hair  of  the  skin,  striation  of  the  nails,  may  be 
expected.  Tlie  skin  is  bluish  and  cool.  There  is  often  infiltration  of  the 
subcutaneous  tissue.  Sometimes  hyperidrosis  is  especially  noticeable. 
Amidrosis  may  occur. 

The  lesion  determines  the  prognosis,  and  the  treatment  calls  for  no 
special  comment. 

ULNAR  NERVE. 

This  nerve  is  frequently  paralyzed,  more  so  than  the  median.  It 
stands  second  to  the  musculo-spiral  in  the  frequency  of  its  disease.     It 

FIGURE  135. 


Showing  Area  op  Anesthesia  in  Ulnar-Nerve  Palsy  (Bowlby). 

is  often  affected  with  other  nerves  by  traumata,  such  as  fractures  with 
callus,  growths,  and  luxations.  Cuts,  bruises,  blows  all  figure  in  the 
etiology.  It  is  subject  to  pressure  paralysis  and  it  enters  into  the 
pathology  of  the  professional  palsies.  It  is  not  often  affected  in  lead 
intoxication.  It  is  an  accompaniment  of  polyneuritis,  syphilitic  neuritis 
and  other  infectious  troubles.  Tumors  develop  upon  the  ulnar  and  it 
has  exhibited  an  ascending  form  of  neuritis. 

The  nerve  supplies  cutaneous  filaments  to  the  lower  part  of  the 
forearm  to  a  small  extent  and  the  palmar  and  dorsal  aspects  of  the 
hand  in  the  inner  half,  to  the  little  finger  and  to  the  inner  or  ulnar  side 
of  the  ring  finger. 

The  muscles  stimulated  by  it  are  the  ulnar  flexor  of  the  carpus, 
the  deep  flexor  of  the  fingers  (its  inner  half) ,  the  short  muscles  of  the 
little  finger  with  the  palmaris  hrevis,  the  interossei  of  the  hand,  the  in- 
ner tzvo  lumbricales,  the  adductor  pollicis  and  the  inner  half  of  the 
flexor  brevis  pollicis.  It  also  furnishes  the  nerve  supply  to  the  joints 
of  the  elbow,  wrist  and  hand. 

Tight  closure  of  the  hand   is  impossible,  the  weakness  being  of 


THE  XOX-XEUROXIC  DISEASES  623 

course  in  the  little  and  ring  fingers.  The  temiinal  phalanges  of  the 
last  three  fingers  cannot  be  fiexed,  nor  can  the  thumb  be  adducted.  On 
account  of  the  paralysis  of  the  interossei  and  lumbricales,  the  claw 
hand  or  the  main-en- grift e  appears.  The  fingers  cannot  be  abducted  or 
adducted. 

Atrophy,  loss  of  reflex  and  the  reaction  of  degeneration  accompany 
this  paralysis  as  in  all  similar  peripheral  palsies. 

The  sensory  syniptoms  are  rarely  absent  in  ulnar  disease.  There 
are  pains,  hyperesthesia  and  anesthesia,  sometimes  all  existing  simul- 
taneously. Hypesthesia  usually  occurs  on  the  volar  surface  of  the 
hand  to  a  line  which  passes  through  the  longitudinal  center  of  the  ring 
finger  and  in  a  corresponding  area  on  the  dorsal  surface;  in  the  little 
finger  and  over  the  ulnar  half  of  the  ring  finger.  Sometimes  the 
sensor}-  disturbance  has  been  limited  entirely  to  the  little  finger. 

Trophic,  vasomotor  and  secretory  changes,  such  as  are  mentioned 
in  connection  with  median  nerve  palsy,  are  rather  common. 

Pressure  palsies  recover  in  a  few  weeks ;  severer  ones  require 
months  and  years. 

FIGURE  136. 


Complete  "  claw-hand"  in  an  old  ulnar  paralysis  (cica- 
trix at  A).    (After  Duchenne  ) 

The  treatment  may  involve  nerve  suture,  neurolysis  (freeing  of  the 
nerve  from  tumors,  etc.),  electricity,  massage  and  the  usual  measures 
described  at  length  under  the  head  of  neuritis. 

A  primary  spontaneous  neuritis  of  symmetrical  distribution  is  a 
rare  condition,  occurring  in  the  ulnar  nei^^es  of  persons  of  neuropathic 
constitution  and  supposed  to  be  due  to  infection.  It  is  very  chronic 
and  scarcely  ever  ends  in  recovery.  It  has  followed  the  acute  infec- 
tious diseases,  particularly  typhoid  fever.  There  is  at  first  pain  and 
paraesthesia  in  the  ulnar  distribution.  The  muscles  become  weak  and 
atrophy  and  the  characteristic  claw^-hand  appears.  Anesthesia  de- 
velops also.  This  is  probably  a  true  neuritis  in  which  the  degenerative 
side  of  the  process  takes  precedence  because  the  infection  is  not  virulent 
enough  to  provoke  gross  inflammation,  but  with  the  aid  of  the  neu- 
ropathic heredity  is  virulent  enough  to  cause  damage  in  the  neurones. 
It  is  a  local,  not  a  true,  primar\-  disease,  as  I  have  explained  at  the  head 
of  this  chapter. 

Morvan's  Disease,  or  Analgesic  Paralysis  zAth  JVhitloz>.'.  There  is 
neuritis  of  the  upper  extremities  in  this  disease,  but  it  is  a  complication 
of  syringomyelia,  to  which  the  reader  is  referred  for  its  more  detailed 
description. 


624  THE  XOX-XEURONIC  DISEASES 

DORSAL  NERVES. 

There  are  twelve  pairs  of  dorsal  nerves,  the  first  pair  entering  into 
the  formation  of  the  brachial  plexus.  Except  this,  and  the  second  and 
twelfth,  which  send  cutaneous  offsets  respectively  to  the  arm  and  hip, 
the  dorsal  nerves  are  almost  entirely  distributed  to  the  walls  of  the 
thorax  and  abdomen.  In  certain  respirator}-  troubles  and  neuralg^ias 
alone  are  they  of  any  special  clinical  interest. 

THE  LUMBAR  PLEXUS. 

Anatomy. — The  liimhar  plexus  is  formed  by  connections  between 
the  anterior  primary  divisions  of  the  four  upper  lumbar  nerves.  It  is 
in  the  substance  of  the  psoas  muscle.  It  is  joined  to  the  sacral  plexus 
by  a  branch  from  the  fourth  lumbar  nerve  to  the  fifth. 

From  the  first  nerve  spring  the  ilio-hypogastric  and  ilio-inguinal 
nerves  and  a  communicating  branch  to  the  second  nerve.  The  second 
nerve  supplies  the  greater  part  of  the  genito-crural  and  external  cutane- 
ous nerves  and  also  transmits  a  branch  to  the  third,  from  which  some 
of  the  fibres  of  the  anterior  crural  and  obturator  nerves  proceed.  There 
are  two  branches  from  the  third  nerve — namely,  a  large  one  forming  a 
part  of  the  anterior  crural  nerve,  and  a  smaller  forming  a  part  of  the 
obturator.  The  fourth  nerve  sends  forth  three  branches.  Two  of  these 
complete  the  obturator  and  anterior  crural  nerves,  while  the  third  con- 
nects with  the  fifth  nerve  and  thus  becomes  a  part  of  the  sacral  plexus. 

This  plexus  thus  innervates  the  lower  part  of  the  abdominal  wall 
and  the  fore  part  and  inner  side  of  the  lower  limb. 

Disease  of  the  lumbar  or  sacral  plexus  is  not  as  frequent  as  of  the 
brachial  plexus.  The  lumbar  plexus  has  been  damaged  by  neoplasms 
in  the  abdomen,  psoas  abscess  and  vertebral  disease.  A  spontaneous 
crural  neuritis  has  been  seen.  Very  rarely  is  the  obturator  nerve  alone 
affected,  though  it  has  been  damaged  in  parturition.  The  same  is  to  be 
said  of  the  anterior  crural  nerve.  The  gouty  diathesis,  alcoholic  intoxi- 
cation and  diabetes  mellitus  have  caused  disease  sometimes  in  the 
crural.  Sometimes  it  has  been  a  total  bilateral  paralysis.  Fractures 
have  damaged  the  nerves  in  a  few  instances ;  but  they  are  well  pro- 
tected. 

Symptoms. — Sensory  symptoms  only  occur  when  the  two  upper 
lumbar  nerves  are  invoh'ed.  These  involve  the  abdominal  wall.  An- 
cesthesia  or  hypcesthesia  may  appear  in  the  area  of  distribution  of  the 
anterior  and  internal  cutaneous  femoris  and  of  the  saphenus  major. 
This  includes  the  anterior  and  inner  surface  of  the  thigh,  the  inner  sur- 
face of  the  leg  and  the  inner  border  of  the  foot  nearly  to  the  great  toe. 
This,  of  course,  represents  disease  in  the  two  lower  lumbar  nerves  and 
their  branches. 

The  motor  paralysis  is  seen  in  the  inability  of  the  patient  to  extend 
the  leg  and  flex  the  hip.  This  is  a  total  paralysis.  If  it  is  bilateral  the 
gait  is  markedly  disturbed.  The  pectineus  and  sartorius  do  not  es- 
pecially cause  any  trouble.  When  the  palsy  is  unilateral,  the  patient  has 
to  step  carefully  and  not  flex  the  knee. 


THE  NOX-NEUROXIC  DISEASES 


62: 


.«»rf™...  the  .....,■,„  and  ..,e  ....!::.  Ztalysirirr/SSt 


FIGURE  137. 


DXIJ 


(From  Quain.) 


-DlAGRAMJiAnc  our- 
LINL  OF  THE  LDMBAR  AND 
SACKAL  PLIIXUSES  WITH  THK 
PRINCIPAL  KERVES  ARISIXO 
FKOM    THEM.       (A.  T. )       i 

DXII,    the    divided   roots  c. 
the  last  dorsal  nerve  ;  LI,  to  V, 
the   roots   of   the    five    lumbar 
Jierres;  the    loops   uniting   the 
■anterior    primary    divisions    of 
these  nei-ves  together,  and  the 
first  with  the  twelfth  dorsal  arc 
shou-n  ;  SI,  to  V,  and  CI,  the 
sacral  and  coccygeal  nerves  ;  p, 
placed   on  some  of  the  nerves 
marks    the    posterior    primary 
divisions  cut  fihort ;  p,  p\    the 
plexus  formed  by  the  union  of 
the   posterior    branches   of   the 
third,   fourth,   and  fifth  sacral 
and   the   coccygeal   nerves ;  d, 
anterior    division   of    the    last 
dorsal  nerve,  from  which  d'  the 
lateral  cutaneous  branch  arises  ; 
1,    ilio-hypogastric    nerve  ;    1'' 
ilio-inguinal ;  2,   genito-crural ; 
2',_  external   cutaneous   of  the 
thigh  ;  ps,  branches  to  the  psoas 
muscle  ;  _  cr,     anterior    crural 
nerve;     il,    branches     to    the 
iliacus  ;    ob,    obturator    nerve  ; 
oh',    accessory   obturator ;    IV','  . 
V,   loop  from    the   fourth    and 
fifth  lumbar,  forming  the  lumbo- 
sacral cord, ;  3,  superior  gluteal 
nerve ;    sc,  great  sciatic  nerve, 
continued     from      the     sacral 
plexus ;  4,  small  sciatic  nei-ve, 
rising  from    the   plexus    poste- 
riorly ;  4',  inferior  gluteal  nerve ; 
5,  inferior  pudendal  ;  5',  poste- 
rior cutaneous  of  the  thigh  and 
leg ;  6,  6,  branch  to  the  obtu- 
rator intemus  and  gemellus  su- 
perior ;  6',   6',  branch    to    the 
gemellus     inferior,     quadratus 
femoris  and  hip-joint ;  7,  twigs 
to    the    pyriformis  ;    8,    pudic 
nerve  ;  9,  visceral  branches  ;  9', 
twig  to  the  levator  ani ;    10, 
perforating     cutaneous    nerve ; 
11,  coccygeal  branches. 


plexus  one  and  hence  is  incomplete  and  more  limited      In  such  ca,e, 
severe  pam  ,s  caused  m  the  region  supplied  bv  the  nerve  tha"  is  irritated 
Thts  occurs  somet„.es  early  and  is  often  due  to  a  neoplasm  ne^r  the 


626  THE  NON-NEURONIC  DISEASES 

Spine.    The  pains  follow  the  course  of  the  crural  and  saphenus  nerves. 
The  paralysis  is  of  the  ordinary  neuritic  type  with  atrophy,  reaction 
of  degeneration,  loss  of  reflexes  and  is  entirely  flaccid. 

OBTURATOR  NERVE. 

This  nerve  rarely  suffers  alone.  It  has,  however,  been  so  affected 
in  tumors  and  difficult  labors.  Adduction  of  the  thigh  is  impossible. 
The  patient  cannot  throw  one  leg"  across  the  other.  There  is  also  some 
impairment  in  both  external  and  internal  rotation.  There  are  sensory 
disturbances  on  the  median  upper  third  of  the  thigh. 

ANTERIOR  CRURAL  NERVE. 

Here  there  is  zveakness  in  the  muscles  on  the  front  of  the  thigh. 
The  leg  cannot  be  normally  extended.  Anesthesia  and  pain  occur  in  the 
crural  area. 

External  Cutaneous  Nerve. — Only  lately  has  an  isolated  paralysis 
of  this  nerve  been  noted.  There  were  pains,  ancesthesia,  parcesthesia 
and  other  sensory  disorders  in  the  area  supplied  by  this  nerve.  Walk- 
ing and  standing  seemed  to  bring  on  the  symptoms. 

Superior  Gluteal  Nerve. — Cowers  mentions  that  this  nerve  is  very 
rarely  diseased  in  the  isolated  form.  The  gluteus  niedius  and  minimus 
are  paralyzed.  There  is  loss  of  abduction  and  circumduction  of  the 
thigh. 

THE  SACRAL  PLEXUS. 

Anatomy. — It  should  be  remembered  that  the  anterior  divisions  of 
the  first  four  sacral  nerves  make  their  exit  from  the  spinal  canal  through 
the  anterior  sacral  foramina,  while  the  fifth  passes  out  between  the 
sacrum  and  coccyx.  The  first  three  and  a  part  of  the  fourth  enter  into 
the  composition  of  the  sacral  plexus.  The  fifth  does  not  form  a  part  of 
the  plexus,  but  ends  on  the  back  of  the  coccyx.  That  part  of  the  fourth 
that  does  not  enter  as  a  constituent  of  the  plexus  supplies  branches  to 
the  viscera  and  muscles  of  the  pelvis  and  a  connecting  branch  to  the 
fifth  nerve.  Sometimes  the  sixth  sacral  nerve,  or  anterior  branch  of 
the  coccygeal  nerve,  in  its  union  by  connecting  filaments  with  the  fifth 
and  fourth  sacral  nerves,  is  said  to  constitute  a  coccygeal  plexus. 

The  first  three  and  part  of  the  fourth  sacral  nerves  then  form  the 
sacral  plexus.  Without  much  interlacement  these  unite  to  form  a  large 
upper  and  a  small  lower  cord  or  band.  The  upper  represents  the  union 
of  the  lumbo-sacral  cord  with  the  first  and  second  and  the  greater  part 
of  the  third  sacral  nerves.  It  is  continued  into  the  great  sciatic  nerve. 
The  lower  band  has  a  plexiform  arrangement  and  represents  the  union 
of  the  smaller  part  of  the  third  sacral  nerve  with  the  plexus  portion 
of  the  fourth.     It  is  prolonged  into  the  pudic  nerve. 

The  sacral  plexus  lies  on  the  anterior  surface  of  the  pyriformis 
muscle  opposite  the  side  of  the  sacrum.  It  escapes  through  the  great 
sacro-sciatic  foramen  and  ends  at  the  lower  border  of  the  pyriformis. 

In  addition  to  the  great  sciatic  and  pudic  nerves,  it  gives  off  a 


THE  NON-NEURON IC  DISEASES  62/ 

number  of  collateral  branches,  such  as  the  superior  gluteal,  which  oc- 
cupies an  intermediate  position  between  the  two  plexuses,  lumbar  and 
sacral,  the  inferior  gluteal,  the  small  sciatic,  the  perforating  cutaneous 
and  branches  to  the  pyriforinis,  obturator  interims,  gemelli  and  quad- 
rat us  fenioris  muscles. 

Diseases  of  the  sacral  plexus  usually  mean  the  sciatic  nerve  and  its 
branches.  Pelvic  fractures  during  parturition,  either  natural  or  artifi- 
cial, fractures  of  the  lumjbar  vertebrae,  are  a  source  of  disease  in  this 
nerve.  The  motor  manifestations  most  commonly  implicate  the  per- 
oneal branch.  This  is  especially  the  case  where  the  pelvis  is  contracted 
and  the  pressure  of  the  head  is  severe  and  prolonged.  The  peroneal 
nerve  arises  from  the  lumbar  sacral  cord  mostly,  which  lies  on  the  in- 
nominate crest  and  not  the  pyriform  muscle,  as  the  rest  of  the  plexus 
does.  Its  fibrillse  are  thought  to  be  especially  sensitive  and.  susceptible 
to  injury,  as  shown  by  its  early  degeneration  in  disease  and  the  early 
functionless  condition  of  its  muscles  after  death.  Among  other  causes 
of  sacral  disease  are  to  be  mentioned  pelvic  tumors,  parametritis  and 
intrapelvic  septic  processes,  subcutaneous  injections  of  ether,  mercury, 
etc.,  nerve-stretching,  fractures  and  dislocations  of  the  femur. 

SCIATICA. 

This  is  sometimes  called  neuralgia  ischiadica  or  malum  cotunnii. 
It  is  a  painful  condition  of  the  sciatic  nerve  and  its  branches,  due  in  my 
opinion,  to  neuritis,  though  many  authors  regard  it  as  a  pure  neuralgia. 

As  stated  by  the  authorities,  there  are  two  forms  of  sciatica,  the 
primary  and  the  secondary.  By  secondary  sciatica  is  meant  pain  in 
the  sciatic  nerve  provoked  by  some  extra-neural  cause,  as  for  instance 
a  tumor  pressing  upon  the  nerve.  It  would  be  well  if  we  could  drop 
the  term  secondary  sciatica  in  this  sense  entirely,  as  the  name  of  a  dis- 
ease of  the  sciatic  nerve ;  for  it  represents  no  more  an  affection  of  that 
nerve  than  would  the  pain  caused  by  a  corn  on  the  foot  represent  an 
affection  of  the  nerve  involved.  The  very  symptom-complex  of  so- 
called  secondary  sciatica  is  different  from  that  of  the  true  or  primary 
form.  In  the  former  the  pain  is  a  referred  pain,  usually  peripheral  in 
location,  and  is  not  elicited  by  direct  pressure  or  by  the  usual  manoeu- 
vres which  elicit  the  pain  in  the  latter. 

Strictly  speaking,  there  is  only  one  form  of  sciatica,  disease  of 
the  nerve  itself.  This  disease,  it  is  sometimes  said,  may  be  functional 
or  organic,  and  hence  true  sciatica  has  been  divided  into  idiopathic 
neuralgia  of  the  nerve,  and  neuritis.  Idiopathic  functional  sciatic  neu- 
ralgia is  the  term  employed  to  cover  all  the  so-called  secondary  neural- 
gias and  all  painful  states  of  the  sciatic  nerve  unaccompanied  by  any 
known  or  observable  changes  in  the  nerve  itself  or  its  central  connec- 
tions. Such  names  as  gastralgia,  cardialgia,  cephalalgia,  myalgia,  neu- 
ralgia, and  a  host  of  others  that  have  become  engrafted  upon  the  science 
of  medicine,  are  the  contributions  of  practical  medicine  ;  and  while  they 
may  be  very  comforting  to  employ  in  certain  obscure  cases,  their  care- 
less and  indiscriminate  application  to  well  recognized  symptom-groups 
and  pathological  conditions  is  an  unwarrantable  looseness  in  the  use 


628  THE  NOX-XEUROXIC  DISEASES 

of  language  which  awakens  a  suspicion  of  ignorance  or  of  indolence. 
Idiopathic  neuralgia  and  simple  neuritis  are  constantly  being  con- 
founded. Though  many  cases  of  so-called  neuralgia  are  clearly  in- 
stances of  neuritis,  it  is  much  more  -convenient  in  the  hurrv  of  gen- 
eral practice  to  call  cases  of  painful  nerves  by  the  undeniable  but 
meaningless  name  of  neuralgia  than  it  is  to  study  the  electrical  reac- 
tions and  other  symptoms  characteristic  of  neuritis.  Dana  found,  after 
a  close  study  of  the  subject,  that  true  idiopathic  neuralgia  is  a  rare 
disease,  constituting  not  more  than  two  or  three  per  cent,  of  all  the 
different  forms  of  nervous  disorders.  Symptomatic  and  reflex  neu- 
ralgias are  of  course  far  more  common.  These  statistics  confirm  those 
of  Classin,  of  Kiel,  who  collected  434  cases. 

On  account  of  the  generally  favorable  termination  of  sciatica,  the 
opportunity  for  the  direct  exammation  of  the  diseased  nerve  rarelv 
presents  itself.  In  those  cases  in  which  it  has  been  examined,  how- 
ever, the  findings  have  almost  invariably  been  those  of  a  neuritis  or 
perineuritis ;  redness  with  swelling  of  the  nerve-sheath,  small  hemor- 
rhages in  recent  cases,  spindle-shaped  intumescence,  dilated  arteries, 
serous  transudations,  migration  of  the  leucocytes,  proliferation  of  the 
connective  tissue,  adhesions  and  secondary  damage  to  the  nerve-fibres. 
In  so  great  a  majority  of  the  cases  have  these  signs  of  inflammation 
been  seen  that  one  is  easily  justified  in  suspecting  that  all  cases  of  pri- 
mar}^  sciatica  are  cases  of  sciatic  neuritis.  This  suspicion  is  moreover 
confirmed  by  a  careful  consideration  of  the  etiology,  symptoms,  and 
therapeutics  of  sciatica.  Among  the  considerable  number  of  cases 
that  have  come  under  my  observation,  I  do  not  recall  one  in  which  I 
was  not  satisfied  that  the  nerve  itself  was  more  or  less  inflamed. 

Etiology. — The  etiology  of  sciatica,  as  given  in  the  text-books, 
is  remarkably  like  that  of  simple  neuritis.  In  one  of  the  recent  works 
sciatica  is  said  to  be  the  result  of  traumatism,  exposure,  gout,  rheuma- 
tism, syphilis,  or  malaria.  Lawson  declares  that  nine-tenths  of  the 
cases  of  sciatica  are  due  to  exposure  to  cold,  while  Erb  insists  upon 
the  preeminence  of  this  above  all  other  causes.  Many  authors,  as,  for 
instance,  Gowers,  Tyson,  Osier,  x'Vnstie,  and  Weir  Mitchell,  speak  of 
syphilis  as  an  infrequent  cause  of  sciatica.  They  doubtless  refer  to 
sciatic  neuritis;  for  just  like  intracranial  syphilis,  which  so  frequently 
affects  the  nerves  of  the  ocular  muscles  without  causing  any  inflam- 
mation in  these  nerves,  so  syphilis  may  cause  a  secondary  sciatica  or 
pain  in  the  nerve  by  a  neoplastic  pressure,  without  giving  rise  to  a 
primary  sciatic  neuritis  except  in  rare  cases.  Infectious  diseases,  such 
as  typhoid  fever,  variola,  diphtheria,  tuberculosis,  intoxicants  such  as 
alcohol  and  nicotine,  diabetes,  and  other  toxsemic  conditions,  may  all 
predispose  to  an  attack  of  sciatica,  as  well  as  to  a  general  neuritis ; 
but  exposure  to  cold  and  damp,  and  direct  injury  of  the  nerve,  are  the 
chief  factors  that  start  the  attack.  Among  the  traumatic  causes  may 
be.  mentioned  contusions  and  wounds  in  the  perineum,  buttocks,  pelvis, 
by  falls,  pressure,  slow,  difficult  parturition  and  hard  fecal  masses. 
Perimetritis  may  cause  it.  The  character  and  location  of  these  causes 
will  determine  the  unilaterality  or  bilaterality  of  the  sciatica. 

It  is  a  noteworthv  fact,  when  considered  in  this  connection,  that 


THE  XOX-XEUROXIC  DISEASES  629 

heredity  and  predisposition  are  of  less  importance  in  the  etiologv  of 
sciatica  than  they  are  in  the  neuralgia  of  other  ner\^es. 

In  persons  suffering  from  varicose  veins,  Quenu  found  the  veins 
in  the  interior  of  the  sciatic  nerves  greatly  dilated.  Of  sixty-seven 
individuals  with  varicose  veins  eleven  were  the  victims  of  sciatica. 

A  case  of  my  own  was  a  German  woman,  fifty-two  years  of  age, 
with  varicose  veins  of  the  right  leg,  who  suffered  at  rare  intervals  with 
slight  attacks  of  pain  along  the  course  of  the  corresponding  sciatic 
nerve.  An  elastic  stocking  and  the  internal  administration  of  hamame- 
lis  afforded  her  prompt  and  marked  relief. 

Men  are  more  frequently  afflicted  with  sciatica  than  women, 
though  this  is  probably  due  to  the  difference  between  the  sexes  in  re- 
gard to  the  incidence  of  the  many  other  causes  of  the  disease.  This  is 
shown  by  the  fact  that  it  is  a  disease  of  middle  life,  being  rare  in  ex- 
treme old  age  and  practically  unknown  in  childhood. 

Pathology  ax'D  Pathogex'esis. — This  is  the  same  as  any  form 
of  peripheral  neuritis.  It  is  true  that  in  some  cases  there  are  no  find- 
ings. It  is  probable  that  in  such  cases  the  changes  have  been  very 
slight  and  evanescent,  or  the  central  representation  of  the  nerve  may 
have  been  functionally  at  fault.  These  constitute  a  small  minority  of 
cases  and  I  am  of  the  opinion  that  if  in  every  case  we  could  examine 
microscopically  the  entire  nerve  we  would  find  more  often  than  we 
now  do  positive  signs  of  neuritis. 

Symptoms. — These  begin  gradually  and  steadily  increase  to  a  cli- 
max in  the  course  of  a  few  days  or  ^v•eeks.  It  is  oftener  the  rule  than 
the  exception  for  the  inflammatory  process  in  neuritis  to  be  more  in- 
tense at  particular  points  in  the  course  of  the  nerve.  Indeed,  a  large 
number  of  these  cases  might  well  be  called  focal  neuritis,  on  account 
of  the  higher  degree  of  the  inflammation  at  these  points  or  foci.  The 
pain  is  usually  sharper  there  on  account  of  the  greater  damage  and 
severer  pressure  upon  the  nervi  nervorum.  And  yet  what  are  these 
tender  points  of  neuritis  but  the  classical  puncta  dolorosa  of  neuralgia ! 
These  puncta  are  described  as  being  usually  situated  in  the  neighbor- 
hood of  bony  prominences.  \'alleix,  who  was  the  first  to  draw  atten- 
tion to  them,  said  they  would  be  found  to  correspond  with  the  poste- 
rior superior  spine  of  the  ilium,  the  spine  of  the  ischium  where  the 
nerve  makes  its  escape  from  the  pelvic  cavity,  the  great  trochanter  of 
the  femur  behind  which  the  nerve  runs  near  the  border  of  the  gluteus 
maximus,  the  head  of  the  fibula,  the  internal  malleolus,  and  the  dorsum 
of  the  foot. 

In  sciatic  neuritis  it  is  easy  enough  to  explain  the  tenderness  of 
the  nerve-trunk  by  means  of  the  inflammatory  irritation  and  pressure 
upon  the  nervi  nervorum ;  but  in  so-called  idiopathic  neuralgia,  in 
which  there  is  supposed  to  be  no  perceptible  lesion  of  the  nerve-trunk, 
it  is  diflicult  to  comprehend  how  such  exquisite  local  pain  is  to  be 
accounted  for.  Idiopathic  neuralgic  pain  is  not  localized  in  the  nerve- 
trunk,  but  rather  in  the  peripheral  distribution  of  the  nerve  and  its 
branches.  At  all  events  it  would  not  be  so  keen  in  the  nerve-trunk  as 
it  is  in  neuritis.     Every  one  knows,  however,  that  the  local  pain  in 


630  THE  NOX-XEUROMC  DISEASES 

sciatica  is  usually  so  severe  that  the  patient  dreads  to  be  touched,  and 
finds  sitting  down  often  a  most  distressing"  act. 

Pathology  has  not  yet  discovered  any  change  in  the  trunk  of  a  nerve 
attacked  with  so-called  idiopathic  neuralgia.  The  change,  whatever  it 
may  be,  is  either  at  the  peripheral  or  central  end  of  the  nerve.  There  are 
no  sensory  cells  in  the  coursa  of  the  nerve  itself  or  its  constituent 
fibers  whereby  painful  impressions  are  received  and  transmitted  to  the 
brain.  And  yet  neuralgia  is  one  of  the  most  painful  of  all  affections, 
and  the  pain,  as  in  sciatica,  is  even  more  intolerable  in  the  nerve-trunk 
than  it  is  at  the  periphery.  Those  who  deny  the  inflammatory  char- 
acter of  these  painful  sciaticas  have  no  easy  task  before  them  to  ex- 
plain the  immediate  cause  of  the  pain.  In  opposition  to  all  the  teach- 
ings of  physiology,  they  must  show^  how  a  relatively  inert  nerve-fiber, 
capable  merely  of  transmitting  different  impulses,  can,  when  unaf- 
fected by  any  perceptible  pressure  or  irritation  within  or  outside  of 
its  own  substance,  give  rise  to  the  most  excruciating  agony.  To  say 
that  this  pain  is  functional  in  character,  and  therefore  does  not  neel 
any  perceptible  change  in  the  nerve  structure  to  account  for  it,  only 
enhances  the  difficulty,  for  functional  pains  are  always  referred  to 
the  extremity  of  the  nerve  and  its  branches  and  never  directly  to  the 
nerve-trunk.  And  again,  to  say  that  the  nervi  nervorum  found  in  the 
course  of  the  nerve-trunk  are  the  peripheral  sources  of  this  so-called 
idiopathic  neuralgia  as  functional  pain,  needs  a  further  explanation  as  to 
how  these  nervi  nervorum  come  to  be  the  sources  of  this  pain  in  the 
absence  of  any  pressure  or  damage  to  them.  Does  it  not  seem  singu- 
lar that  this  mysterious,  imperceptible  agent  of  idiopathic  neuralgia 
can  thus  arouse  to  the  highest  degree  the  function  of  a  sensory  nerve 
and  yet  not  at  the  same  time  affect  the  motor  strands?  The  motor 
nerves  along  the  course  of  their  trunks  are  like  the  sensory  nerves ; 
yet  motor  spasm,  pure  and  simple,  is  not  a  symptom  of  idiopathic 
neuralgia. 

In  typical  neuritis  there  are  associated  with  the  pain  along  the 
course  of  the  nerve-trunk  peculiar  scjisatioiis,  parccsthcsicc,  and  various 
degrees  of  motor  paresis  in  the  parts  supplied  by  the  nerve  and  its 
branches.  In  fact,  the  combination  of  pain  in  the  course  of  the  nerve- 
trunk  with  various  spontaneous  irritative  motor  and  sensory  phenomena 
at  its  distal  extremity,  is  almost  pathognomonic  of  an  inflammation  of 
the  nerve.  The  pressure  and  irritation  of  the  nervi  nervorum  and  re- 
current fibers  sufficiently  explain  the  former,  while  interference  with 
the  power  of  conduction  by  the  same  pressure  readily  accounts  for 
the  latter.  And  yet  some  of  the  authorities  still  assert  that  in  simple 
neuralgia  of  the  sciatic  nerve  there  occur  various  pareesthesise,  tonic 
and  clonic  spasms  in  the  leg,  and  even  at  times  a  considerable  degree 
of  paralysis.  In  other  words,  when  the  nerve  is  apparently  quite  un- 
changed histologically,  it  is  affected  functionaUy  in  such  a  mysterious 
wa}^  as  to  give  rise  to  a  paralysis  and  symptoms  of  irritation  at  the 
same  time.  The  argument  itself  is  a  reductio  ad  ahsurdnm.  The 
nerve,  it  is  maintained,  is  so  sensitive  that  the  condition  is  deemed 
worthy  of  the  dignity  of  a  special  name,  neuralgia ;  while  at  the  same 
time  the  nerve  is  so  dead  in  function  as  to  fail  in  the  proper  conduc- 


THE  NON-NEURO^TIC  DISEASES  63  I 

tion  of  received  impressions.  Usuall}",  irritation  is  the  cause  of  mus- 
cular spasm ;  here,  however,  irritation  is  made  more  frequently  to  ac- 
company paralysis.  There  is  a  conflict  here  between  physiology  and 
pathology  which  those  who  insist  upon  the  non-inflammatorv  char- 
acter of  idiopathic  sciatica  will  do  well  to  explain. 

The  pain  of  sciatica  is  a  localised  pain,  rarely  dififuse,  and  is  bor- 
ing, tearing,  and  hurning  in  character.  It  is  often  so  localized  that 
the  patient  can  almost  feel  the  entire  nerve  like  a  cord  passing  down 
the  back  of  his  leg.  Like  all  inflammatory  pains,  it  varies  in  intensity 
and  is  increased  by  nwz'ement  and  pressure.  \A^alking,  straining, 
coughing,  prolonged  sitting  increase  it.  It  may  be  excited  by  the 
finger  in  the  rectum  or  vagina.  Placing  the  patient  on  his  back  and 
attempting  extreme  flexion  of  the  legs,  on  the  body  is  an  excellent 
diagnostic  manoeuvre,  as  it  often  cannot  be  done  on  account  of  the  ex- 
treme pain  produced.  Sometimes  the  skin  is  red  and  slightly  adema- 
tous,  and  the  local  temperature  may  be  somewhat  elevated.  The  earli- 
est indications  of  involvement  of  the  nerve-fibers  are  the  peripheral 
parcesthesia  and  hyperesthesia  for  the  sensory,  and  -fibrillary  tzvitch- 
in'gs  and  tonic  contractions  of  the  muscles  for  the  motor.  The  reflexes 
are  somewhat  increased  at  first,  but  diminished  in  old  cases.  The 
electric  excitability  is  at  first  enhanced,  and  then  more  or  less  lost. 
In  subacute  and  chronic  cases  there  will  be  some  reaction  of  degenera- 
tion. Trophic  disturbances  sometimes  observed  include  muscular 
atrophy^  herpes,  excessive  perspiration,  and  even  joint  affections. 

In  simple  neuritis,  posture  is  at  times  almost  as  pathognomonic  as 
is  pain  upon  movement.  See  illustration  where  the  patient  shows  in 
her  comparative  attitude,  the  painful  and  weakened  condition  of  the 
•  left  leg.  The  faulty  attitude  of  the  body,  so  characteristic  in  sciatica, 
is  an  old  and  well  recognized  symptom.  Sometimes  the  patient  leans 
toward  the  painful  side,  sometimes  away  from  it ;  but  always  in  a 
direction  to  modify  the  severity  of  the  pain.  By  the  manoeuver  the 
nerve  is  probably  lifted  away  from  certain  prominences  in  the  pelvis 
against  w^hich  it  usually  rests.  When  there  is  scoliosis  of  the  lumbar 
column,  the  concavity  is  usually  towards  the  sound  side.  Various  ex- 
planations of  this  have  been  given,  none  of  which  are  entirely  satis- 
factory. Many  think  it  is  due  to  the  eft'ort  to  relieve  pressure  on  the 
sensory  nerve  and  its  branches  ;  others  think  it  is  due  to  a.  muscular 
weakness ;  still  others  hold  that  it  is  dependent  upon  the  muscular 
spasm  and  contracture.     Occasionally  kyphosis  may  be  seen. 

Neuralgia  of  other  nerves  generally  occurs  under  very  dift'erent 
conditions  from  those  under  which  neuralgia  of  the  sciatic  usually 
takes  place.  The  victims  of  such  neuralgias  often  suffer  from  migraine, 
pains  in  some  of  the  special  nerves  of  the  head  and  of  the  viscera,  which 
pains  are  remarkably  disposed  to  become  periodic.  Headaches  an  1 
visceral  pains  are  quite  infrequent  among  patients  suffering  from  pri- 
mary simple  sciatica. 

Diagnosis. — Sciatica  is  more  often  diagnosed  in  practice  than  it 
actually  occurs.  Either  from  the  obscurity  of  the  case  or  the  lack  of 
care  in  the  examination,  various  lesions  of  the  pelvis,  the  hip-joint,  the 


632 


THE  NON-NEURONIC  DISEASES 


Spine  and  elsewhere,  involving  the  sciatic  nerve  and  causing  it  to  be 
painful,  pass  under  the  name  of  sciatica. 

No  disease  demands  a  more  earnest  effort  at  differential  diagno- 
sis.    Its  clinical  picture  is  characteristic  enough  and  there  is  no  ex- 


FI&URE  1 38. 


FIGURE  139- 


Subacute  sciatic  neuritis.  Dr.  Fitch's  case.  The  left  side  is  the  affected 
one,  as  shown  by  the  difference  in  the  attitude,  when  resting  upon  one  or  the 
other  leg. 

cuse,  except  in  the  rarest  instances,  for  some  of  the  gross  blunders 
that  are  sometimes  made.  The  onset  and  location  of  the  pain,  its 
variation  under  certain  characteristic  manoeuvers ;  the  puncta  dolorosa 
and  general  tenderness  along  the  course  of  the  nerve,  the  bodily  atti- 


THE  NON-NEURONIC  DISEASES  633 

Hide  and  disorders  of  motility,  the  etiology  and  course  of  the  entire 
affection  are  distinctive. 

As  I  am  convinced  that  all  forms  of  genuine  peripheral  sciatica 
are  neuritic  in  nature,  it  is  unnecessary  to  attempt  a  differential  diag- 
nosis between  what  is  called  sciatic  neuralgia  and  sciatic  neuritis.  The 
sensory  phenomena,  the  atrophy,  the  reaction  of  degeneration,  the 
altered  reflexes  are  the  same  in  both  but  diff'er  very  widely  in  degree 
in  different  cases.  In  some  instances  they  appear  only  slightly  and 
then  not  until  late  in  the  disease.     These  are  the  chronic  cases. 

Coxalgia  from  tuberculosis  or  other  disease  of  the  hip- joint  is 
characterized  by  the  peculiar  attitude  of  the  leg  and  the  referred  pains 
in  the  knee-joint.     The  sciatic  signs  are  wanting. 

Hysteria,  hysterical  sciatica,  hemorrhoids,  arteriosclerosis,  arteritis 
obliterans,  varicose  veins,  various  vasomotor  spasmodic  conditions, 
need  but  to  be  mentioned  as  causes  of  pains  in  the  legs  that  may  simu- 
late sciatic  neuritis.  None  but  a  tyro  in  medicine,  or  one  who  is 
superficial  in  his  examinations,  would  mistake  these  conditions  with 
their  distinctive  subjective  and  objective  exhibitions  for  a  true  dis- 
ease of  the  sciatic  nerve. 

A  bursitis,  following  gonorrhoea,  malaria  or  trauma  may  cause 
an  achillodynia,  or  pain  at  the  insertion  of  the  tendo  Achilles,  upon 
walking  and  standing. 

Inflammation  of  the  calf-muscles,  a  myositis,  may  be  the  cause  of 
the  pain  in  some  cases.  The  other  distinctive  signs  and  history  of 
sciatica  will  be  absent. 

The  gouty  diathesis,  faulty  footwear,  excessive  use  of  the  feet 
in  standing,  neurasthenia,  may  provoke  pain  in  and  about  the  fourth 
metatarso-phalangeal  articulation.  This  is  Morton's  metatarsal gia  and 
is  usually  relieved  when  the  cause  is  discovered. 

Prognosis. — The  underlying  diathesis  and  predisposition  may  de- 
termine the  course  and  prognosis  of  sciatica.  Acute  cases  due  to 
acute  causes  usually  get  well  in  a  few  weeks.  Chronic  cases  sometimes 
run  their  course  with  more  or  less  periodic  exacerbations.  Remissions 
and  even  intermissions  occur.  Rheumatic  cases  are  usually  favorable. 
Very  old  cases,  senile  cases  and  those  due  to  unchangeable  causes  can- 
not hope  for  more  than  occasional  amelioration,  with  or  without  treat- 
ment.    Permanent  lameness  occurs  in  some. 

Treatment. — In  the  management  of  sciatica  the  methods  that 
afford  the  highest  degree  of  success  are  not  only  different  from  those 
employed  in  the  treatment  of  other  neuralgias,  but  they  are  more  or 
less  identical  with  those  that  prove  to  be  most  efficacious  in  the  man- 
agement of  neuritis.  Counter-irritation  and  the  actual  cautery  even, 
the  internal  administration  of  vasomotor  sedatives,  the  free  use  of 
cathartics,  diuretics,  and  diaphoretics,  are  the  chief  measures  depended 
upon  in  the  subacute  and  acute  stage.  Analgesics,  narcotics,  and  sen- 
sory depressants  produce  less  permanent  results  in  sciatica  than  they 
do  in  other  forms  of  neuralgia,  doubtless  because  they  do  not  affect 
the  organic  changes  underlying  the  trouble. 

According  to  Pliny,  the  victims  of  sciatica  in  his  day  had  their 
pains  assuaged  by  the  soft  tones  of  the  flute.  From  this  ancient  musical 


634  THE  XOX-XEUROXIC  DISEASES 

method  to  the  modern  hypnotic  it  is  not  such  a  far  leap.  Pain  may 
become  a  habit  even  after  the  organic  cause  of  the  pain  has  disap- 
peared, a  habit  which  often  needs  only  moral  and  mental  treatment  for 
its  relief.  In  such  cases,  and  they  are  usually  long-standing  ones, 
electricity,  baths,  moderate  exercise,  and  general  hygienic  treatment 
will  do  much.    2^Iost  of  these  cases  were  undoubtedly  neuralgias. 

Drugs  are  useful,  though  secondary  in  the  treatment  of  sciatica. 
In  the  acute  stage,  general  and  absolute  rest,  even  to  the  point  of  strap- 
ping the  limb  if  necessary,  is  a  sine  qua  non.  To  paralyze  the  sensi- 
bility and  depress  the  excited  circulation,  opium  and  its  alkaloids,  acon- 
ite, belladonna,  antipyrin,  phenacetin.  acetanilid,  are  all  most  useful. 
So  many  cases  are  associated  with  the  rheumatic  and  gouty  diatheses 
that  I  tind  myself  making  large  use  of  the  salicylates  and  colchicum,  and 
with  general  good  results.  The  deep  injection  of  ether  and 
chloroform,  though  useful  sometimes,  has  not  proved  uniformly  so  in 
my  hands.  In  old  cases,  nerve-stretching  may  be  done  surgically,  or 
less  radically  by  placing  the  patient  on  his  back  and  flexing  the  legs 
on  the  body  as  far  as  possible.  Sometimes  this  has  broken  up  a  long- 
standing sciatica,  possibly  doing  it  by  breaking  up  small,  old  adhesions 
and  restoring  the  circulation. 

After  the  trouble  has  become  chronic  and  all  acute  signs  of  in- 
flammation have  disappeared,  I  resort  to  the  steady  use  of  strychnine, 
preferably  by  the  subcutaneous  method  as  recommended  by  Ley  den, 
in  doses  of  from  1-70  to  1-20  of  a  grain  twice  a  day.  Massage,  baths, 
and  the  steady  use  of  mild  currents  of  electricity  should  be  made  every 
day.    For  the  general  principles  of  treatment  see  the  section  on  neuritis. 

Peroneal  or  External  Popliteal  Nerve. — It  is  a  curious  fact  that 
in  all  sciatic  diseases,  the  symptoms  of  the  peroneal  are  more  prominent 
than  of  other  branches.  As  an  isolated  paralysis  the  peroneal  is  far 
more  frequently  aft'ected  than  the  tibialis  posticus.  In  my  own  opinion 
there  is  a  developmental,  biological  reason  behind  this,  though  as  yet 
we  cannot  determine  just  what  it  is.  It  is  one  of  the  curious  facts  of 
nature  that  goes  with  such  exhibitions  as  the  localization  of  syphilitic 
damage  in  special  neurones  in  tabes,  and  the  causation  of  a  thyroid-like 
disease,  acromegaly,  out  of  a  hypophyseal  lesion.  Note  the  frequency 
of  its  disease  in  acute  anterior  poliomyelitis  in  this  connection. 

The  nerve  may  be  injured  by  fracture  of  the  fibula  and  callus, 
by  lacerations  in  running  and  making  missteps,  and  by  forcible  exten- 
sion of  the  leg.  It  has  been  badly  compressed  by  a  tourniquet,  by 
sleeping  cross-legged,  by  wearing  of  stilts  and  by  prolonged  stooping 
in  certain  occupations,  like  potato-picking. 

The  nerve  supplies  the  tibialis  an  tic  us,  the  long  extensor  of  the 
toes,  the  short  extensor  and  the  peronei.  Consequently,  the  foot  drops ; 
it  cannot  be  flexed  at  the  ankle.  Ultimately  talipes  equinus  develops. 
The  first  phalanges  of  the  toes  cannot  be  extended.  The  unopposed 
interossei  cause  persistent  flexion  of  the  first  phalanges.  This  leads 
to  the  pied-en-griffe  appearance,  ^^^alking,  of  course,  is  difficult  and 
the  toes  drag  on  and  scrape  the  floor.  The  dorsum  of  the  foot  and 
outer  half  of  the  leg  is  apt  to  be  ancesthetic. 

The  paralysis  is  of  the  degenerative  type  with  atrophy,  loss  of  re- 


THE  XOX-XEUROXIC  DISEASES  635 

flexes,  reaction  of  degeneration.  It  is  therefore  flaccid.  Anomalies 
occur  in  both  the  motor  and  sensory  phenomena.  Thus  the  tibiahs 
anticus  may  escape  the  palsy  and  the  anaesthesia  may  not  limit  itself 
strictly  to  the  peroneal  area. 

Trophic  and  vasomotor  symptoms  occur. 

Tibialis  Posticus,  or  Internal  Popliteal.  Here  the  popliteus.  calf 
muscles,  tibialis  posticus  and  long  flexors  of  the  toes  are  mvolved.  The 
plantar  muscles  are  implicated.  The  ankle  joint  cannot  be  extended 
and  the  flexed  leg  cannot  be  rotated  inward.  Talipes  calcaneus  is  the 
■deformity  that  ultimately  results.  The  patient  cannot  raise  himself  on 
his  toes.  The  sole  of  the  foot  and  the  lower  half  of  the  outer  part  of 
the  back  of  the  leg  is  ancBsthetic. 

Plantar  Xerves. — These  rarely  are  diseased  alone.  Disease  of  the 
internal  causes  anaesthesia  on  the  inner  part  of  the  sole  and  the  plantar 
surface  of  the  three  inner  toes  and  half  of  the  fourth.  The  short  flexor 
•of  the  toes  is  paralyzed,  the  plantar  muscles  of  the  great  toe  except 
the  adductor  and  the  two  inner  lumbricales.  Disease  of  the  external 
reveals  itself  in  anaesthesia  in  the  outer  half  of  the  sole,  the  little  toe 
and  outer  half  of  the  fourth :  paralysis  of  the  flexor  accessorius,  of 
the  muscles  of  the  little  toe,  all  the  interossei,  the  two  outer  lumbricales 
and  the  adductor  of  the  hallux.  As  the  toes  gradually  become  flexed 
persistently  at  the  last  two  joints,  and  extended  at  the  others,  walking 
is  badly  interfered  with  and  the  appearance  is  that  of  the  pied-en- 
_griffe. 

The  prognosis  and  treatment  of  all  of  these  neuritic  troubles  of 
the  lower  limbs  follow  the  same  line  that  they  do  in  the  similar  troubles 
in  the  upper  limb.  For  the  general  principles,  the  reader  is  referred  to 
the  section  headed  neuritis. 


636 


THE  NON-NEURONIC  DISEASES 


The  following  table  is  taken  from  Dana's  work  and  is  a  compilation  from 
Starr,  Mills,  Sachs,  Thorburn,  Dana  himself  and  others. 

Muscles  of  Tongue,  Palate,  and  Pharynx. 


Diseases  in 

Name  of 

Normal 

Symptoms  of  Defi- 

Innervated 

Represented 

which  Muscle  is 

Muscle. 

Function. 

cient  Action. 

by 

in 

commonly  In- 
volved. 

G  e  n  i  o  - 

Pushes  tongue 

Tongue  when  pro- 

The twelfth 

Medulla. 

glossus. 

to  opposite 

truded  deviates  to 

nerve  ( h  y- 

side. 

paralyzed  side. 

poglossal). 

S  t  yloglos- 

Raises  tongue 

Tongue  cannot  be 

T  li  e  twelfth 

Medulla. 

Bulbar   pal- 

3US. 

backward  and 

moved  backward 

nerve. 

sies     (acute 

upward. 

or   hollowed   out 
(action    deficient 
in  many  healthy 
subjects). 

and  chron- 
ic) ;  in   spe- 
cific and  tu- 
■    b  e  r  c  ulcus 

L  i  ngu  al 

All  movements 

When     lying    in 

The    twelfth 

Medulla. 

diseases    of 

muscle 

of  the  tongue 

mouth    deviation 

nerve. 

base  ;  dys- 

proper. 

itself. 

to   healthy  side  ; 
w  hen  protruded 
deviates  to  para- 
lyzed side;  if  one 
or  both  halves  are 
atrophied  tongue 
looks  shrivelled. 

t  r  0  ph  i  es 
(rare). 

A  zy gos 

Shortening    of 

Uvula  deviates  to- 

Probably 

Medulla, 

As  above. 

UVUlSB- 

uvula. 

ward  sound  side  ; 
if  both  sides  are 
paralyzed     there 
are     nasal    tone 
and  regurgitation 
through  nose 

pharyngeal 
plexus; 
seventh 
nerve  (?). 

Diseases  in 

Name  of 

Normal 

Symptoms  of  Defi- 

Innervated 

Represented 

which  Muscle  is 

Muscle. 

Function. 

cient  Action. 

by 

in 

commonly  In- 
volved. 

Levator 

Raises  the  ve- 

Arch   cannot    b  e 

As  above. 

Medulla. 

As  above  ;   see 

palati. 

lum  palati. 

raised  in  the  in- 
tonation of  "ah;" 
if  paralysis  is  bi- 
lateral flapping  of 
arch  and  regurgi- 
tation   of    food 
through  nose. 

also  seventh- 
nerve  affec- 
tions. 

Palat  0- 

Prevent  food 

Regurgitation    o  f 

The   fifth 

Pons, 

Basilar  a  ff  e  c- 

p  h  a  r  y  n- 

from  passing 

food ;      nasal 

nerve 

tions. 

geal  mus- 

toward up- 

speech. 

cles. 

per  part  of 
pharynx  and 
post  er i  o  r 
nares. 

Stylo- pha- 

Helps  to  draw 

Imperfect  degluti- 

Glosso •  pha- 

Medulla. 

Bulbar      affec* 

ryngeus. 

larynx   up- 

tion ;    food    gets 

ryngeal. 

tions  and  dis- 

ward so  as  to 

into  vdndpipe. 

eases    of    the 

be  closed  by 

base. 

epiglottis  and  j 

overtopped  ( 

by  tongue. 

Cons  tric- 

Help  to   push 

Food  is  swallowed 

Ph  aryngeal 

Medulla 

Diseases  of  the 

tors    of 

food  into  gul- 

very imperfectly; 

plexus. 

base  (bulbar). 

pharynx. 

let. 

sticks  in  throat. 

Laryngeal 

Movements  of 

Hoarseness    and 

Recurrent 

Medulla 

Bulbar  trou- 

muscles. 

vocal  cords  in 

difficulty    in 

la  ryngeal 

bles     (similar 

respiration 

breathing;  laryn- 

nerve  ex- 

symptoms 

and  in  articu- 

goscopic examina- 

cepting the 

may  be  caused 

lation. 

tion  reveals  false 

crico  - 1  h  y- 

by  tumors  and 

position  of  vocal 

roid   m  u  s- 

foreigh  bodies 

cords  (see  special 

cle. 

in  larynx). 

text-books) 

TllK   XOX-XKL'UOXIC   DISEASES 
MrscLES  OF  Head  ajstd  Xeck. 


^W 


Diseases  in 

Name  of           Normal 

Symptoms  of  Defi- 

Innervated 

Represented 

which  Muscle  is 

Muscle.     1       Function. 

1 

cient  Action. 

by 

in 

commonly  In- 
volved. 

S  t e  rn  0- 

Raises  and 

Inability    to    raise 

Spinal  ac- 

Medulla and 

In  bulbar   and 

c  1  e  i  do  - 

turns  face  to 

head  from  bed.  or 

cessory. 

second   and 

cervical -cord 

mastoid. 

opposite  side; 

other    horizontal 

third    cer- 

affections ;  in 

head  inclines 

position,  if   both 

vical     s  e  g- 

later  stages  of 

to  same  side; 

muscles  are  affect- 

ments. 

p  r  0  g  r  e  s  sive 

if  both   mus- 

ed; if  one  muscle 

muscular 

cles   act  con- 

is   affected,    no 

atrophies; 

jointly     head 

marked  change  of 

occasionally 

is  breught 

position,  unless 

in  neuritis. 

foTO-ard; 

opposite     muscle 
is    contractured  ; 
spasm  of  muscle 
frequent ;  head  in- 
clined to  one  side. 

H  e  c  t  us 

To  flex  head. 

Cannot  flex  head" 

Opper  cervi- 
cal. 

L'pper    c  e  r- 

capitis  1 

so    as    to   bring 

vical    s  e  g- 

anticus 

chin  on  chest. 

ments. 

major. 

1 
Rectus  To  flex  head. 

capitis 

anticus 

minor.        ; 

Diseases     o  f 

the   cervical 

"Rectus 

Slight  rota- 

Deficient   rota- 

region  (my- 

capitis 

tion. 

tion     scarcely 

1 

-  elitis,    men- 

lateralis. 

noticeable,     un- 
less  stemo-clei- 
do-mastoids  are 
diseased. 

1    i  n  g  i  t  i  s  , 
tumor;  pro- 
gressive 
wasting    0  f 

S  c  a  1  e  n  i  'i 

Elevate  r  i  b  s- 

Deficient  inspi-| 

Lower  cervi- 

L<:iwer cervi- 

muscles) 

anterior  ' 

1  when  verte- 

ratory     m  o  v  e- 

cal  nerves. 

e  a  1    s  e  g- 

m  e  d  i  -  : 

'  bi-al     column 

ments. 

ments. 

us,    e  t 

is  fixed  ;    aid 

po  ste- 
rior. 

in    i  n  s  p  i  r  a- 

. 

i 

tion  ;  slight 

lateral      flex- 

ion. 

Flexion  of  ver- 

Imperfect flexion 

Lower  cervi- 

LOD gus 

tebral     c  o  1  - 

of  upper  spine,   j 

cal  nerves. 

. 

colli. 

umn. 

1 

638  THE  NON-NEUKONIC  DISEASES 

Muscles  of  Shoulders  and  Upper  Extremity. 


Diseases  in 

Name  of 

Normal 

Symptoms  of  Defi- 

Innervated 

Represented 

which  Muscle  is- 

Muscle. 

Function. 

cient  Action. 

by 

in 

commonly  In- 
volved. 

T  rapezius 

Pulls   head  Deficient   back- 

Spinal  acces- 

Medulla and 

Progressive^ 

1.     Cla- 

backward ;  ro- 

ward movement 

sory 

second  and 

m  u  sc  u  lar 

vicular 

tates  slightly 

of  head;   not 

third  cervi- 

wasting  ;    dis- 

portion 

toward  side  of 

maiked  as  a  rule 

c  a  1    s  e  g- 

eases    of   me- 

(respi- 

muscle,   BO 

because  deep 

ments. 

dulla  and  up- 

ratory  ; 

that    chin    is 

muscles   perforin 

per     cervical 

ou  t  e  r 

turned  to  op- 

this   function  ; 

cord  ;    clavic- 

third of 

posite  side; 

shoulder  does  not 

ular      portion 

clav  icle 

contraction  of 

move   during  in- 

least frequent- 

to occipi- 

both clavicu- 

spiration. 

ly  involved. 

tal  bone) 

lar     portions 
bends    head 
backward  ; 
slight     eleva- 
tion of  shoul- 
ders; aids  in 
deep  inspira- 
tion. 

2.Middle 

Raises     shout- 

Acromion  depress- 

Spinal acces- 

As above. 

As  above. 

portion 

der-blad  e ; 

ed   by  weight  of 

sory  nerve. 

(from 

elevation    0  f 

upper  extremity ; 

acromion 

acromion 

inner   upper    an- 

and outer 

(clavicle  goes 

gle  may  be  pulled 

spine    0  f 

along). 

upward  bylevaior 

scapula  to 

anguli     scapulas; 

ligament. 

internal  lower  an- 

n u  c  h  se 

gle  is  nearer    to 

and   u  p- 

median  line. 

per  dorsal 

spines  V. 

3.    Lower 

Adduction    0  f 

Margin  of  scapula 

Spmal  acces- 

Medulla and 

portion 

scapula  to- 

is about  ten  cm. 

sory  nerve. 

second  and 

and    a  d- 

ward  median 

distant,  instead  of 

third  cervi- 

ductor 

line. 

being  Ave  or  six 
cm.  distant  from 
median  line  ;  loss 
of  adductor  may 
be  covered  up  by 
action  0  f    rhom- 
boids ;    rounding 
of  back. 

c  a  1    s  e  g  - 
ments. 

R  h   0  m  - 

Oblique  move- 

Deep   groove    be- 

Fifth   cervi- 

Fourth and 

As  above. 

boids. 

ment  of  scap- 

tween inner  mar- 

cal. 

fifth    cervi- 

ula  from  be- 

gin of  scapula  and 

ca  1    se  g- 

low,    upward 

thorax;  if  serra- 

ments. 

and   inward, 

tus  is  normal,  this 

so  tliat  infe- 

groove    disap- 

rior  angle   is 

pears  if  arm  is  ex- 

brought near- 
er  the  medi- 
an line;    hold 
spinal  margin 
of  scapula 
down  to  tho- 
rax. 

tended  forward  ; 
shoulder  blade 
cannot  be  approx- 
iiuated  to  median 
line.     (According 
to  Duchenne  this 
can  be  effected  by 
upper  porlion  of 
latissimus  dorsi.) 

Levator 

Draws  superi- 

Isolated  paralysis 

Third    and 

Second    and 

Dystrophies 

an  gul i 

or  inner  angle 

rare. 

fifth    cervi- 

fourth     (?) 

and    cervical 

scapulas. 

of  scapula  up- 
war  d ;  aids 
in    shrugging 
of  shoulilers. 

cal  nerves. 

cervical 
segments. 

diseases. 

Serratus 

Rotation  of 

Scapula  puUecfup- 

Posterior 

Fifth  and 

Progressive 

magnus. 

shoulder- 

ward;  lower  inner 

thoracic 

sixth  cervi- 

muscular  atro-' 

blade  out- 

angle nearer  the 

nerve. 

cal     seg- 

phies   (  d  y  s- 

ward,    and 

median  line;  arm 

ments. 

trophies);neu-- 

slight    eleva- 

cannot be  raised 

ritis  of  part  of 

tion  of  acro- 

above   horizontal 

the   brachial 

mion;  holds 

position:  if  ai'm  is 

plexus  ;    after 

inner  margin 

stretched  f  orwaid 

traumatic    in- 

of scapula  to 

scapula   is   re- 

juries to  shoul- 

thorax ;brings 

moved  from  tho- 

der :  in  cervi- 

arm from  hor- 

rax   ("winged 

cal-cord  affec- 

izontal to  ver- 

scapula");   dur- 

tions. 

tical  position. 

ing  abduction  of 
arm,    scapula    i? 
moved  nearer  to 
median  line,  and 
crowds  trapezius 
and    rhomboids 
forward. 

THE  NON-NEUROXTC  DISEASES 


639 


Muscles  of  Shoulders  axd  Upper  'ExTREymY.—Contm'ued. 


Name  of 
Muscle. 


Deltoid 
(three  d  i  - 
visions). 


Iiif  raspi-  "I 
natus.    ) 

Teres  | 
minor.  J 

Sub  s  c  a  p  - 
ularis. 


Supras  p  i  - 
natus. 


Latissimus 
dorsi. 


formal 
Function. 


Teres  ma- 
jor. 


Pectoralis 
major. 


To  raise  arm 
to  horizontal 
position,  and 
forward,  out- 
ward,or  back- 
ward ;  move- 
ments possi- 
ble only  if 
scapula  is 
fixed  by  ac- 
tion of  serra- 
tus  and  tra- 
pezius. 

Rotator  hu- 
meri posticus 
(  Duch^nne ) ; 
rotate  arm 
outward. 

Rotator  hume- 
r  i  a  q't  i  c  u  s 
(Duchenne)  ; 
rotates  arm 
inward 

Helps  to 
steady  shoul- 
der-joint and 
to  elevate 
arm  forward 
and  outward: 
outer  an^leof 
scapula  is  de- 
pressed. 

Pulls  the  arm 
when  raised, 
downward 
and  b  a  c  k- 
ward;  if  arm 
is  at  rest  up- 
p  e  r  portion 
brings  scap- 
ula nearer 
the  median 
line;  united 
action  of  up- 
per third  of 
both  muscles 
causes  exten- 
sion of  dorsal 
trunk  ;  single 
action  causes 
lateral  jnove- 
ment  of  trunk. 

Rotates  raised 
humerus  in- 
ward; adduc- 
tion of  arm  to 
thorax;  slight 
elevation  o  f 
shoulder. 

Clavicular 
portion  d  e  - 
presses  h  u  - 
merus  from 
raised  p  o  s  i- 
tion  to  hori- 
zontal ;  ad- 
duction of 
arm,  as  in 
giving  a  bless- 
ing;  sternal 
portion  d  e  - 
presses  arm 
com  pletely, 
and  if  arm  is 
at  rest  draws 
acromion  for- 
w  a  r  d  and 
backward. 


Symptoms  of  Defi- 
cient Action. 


Can  raise  shoulder 
but  not  arm; 
shoulder  flattened 
(atrophy) ;  groove 
between  acromion 
and  head  of  hu- 
merus ;  each  di- 
vision of  deltoid, 
maj'  be  paralyzed 
singly. 


Arm  cannot  be 
moved  outward. 

Difficulty  in  writ- 
ing (Duchenne). 

Arm  cannot  be 
moved  inward  ; 
scapula  is  rubbed 
against  ribs. 

-According  to  Du- 
chenne, humerus 
is  separated  still 
farther  from  acro- 
mion, if  supra- 
spinatus  is  affect- 
ed in  addition  to 
deltoid. 

Arm  cannot  b  e 
moved  backward : 
insufficient  exten- 
siou  of  dorsal 
spine;  trunk  can- 
not be  moved  lat- 
erally. 


Very  few  symp- 
toms; action  sup- 
plied b  y  other 
muscles. 


Imperfect  adduc- 
tion of  arm ;  pa- 
ralysis can  be  dis- 
covered best  by 
extending  arms 
and  trying  to 
press  volar  sur- 
faces against 
each  other. 


Innervated 

by 


Circumflex. 


Supra- 
scapular. 
C  i  r  c  u  m- 

flex. 

Subscapu- 
lar nerve. 


Suprascapu- 
lar, 


Subscapu- 
1  a  r,  also 
branches  of 
dorsal  and 
lumbar 
nerves  pass- 
ing through 
muscle. 


Fourth    cer -  .\s  above, 
vical. 


Sixth  and 
seventh  cer- 
vical. 


Subscapular. 


Anterior 
thoracic. 


Represented 


Diseases  in 
which  Muscle  is 
commonly  In- 
volved. 


Fourth,  flfth, 
and  sixth 
cervical 
segments. 


Fourth,  flfth, 
and  sixth 
cervical 
segments. 


As  above  ;  also 
in  Erb's  form 
of  obstetrical 
paralysis. 


As  in   case  of 
deltoid. 


Seventh  cer- 
vical. 


Fifth,  sixth, 
and  seventh 
cervical. 


As  in  progres- 
sive atrophies 
and  dystro- 
phies; in  cer- 
vico -dorsal 
lesion  s ;  in 
neuritis. 


As  above. 


Amyotrophies 
and  dystro- 
phies, chiefly; 
also  in  lesions 
of  brachial 
plexus. 


640 


THE  NON-NEUKONIC  DISEASES 
Muscles  of  Arm,  Forearm,  and  Hand. 


Fame  of 
Muscle. 


Triceps . . 


Normal 
Function. 


Biceps. 


Supinator 
longus. 


Supin  a  t  o  r 
brevis. 


Exte  nso  r 
carpi  ra- 
d  i  a  1  i  s 
longus  et 
brevis. 


Extensor 
carpi  ul- 
naris. 


Extensor 
d  i  g  i  t  o  - 
rum  com- 
munis. 

Extensor 
indicis. 

Extensor 
minimi 
digiti. 

Flexor 
carpi 
i-adialis. 

Flexor 
carpi 
ulnaris. 

Pal  maris 
longus. 


Extends  fore- 
arm; long 
head  of  tri- 
ceps, and  cor- 
aco-brachialis 
help  to  keep 
head  o  f  hu- 
merus in  posi- 
tion. 

Flexion  and 
supination  of 
forearm. 


Flexes  f  o  r  e  - 
arm  and  aids 
in  pronation. 


Supinates 
hand  w  li  e  n 
forearm  is  ex- 
tended. 

Extension 
and  abduc- 
tion of  wrist; 
the  shorter 
muscle  has 
pure  exten- 
s  i  o  n  action 
only. 

Extension  and 
abduction  of 
wrist. 


Extension  of 
fi  r  s  t  pha- 
langes of  all 
fingers  and 
abduction. 


Flexion  of 
wrist  and  pro- 
nation. 

Flexion  of 
wrist  and 
supination. 

Flexion  of 
wrist  only. 


Symptoms  of  Defi- 
cient Action. 


Arm  cannot  be  ex- 
tended except  by 
its  own  weignt;  if 
long  head  of  tri- 
ceps is  affected 
subluxation  o  f 
head  of  humerus 
occurs  easily. 

Flexion  deficient, 
but  can  be  carried 
out  in  part  by 
other  muscles. 


Flexion  and  prona- 
tion deficient; 
muscle  does  not 
stand  out  promi- 
nently if  arm  is 
flexed  and  a  t- 
tempt  is  made  by 
another  to  extend 
it  forcibly;  if  mus- 
cle i  s  atrophied 
arm  i  s  spinule- 
shaped. 

Deficient  supina- 
tion of  band. 


Wrist  cannot  be 
flexed  dorsally 
(extended)  or  ab- 
ducted; flattening 
of  forearm. 


Wrist  cannot  be 
flexed  dorsally  or 
adducted;  "drop- 
wrist  "  is  charac- 
teristic of  paraly- 
sis of  extensors. 

First  phalanges 
cannot  be  ex- 
tended nor  fingers 
abducted ;  grasp 
is  weak  because 
flexor  muscles  are 
shortened  and 
cannot  contract 
forcibly. 

Deficient  flexion. 


Flexion  and  supi- 
nation impaired. 

Flexion  impaired; 
no  a  n  o  m  a  1  ous 
position  of  hand 
from  paralysis  of 
wrist  as  hand  falls 
by  its  own  weight; 
the  flexors  o  f 
fingers  may  act  as 
substitutes. 


Innervated 
by 


Musculo- 
spiral. 


Musculo -cu- 
taneous. 


Musculo- 
spiral. 


Musculo- 
spiral. 


Muse  u  lo- 
spiral. 


As  above. 


Musculo- 
spiral. 


Median  . 


Ulnar. 


Median 


Represented 


Sixth,  sev- 
enth, eighth 
cervical  seg- 
ments. 


Fourth,  fifth, 
sixth  cervi- 
cal. 


Fourth,  fifth 
cervical. 


Diseases  in 
which  Muscle  is 
commonly  In- 
volved. 


Fifth    cervi- 
cal. 


Seventh  cer- 
vical. 


Seventh  cer- 
vical. 


Seventh  cer- 
vical. 


Eighth  c  e  r- 
vical. 

Eighth   cer- 
vical. 

Eighth   c  e  r- 
vical. 


]  Poliomyelitis 
and   other 
affections  of 
cervical 
cord  ;    trau- 
matic   inju- 
ries ;  amyo- 
-  t  r  o  p  h  ies 
and    dystro- 
phies (tri- 
ceps   e  s- 
c  a^pes    i  n 
many    pe- 
ripheral 
J    palsies.) 
As  above  ;   in- 
volved  in  pe- 
ripheral   neu- 
ritis (traumat- 
ic),    nob    in 
lead  palsy. 


Diseases  as 
above ;  also 
i  n  peripheral 
palsies. 

As  before  ;  es- 
pec  iall  y  in 
neuritis. 


As  above. 


As  above. 
As  above. 
As  above. 


THE  NON-NEURONIC  DISEASES 
Muscles  of  Arm,  Forearm,  a,nd  Hand. — Continued. 


64  T 


Name  of 
Muscle. 


d  i  g  i  t  o 
rum  sub- 
limis. 
Flexor 
d  i  g  i  t  o- 
rum  pro- 
fundus. 


Interossei 
and  lum- 
bricales. 


Normal 

Function. 


Plexor  Flexes  second 


Thenar 

muscles : 

Extensor 

Eollici  s 
revis. 


■Exten  sor 
pol  1  icis 
longus. 


Abd  uctor 
pollicis 
longus. 


Abductor 

g  611  icis 
revis. 
Opponens 
pollicis 
and  outer 
portion  of 
the  flexor 
brevis. 
Abductor 

gollicis 
revis ; 
flex  o  r 
brevisand 
adductor. 


Flexor 
pollicis 
longus. 


phalanx    to- 
ward first. 

Flexes  last 
two  phalanges 
toward  first. 


Abduction  and 
adduction  of 
fingers  if  first 
phalanges  are 
extended; 
flexion  of  first 
phalanges 
and  s  i  m  u  1- 
taneous  e  x  - 
tension  of  sec- 
ond and  third 
phalanges. 

E.xtends  first 
phalanx  and 
abducts  meta- 
carpal bone  ; 
'acts  with  ad- 
ductor polli- 
cis longus. 

Extends  both 
phalanges  of 
thumb  ;  also 
adduction  of 
m  e  t  acarpal 
bone  and 
backward 
movement  of 
thumb. 

Abduction  of 
metacarpal 
bone  ;  aids  in 
flexion  of 
hand. 


^Opposition 
of  thumb. 


Flex  first  pha- 
lanx and  ex- 
tend second 
phalanx  (like 
i  n  terossei), 
also  have  an 
abduction 
and  adduc- 
tion action. 

Flexes  end 
phalanx. 


Second  phalanx 
cannot  be  flexed. 


Symptoms  of  De- 
ficient Action. 


Innervated 
by 


Median  , 


Last  two  phalanges  Ulnar    and 
cannot  be  flexed.      Median. 


Fingers  cannot  be 
abducted  or  ad- 
ducted;  inter- 
osseous  spaces 
are  very  marked ; 
"Main  en  griffe  " 
due  to  extension 
of  first  phalanges 
and  flexion  o  f 
Second  and  third 
phalanges. 

Impairment  of  ex- 
tension and  ad- 
duction ;  flatten- 
ing of  ball  of 
thumb. 


Deficient  extension 
a  n  d  adduction  ; 
second  phalanx  is 
flexed  toward 
first. 


Deficient  abduc- 
tion of  metacar- 
pal bone  ;  if  this 
muscle  and  ex- 
tensor pollicis 
brevis  are  par- 
alyzed adduction 
results. 


No  opposition 
movement. 


No  flexion ;  if  mus- 
cles are  paralyzed 
and  atrophied, 
ape  hand  is 
formed. 


No  flexion  of  end 
phalanx. 


Represented 


Ulnar,  which 
also  s  u  p  - 
plies  third 
and  fourth 
1  u  m  b  r  i- 
cales;  medi- 
an supplies 
first  two  and 
sometimes 
third  lum- 
bricales. 

Musculo- 
spiral. 


Musculo- 
spiral. 


M  u  scu 1 o- 
spiral. 


Musculo- 
spiral. 


Median. 


Median 
ulnar. 


Median. 


and 


Eighth  cer- 
vical. 


Eighth  cer- 
vical. 


Eighth  cer- 
vical, first 
dorsal. 


First  dorsal. 


First  dorsal. 


First  dorsal. 


First  dorsal. 


Diseases  in 
which  Muscle  is 
commonly  In- 
volved. 


As  above; 
muscle  should 
be  tested  with 
special  care 
i  n  cases  o  f 
traumatic  in- 
juries. 

As  above ;  oft- 
en the  first 
muscles  to  be 
affected  in 
p  r  o  g  r  e  s  sive 
spinal  a  t  r  o- 
phies. 


As  before; 
more  es  pe- 
ciallv  in  amyo- 
tropnies  and. 
neuritis. 


As  above. 


As  above. 


As  above. 


As  above. 


As  above. 


642 


THE  NON-NEURONIC  DISEASES 
Muscles  of  Back  and  Lower  Extremities. 


Name  of  Muscle. 


Erector  spinse;  sa- 
cro-lumbalis;  lon- 
gissimus  dorsi. 

AbdomiBal  muscles. 


Quadratus     lumbo- 

rum. 
Adductor  muscles. 

Sartorius. 

Quadriceps  femoris. 

Ilio-psoas. 

Tensor  fasciae  latae. 

"External  rotators:  1 
Pyrif  ormis 
Gemelli. 

Quadratus  femoris. 
Internal  obturator 
External  obturator  f 

Gluteal  muscles. 

Biceps  ;  semitendi- 
nosus  and  semi- 
membranosus. 

Gastrocnemius  (al- 
so plantarius  and 
soleus). 

Anterior  tibial  mus- 
cles (tibialis  anti- 
cus,  extensor  digi- 
torum,  and  exten- 
s  o  r  pollicis  lou- 
gus). 

Peroneus  longus. 


Posterior  tibial  mus- 
cle. 

Peroneus  brevis. 

1  n  terossei  pedis  et 
lurnbricales 

Adductor:  flexor 
brevis  and  abduc- 
tor liallucis. 


Innervated  by 


Dorsal  nerves.  Second  to 
twelfth  dorsal  segments. 


Dorsal  nerves.  Second  to 
twelfth  dorsal. 


Lumbar  nerves. 

Obturator   nerve,    great 

sciatic  and  crural. 
Crural.    Third  lumbar 
•   segment. 
Crural.    Third  lumbar. 


Crural  (lumbar  plexus). 

Fourth  lumbar. 
Superior  gluteal.  Fourth 

lumbar. 

Sacral  plexus  (muscular 
branches).  Fifth  lum- 
bar. 

Obturator  nerve  (lum- 
bar plexus). 

f  Inferior  gluteal  (sacral 
plexus).  First  and  sec- 

i     ond  sacral. 

I  Gluteal  superior.    First 

[     and  second  sacral. 

Sciatic.  Fifth  lumbar 
segment. 


Internal  popliteal.    Fifth 
lumbar. 

Anterior  tibial.     Fifth 
lumbar  and  first  sacral. 


Peroneal.  First  and  sec- 
ond  sacral    segments. 

Posterior  tibial  nerve. 
First  and  second  seg- 
ments. 

Peroneal.  First  and  sec- 
ond segments. 

Posterior  tibial.  First 
and  second  segments. 

Posterior  tibial.  First 
and  second  segments. 


Symptoms  of  Deficient  Action. 


Lordosis  of  lower  spine;  perpendicular 
line  from  shoulder  falls  behind  os  sa- 
crum: unilateral  palsy  causes  deflection 
of  spine  toward  sound  side. 

Lordosis  with  protrusion  of  nates  and 
abdomen;  other  actions  deficient;  can- 
not straighten  up  from  recumbent 
position  without  assistance  of  hands. 

Lateral  movements  of  lower  vertebrea 
imperfect. 

No  adduction;  thigh  rolls  outward. 

Flexion  impaired;  acts  imperfectly. 

Leg  cannot  be  extended;  to  test  it  ask 
patient,  who  is  lying  down  with  hip 
bent,  to  stretch  out  the  leg,  when  pa- 
tient is  sittiug  down  to  extend  leg. 

j  Flexion  difficult:  in  bed  thigh  cannot  be 
V    flexed:  difficulty  rising  from  horizon- 
tal position. 


Deficient  outward  rotation 
inward. 


leg  turned 


No  extension  of  thigh:  great  difficulty  in 
climbing:  no  abduction  of  thigh;  wad- 
dling gait,  exaggerated  movement  of 
pelvis. 

deficient  flexion;  action  of  quadriceps 
may  cause  excessive  extension  ;  in 
standing  thigh  is  fiexed  to  excess ; 
trunk  moved  backward 

Deficient  flexion  of  foot  ;  heel  cannot  be 
raised  ;  cannot  stand  on  tiptoes. 

Deficient  extension;  "dropfoot,"  toes 
scrape  floor  ;  to  clear  this,  excessive 
flexion  at  knee  and  hip  ;  contracture  of 
fiexors  and  pes  equinus  or  equinovarus. 


Deficient  abduction  ;  plantar  arch  les- 
sened; increased  by  contracture.  Flat- 
foot  ;  walking  tiresome. 

I  Deficient  abduction  or  adduction  ,   de- 
!    formities  result  from  deficiencies. 

Abduction  and  adduction  of  toes  defl- 
cieut ;  paralysis  of  interossei ;  hyperex^ 
tension  of  first  phalanges;  second  and 
third  flexed  (clawed  foot). 

Deficient  flexion  of  toes  ;  foot  cannot  be 
pushed  off  ground  easily. 


THE  XOX-XEUROXIC  DISEASES  643 

DISEASES  OF  THE  CRANIAL  XER\'ES. 

The  olfactory  and  optic  nerves,  so-called,  are  parts  of  the  brain 
and  will  be  discussed  in  another  part  of  the  book.  Thev  are  not 
nerv'es  in  the  sense  of  being  mere  bundles  of  neuraxones  remote  from 
their  ganglionic  centers.  They  are  part  and  parcel  of  the  great  intra- 
cranial ganglionic  centers  and  tracts.  The  olfactory  bulb  is  actually 
a  cerebral  lobe,  and  the  optic  nerves  are  pure  cerebral  tracts. 

The  other  cranial  nerves  are  identical  in  structure  with  the  spinal 
nerves.  They  spring  from  motor  and  sensory  roots.  The  former  have 
their  cells  bunched  together  in  nuclei  which  are  the  mere  forward  ex- 
tension or  homologous  representation  of  the  anterior  horns  of  the 
cord.  *  The  latter  have  their  cells  collected  m  the  ganglia  ( Gasserian, 
jugular,  petrosal,  geniculate,  etc.)  found  on  the  roots  of  the  sensory 
nerv^es.  Like  the  spinal  sensory  nerves,  the  processes  from  these  root- 
ganglion  cells  divide  T-like,  the  peripheral  end  going  out  to  the  skin 
and  special  end-organs  and  the  central  end  penetrating  the  medulla 
to  terminate  in  arborizations  in  nuclei  which  are  the  homologues  of 
the  gelatinous  substance  of  Rolando  of  the  posterior  horns  of  the  cord. 

In  one  respect,  however,  the  cranial  nerves  differ  from  the  spinal 
nerves  and  thus  obtain  all  their  confusing  arrangement.  It  is  a  mere 
non-essential  anatomical  difference,  which  is  the  result  of  the  working 
of  the  great  biological  law  of  adaptation  and  in  no  way  changes  the 
physiology  or  physiological  anatomy  of  the  cranial  nerves. 

The  motor  and  cranial  strands  do  not  keep  so  rigidly  apart  and 
regularly  arranged  serially  among  the  cranial  ner\^es  as  they  do  among 
the  spinal. 

The  third,  fourth,  motor  branch  of  the  fifth,  sixth,  seventh,  and 
twelfth  are  pure  motor  nerves.  Their  sensorv  correspondents  are 
wrapped  up  together  in  the  great  trigeminal  sensory  nerve.  This  is 
shown  by  the  study  of  the  nuclei  of  origin  of  all  these  nerves. 

The  ninth,  tenth  and  accssor}'  part  of  the  eleventh  belong  to  the 
visceral  system  and  spring  from  nuclei  on  their  roots  while  the  motor 
parts  originate  in  central  gray  matter  that  is  homologous  with  the  vesi- 
cular column  of  Clarke.  The  spinal  part  of  the  eleventh  nerve  is  a 
pure  spinal  nerve.  In  some  lower  animals  the  twelfth,  or  hypoglossal 
nerve,  is  outside  of  the  cranium  entirely  and  in  every  respect  simu- 
lates a  spinal  motor  nerve. 

The  important  point  in  these  biological  observations  to  the  prac- 
tical clinician  is  that  diseases  of  these  cranial  nerves  differ  in  no  re- 
spect whatever  from  diseases  of  the  spinal  nerves.  The  essential 
differences  in  their  semeiolog}-  depend  entirely  upon  the  organs  and 
structures  which  they  innervate.  Disease  of  those  that  go  to  the  heart 
muscle  will  naturally  awaken  more  significant  manifestations  than 
those  that  go  to  the  face  muscles.  The  symptoms  that  arise  from  dis- 
ease of  those  that  terminate  in  the  ear  will  naturally  be  different  from 
the  symptoms  of  disease  in  those  that  end  in  the  taste  bulbs  of  the 
tongue.  But  the  sarme  holds  true  with  the  spinal  nerves.  From  all 
points  of  view,  therefore,  the  cranial  nerves  must  be  regarded  in  the 
same  light  as  the  spinal  nerves. 


644 


THE  NON-NEURON  IC  DISEASES 


FIGURE  140. 

-A.  Semtdiacrammatic  view  of  a  deep  dissection  of  the  cranial  nervss 
ON  THE  LEFT  SIDE  OF  THE  HEAD  (from  various  authors  and  from  nature).  B.  Explan- 
atory OUTLINE  OF  THE   SAME.      (A.T. )      -^ 


The  Roman  numerals  from  I  to  XII  indicate  the  roots  of  the  several  cranial  nerves  as 
they  lie  in  or  near  their  foramina  of  exit ;  V,  is  upon  the  large  root  of  the  fifth  with  the 
Gasserian  ganglion  in  front ;  C  I,  the  suboccipital  or  first  cervical  nerve  ;  C  VIII,  the 
eighth.  The  branches  of  the  nerves  are  marked  as  follows,  viz.  : — 1,  supraorbital  branch 
of  the  fifth  ;  2,  lachrymal  passing  into  the  gland  ;  3,  nasal  passing  towards  the  anterior 
internal  orbital  canal,  and  giving  the  long  root  to  the  ciliary  ganglion,  4' ;  3',  termination  of 
the  nasal  nerve  ;  4,  lower  branch  of  the  third  nerve ;  5,  superior  maxillary  division  of  the 
fifth  passing  into  the  infraorbital  canal ;  5',  the  same  issuing  at  the  infraorbital  foramen 
and  beipg  distributed  as  inferior  .palpebral,  lateral  nasal,  and  superior  labial  nerves,  5"  ; 
6,  ganglion  of  Meckel  and  Vidian  nerve  passing  back  from  it ;  6',  palatine  and  other 
nerves  descending  from  it ;  6",  large  superficial  petrosal  nerve  ;  7,  posterior  dental  nerves  ; 
7',  placed  in  the  antrum,  which  has  been  opened,  points  to  the  anterior  dental  nerve  ;  8, 
inferior  maxillary  division  of  the  fifth  immediately  below  the  foramen  ovale  ;  8',  some  of 
theniuscular  branches  coming  from  it ;  8+,  the  auriculo-temporal  branch  cut  short,  and 
above  it  the  small  superficial  petrosal  nerve  connected  with  the  facial ;  9,  buccal  and  ex- 
lemal  pterygoid  ;  10,  lingual  or  gustatory  nerve ;  10',  its  distribution  to  the  side  and 
front  of  the  tongue  and  to  the  sublingual  gland  ;  10",  submaxillary  ganglion  ;  below  10,  the 
chorda  tympani  passing  forwards  from  the  facial  above  12,  to  join  the  lingual  nerve  ;  11, 


(From  Quaiii. ) 


THE  NON-NEURONIC  DISEASES 


64: 


FIGURE  140. 

inferior  dental  nerve  ;  11',  the  same  nerve  and  part  of  its  dental  distribution,  exposed  by 
removal  of  the  jaw  ;  11",  its  termination  as  the  mental  nerve  ;  11'",  its  mylo-hyoid  branch  ; 
12,  twigs  of  the  facial  nerve  -immediately  after  its  exit  from  the  stylo-mastoid  foramea 


B. 


19" 


to  the  posterior  belly  of  the  digastric  and  to  the  stylo-hyoid  muscle  ;  12',  temporo-facial 
division  of  the  facial  ;  12",  cervico-facial  division  ;  13,  trunk  of  the  glosso-pharyngeal 
passing  round  the  stylo-pharyngeus  muscle  after  giving  pharyngeal  and  muscular  bi-anches ; 
13',  its  distribution  on  the  side  and  back  part  of  the  tongue  ;  14,  spinal  accessory  nerve  ; 
14',  the  same  after  having  passed  through  the  sterna- mastoid  muscle  uniting  with  branches 
from  the  cervical  nerves  ;  15,  hypoglossal  nerve  ;  IS',  its  twig  zo  the  thyro-liyoid  muscle  ; 
15",  its  distribution  to  the  muscles  of  the  tongue;  16,  its  descending  branch  giving  a 
direct  offset  to  the  anterior  belly  of  the  omo-hyoid  muscle,  and  receiving  the  communi- 
cating branches  16  +  ,  from  the  cervical  nerves  ;  17,  pneumo-gastric  nerve ;  17',  its  superior 
laryngeal  branch  ;  17",  external  laryngeal  twig  ;  18,  superior  cervical  ganglion  of  the  sym- 
pathetic nerve,  uniting  with  the  upper  cervical  nerves,  and  giving  at  18'  the  superficial 
cardiac  nerve  ;  19,  the  trank  of  the  sympathetic  ;  19',  the  middle  cervical  ganglion, 
uniting  with  some  of  the  cemcal  nerves,  and  giving  19",  the  large  or  middle  cardiac 
Tiei"ve  ;  20,  continuation  of  the  sympathetic  nerve  down  the  neck  ;  21,  great  occipital 
nerve  ;  22,  thu-d  occipital. 

(From  Quain.) 


646  THE  KOX-XEUKOXIC  DISEASES 

I  will  now  discuss  some  of  the  more  prominent  diseases  of  them, 
thus  continuing  the  discussion  of  the  peripheral  nerve  diseases,  part 
of  which  I  have  taken  up  in  the  previous  section  upon  the  spinal  nerves. 

The  diseases  that  involve  the  cranial  nuclei  and  which  produce 
ofttimes  clinical  pictures  that  cannot  be  sharply  dififerentiated  from  the 
clinical  pictures  presented  by  disease  in  the  respective  nerve-trunks, 
will  be  considered  among  the  affections  of  the  medulla.  In  this  I  am 
following  the  same  general  plan  as  evidenced  in  the  separation  of  the 
spinal  nerve  diseases  from  those  of  the  gray  matter  of  the  cord.  There 
is  no  logical  congruity  in  separating,  for  instance,  focal  poliomyelitis 
from  peripheral  neuritis  and  throwing  together  ophthalmoplegia  and 
peripheral  ocular  nerve  palsies. 

OCULOMOTOR  OR  THIRD  CRANIAL  XERA'E. 

This  nerve,  like  the  fourth  and  sixth  nerves,  arises  from  the 
nucleus  in  the  floor  of  the  aqueduct  of  Sylvius.  It  appears  in  the  inter- 
peduncular space,  passes  forw'ard  to  enter  the  orbit  by  the  inner  end  of 
the  sphenoidal  fissure,  and  supplies  all  the  muscles  of  the  eyeball,  ex- 
cept the  superior  oblique  and  the  external  rectus.  Through  the  lenticu- 
lar ganglion  it  also  supplies  the  sphincter  muscle  of  the  iris  and  the 
ciliarv  }imsclc.  The  clcTOtor  of  the  eyelid  is  also  furnished  with  a 
branch. 

Etiology. — A  general  diathesis  often  underlies  ocular  palsy  and 
the  trouble  is  thus  but  a  side  manifestation  of  another,  more  extensive 
disease.  With  such  an  underlying  diathesis,  as,  for  instance,  rheuma- 
tism, cold  can  play  a  very  important  part  in  initiating  the  local  trouble. 
Sometimes  the  rheumatic,  unilateral  ophthalmoplegia  has  merely  re- 
sulted from  the  extension  of  the  disease  from  a  focus  somewhere  in 
the  neighborhood. 

Infection,  especially  diphtheritic  infection,  is  responsible  in  some 
cases.  The  resulting  neuritis  may  aft'ect  the  whole  or  part  of  the  nerve. 
The  muscles  of  accommodation  are  particularly  liable  to  be  paralyzed. 
The  sixth  nerve  often,  the  fourth  rarely,  is  included  in  this  form  of 
palsy.  It  is  not  possible  at  times  to  distinguish  this  neuritis  from  nu- 
clear disease  due  to  the  same  cause.  Influenza,  acute  rheumatism,  scar- 
latina, pneumonia,  are  some  other  forms  of  infection  that  have  given 
rise  to  ophthalmoplegia.  Tumors,  thrombosis  of  the  cavernous  sinus 
and  neighboring  exostoses  are  in  the  etiology^  Gummatous  tumors 
and  other  syphilitic  conditions  at  the  base  of  the  brain  are  all  well 
known  causes  of  ocular  palsy.  There  is  also  a  primary  gummatous 
neuritis  of  the  nerve  itself.  Toxcemia,  such  as  occurs  in  alcoholism, 
lead-poisoning,  and  eating  of  tainted  food  (oysters,  fish,  meat,  bologna) 
has  been  responsible  in  a  few  instances.  In  diabetes  paralysis  of  the 
ciliary  muscles  and  disturbances  of  accommodation  are  of  common 
observation.  The  latter  has  been  attributed  to  intestinal  auto-intoxica- 
tion (Panas).  Mydriasis  was  also  present.  Most  of  these  cases,  if 
not  all  of  them,  are  better  attributed  to  nuclear  disease. 

Intracranial  traumata  need  merely  to  be  mentioned  to  be  recog- 
nized as  possible  causes.     Bone  lesions  in  the  orbit  must  not  be  over- 


■     THE  NON-NEURONIC  DISEASES  647 

looked.     Fractures,  aneurisms,    tumors,    exostoses,    hemorrhages,  ex- 
udates, are  all  liable  to  injure  the  nerve. 

Obstetrical  (forceps)  palsy,  through  pressure,  has  been  seen  in 
the  oculomotor.  Pressure  of  a  damaging  sort  may  be  exercised  other- 
wise also  upon  the  nerve. 

In  tabes,  uiultiple  sclerosis,  and  other  general  and  intracranial 
diseases,  oculomotor  neuritis  is  uncommon. 

Symptoms. — Remembering  the  muscles  supplied  by  the  third 
cranial  nerve,  it  is  an  easy  matter  to  correlate  the  disease  with  the 
abnormal  movements  of  the  lid,  eyeball  and  iris. 

Ptosis  is  a  prominent  symptom.  The  lid  hangs  down  almost  to 
the  lower  lid.  The  eye  is  not  absolutely  closed  and  the  lid  can  be 
slightly  raised  because  the  fibres  of  the  occipito-frontalis  muscle  ex- 
ercise some  effect  upon  it.  Place  the  hand  upon  the  brow  or  get  the 
patient  to  fix  the  occipito-frontalis  and  it  will  be  very  noticeable  that 
he  cannot  move  the  lid  a  particle. 

As  the  internal  rectus  is  innervated  by  the  third  nerve  and  the 
external  by  the  sixth  the  ball  of  the  eye  cannot  be  rolled  inward  or 
made  to  follow  the  finger  towards  the  nose.  Only  outward  can  the 
ball  be  moved.  Contracture  of  the  external  rectus  ultimately  causes 
a  downward,  outward  strabismus.  Other  movements  of  the  ball  are 
impossible. 

The  iris  remains  a  trifle  larger  than  normal.  It  cannot  contract. 
It  dilates  more  rapidly  than  usual  under  atropine.  Neither  light  nor 
convergence  contracts  it. 

Diplopia,  slight  exophthahnos  and  consequent  disturbance  of  vis- 
ion result  from  the  displacement  of  the  line  of  fixation  and  relaxation 
of  the  affected  muscles.       ^^^ 

Pains  ma}'  accompany  the  rheumatic  and  compression  form  of 
the  trouble. 

The  above  picture  represents  a  total  paralysis  of  the  nerve.  This 
usually  is  the  case  in  peripheral  disease,  though  not  always  so.  In 
nuclear  disease  there  is  more  frequently  a  separation  of  the  internal 
from  the  external  ophthalmoplegia.  A  bilateral  palsy  of  the  sphincter 
iridis  and  ciliary  muscle,  or  a  bilateral  external  palsy  with  retention 
of  accommodation  is  almost  pathognomonic  of  central  disease.  Per- 
ipheral disease  may  be  inferred  when  neighboring  cranial  nerves  are 
affected. 

Though  it  is  impossible  of  actual  demonstration  we  assume  tlmt 
the  paralysis  is  atrophic  and  flaccid,  as  in  all  peripheral  palsies. 

There  is  a  recurrent  or  periodical  ocular  palsy  that  should  re- 
ceive some  mention  here.  Cases  have  been  seen  by  Saundby,  Snell, 
Gubler,  Mobius,  Senator,  Buzzard,  Pfliiger,  Charcot,  Manz,  Oppen- 
heim  and  others. 

Every  few  days,  weeks  or  months  the  eyelid  falls  and  remains 
down  for  a  variable  time.  The  trouble  is  mostly  unilateral.  With  the 
paralysis  there  has  been  headache,  pain  in  the  eyeballs,  nausea  and 
vomiting.  The  disease  is  supposed  to  be  related  to  migraine,  though 
it  is  not  strictly  identical  with  it.  It  may  last  a  week.  The  whole 
nerve  is   usually  involved.     Albuminuria  has   accompanied   it.      Both 


64S  IHE  NON-NEURONIC  DISEASES 

sexes  are  subject  to  it  and  it  has  been  seen  in  children.  Female  adults 
are  more  frequently  its  victims.  It  is  a  mysterious  trouble  and  noth- 
ing is  known  of  its  cause.  The  most  plausible  hypothesis  is  that  of 
Charcot  who  likens  the  disease  to  hemicrania. 

Prognosis. — This  is  entirely  dependent  upon  the  cause.  Infec- 
tious cases  as  a  rule  recover.  Properly  treated  syphilitic  cases  offer 
most  favorable  prognoses.  Less  favorable,  but  still  not  absolutely  bad, 
are  the  traumatic  cases.  If  the  nerve  is  not  too  severely  damaged  and 
the  cause  can  be  removed  the  outlook  is  good.  Inoperable  brain  tumors 
of  course  render  the  accompanying  ocular  palsy  hopeless.  Tabetic 
ocular  palsies  usually  recede,  though  not  always.  The  prognosis  of 
an  isolated  iridoplegia  is  grave  because  it  may  be  the  advance  sign  of 
tabes  or  general  paresis.  It  occurs,  however,  in  alcoholism  and  syph- 
ilitic cerebral  disease  and  under  treatment  may  recover. 

Treatment. — First,  remove  the  cause  as  promptly  and  completely 
as  possible.  If  rheumatism,  syphilis,  influenza,  diphtheria  or  other 
infection  is  present  it  must  be  attacked  with  the  usual  medicines. 
Sweating  must  be  encouraged.  General  antiphlogistic  treatment,  with 
local  vesication  and  bloodletting,  must  be  instituted.  Later  on  electrical 
treatment  may  be  tried,  though  it  is  not  very  effective.  Galvanism  is 
the  best  current  to  use,  with  the  cathode  on  the  back  of  the  neck  and 
the  anode  directly  over  the  eye.  The  electrodes  may  be  placed  up  on 
the  opposite  temples.  The  seance  should  be  only  three  or  four  minutes 
and  the  current  just  strong  enough  to  contract  the  facial  muscles. 
Faradism  should  never  be  used. 

Hypodermics  of  strychnine  are  often  of  much  benefit.  Prisms 
and  protectors  over  the  affected  eye  may  give  relief  from  the  double 
vision.  Ophthalmic  surgery  has  been  resorted  to  for  overcoming  the 
ptosis. 

TROCHLEAR,   PATHETICUS,   OR  FOURTH   CRANIAL 

NERA'E. 

This  is  the  smallest  of  the  cranial  nerves  and  yet  has  a  long  course. 
It  springs  from  the  nucleus  in  the  floor  of  the  aqueduct  of  Sylvius.  It 
emerges  from  just  beneath  the  corpora  quadrigemina,  curves  outward 
around  the  superior  peduncle  of  the  cerebellum  and  the  outer  side  of 
the  crus  cerebri,  passes  forward  in  the  outer  wall  of  the  cavernous  sinus 
and  into  the  orbit  by  way  of  the  sphenoidal  fissure,  and  ultimately  termi- 
nates in  the  end-plates  of  the  superior  oblique  muscle. 

Paralysis  of  this  muscle  causes  the  eye  to  turn  slightly  inward 
when  looking  down.  There  may  be  diplopia  in  the  lower  half  of  the 
visual  field.  It  is  noticeable  when  the  patient  descends  a  flight  of  steps, 
all  of  which  seem  to  be  double. 

THE   ABDUCENS,   OR   SIXTH    CRANIAL    NERVE. 

This  nerve  also  originates  in  the  nucleus  in  the  floor  of  the  aque- 
duct of  Sylvius.  It  supplies  the  external  rectus  of  the  eyeball  and  thus 
is  appropriately  considered  in  connection  with  the  previous  two  nerves. 


THE  XOX-XEUROXIC  DISEASES  649 

It  is,  of  all  the  cranial  nerves,  the  one  most  frequently  diseased.  This 
is  largely  on  account  of  its  long,  exposed  course  at  the  base  of  the 
brain.  Emerging  just  behind  the  pons  \'arolii  above  the  pyramids,  it 
passes  forward  close  to  the  floor  of  the  cavernous  sinus,  enters  the  orbit 
through  the  sphenoidal  fissure  and  terminates  in  the  external  rectus.. 
Its  paralysis  results  in  internal  strabismus  and  limitation  of  ex- 
ternal movements  of  the  eyeball.  Diplopia  is  present  and  may  be 
homogeneous.  The  head  is  usually  turned  towards  the  side  of  the 
paralyzed  muscle.  Gummatous  disease  particularly  attacks  the  abdu- 
cens  nerve. 

TRIFACIAL.   TRIGEMIXAL,   OR  FIFTH   CRANIAL   XERVE. 

This  is  a  combined  motor  and  sensory  nerve.  The  motor  root 
springs  from  a  nucleus  in  the  floor  of  the  fourth  ventricle  and  the 
Sylvan  aqueduct.  The  sensory  root,  which  represents  the  central 
processes  of  the  neurones  whose  cell-bodies  are  in  the  Gasscrian 
ganglion  king  on  the  petrous  part  of  the  temporal  bone,  is  traceable 
under  the  superior  cerebellar  peduncle  in  the  pons  to  the  nucleus  of 
Rolando  in  the  medulla. 

Starting  from  the  sides  of  the  pons  \'arolii,  nearer  its  upper  than 
its  lower  border,  the  small  or  motor  root  lies  at  first  above  the  large 
or  sensory  one.  Both  branches  then  pass  forward  to  the  middle  fossa 
of  the  skull  enter  a  recess  of  the  dura  over  the  summit  of  the  petrous 
bone,  where  the  ganglion  in  the  sensory  portion  of  the  nerve  is  found. 
The  motor  trunk  passes  beneath  the  ganglion  to  join  the  lowest  of  the 
three  branches  of  the  ganglion  just  below  the  foramen  ovale.  The  three 
branches  that  project  from  the  Gasserian  ganglion  are  the  ophthalmic, 
which  enters  the  orbit  and  emerges  in  the  terminal  supra-orbital  nerve 
that  runs  up  on  the  forehead ;  the  superior  maxillary,  which  is  continued 
fonvard  to  emerge  from  the  supra-maxillary  foramen  between  the 
orbit  and  the  mouth ;  and  the  inferior  maxillary  which  is  distributed  to 
the  external  ear.  the  tongue,  the  lower  teeth  and  by  the  branch  that 
emerges  from  the  infra-maxillary  foramen  in  the  lower  jaw.  The 
motor  branch  terminates  in  the  muscles  of  mastication,  namely,  the 
temporal,  the  masseter  and  the  tzi'o  pteragoids. 

This  is  the  great  sensory  nerve  of  the  face,  probably  the  most 
important  sensory  nerve  in  the  body.  It  imparts  common  sensibility 
to  the  face,  the  fore  part  of  the  head,  the  eye,  the  nose,  the  ear  and 
the  mouth,  including  the  greater  portion  of  the  tongue.  To  the  ante- 
rior two-thirds  of  the  latter  it  is  believed  to  confer  the  power  of 
taste,  the  taste  fibres  coming  really  from  the  glosso-pharyngeal  by  way 
of  the  facial  and  the  chorda  tympani. 

In  the  orbital  cavit\-.  fibres  from  the  sympathetic  nerve  run  along 
beside  the  ramus  ophthalmicus  of  the  fifth  nerve  and  innervate  the 
dilator  muscle  of  the  pupil  after  emerging  from  the  cdiary  ganglion. 
To  the  second  branch  of  the  fifth  is  attached  the  spheno-palatine  gan- 
glion which  is  connected  with  the  geniculate  ganglion  of  the  facial 
nerve  bv  the  Mdian.  or  large  superficial  petrosal  nerve. 

To' the  third  branch  is  attached  the  otic  ganglion,  which  also  is 


650 


THE  NOX-NEUROXIC  DISEASES 


connected  with  the  geniculate  ganghon  of  the  facial  by  the  small  super- 
ficial petrosal  nerve.  This  last  nerve  sends  a  branch,  Jacobson's  tym- 
panic nerve,  to  the  glosso-pharyngeal. 

The  innervations  of  the  trigeminal  nerve  have  lately  been  seen 
to  be  very  variable. 

Not  often  does  isolated  disease  of  this  nerve  occur.  The  nature 
of  its  neuralgic  manifestations  have  been  described  under  the  head  of 
neuralgia  elsewhere. 

Etiology. — Neighboring  bone  disease,  caries,  exostoses,  tumors, 
chronic  meningitis  and  syphilitic  disease  have  damaged  the  nerve.  I 
have  lately  seen  a  case  of  guuunatous  neuritis  in  it.  Tra\imata  and 
infection,  especially  rheumatism,  have  been  responsible  for  its  disease  in 

FIGURE  141. 


Course  of  the  facial  nerve  and  its  anastopMses  with  the  trigeminal  and  glossopharyngeal  nerves, 

(After  Leuhe.) 

some  cases.  Surgical  operations  in  and  about  the  orbit  and  maxillary 
bones  are  to  be  included  sometimes  in  the  etiology.  I  have  seen  the 
nerv'e  manifest  paralytic  symptoms  in  cases  of  ear  disease.  As  a  col- 
lateral trouble  in  brain  tumor,  hemorrhage,  pontile  encephalomalacia. 
tabes  and  syringomyelia,  disease  of  the  trifacial  is  not  an  uncommon 
event. 

Symptoms. — The  symptoms  depend  upon  the  character  and  loca- 
tion of  the  lesion.  If  one  remembers  the  physiological  anatomy  of  the 
nerve,  the  symptoms  may  easily  be  inferred.  ^lotor,  sensory  and 
trophic  manifestations  occur  in  total  paralysis  of  the  nerve. 

The  jaw  cannot  be  closed,  nor  m^oved  laterally  as  it  is  slightly,  in 
chewing  food.  The  anaesthesia  involves  the  face  in  front  of  a  line 
passing  transversely  across  the  top  of  the  head,  down  through  the 
external  auditory  meatuses  and  along  the  lower  edge  of  the  lower 
jaw.  The  accompanying  diagram,  with'  figures  corresponding  with 
the  branches  of  the  ner\-e.  will  show  its  cutaneous  distribution  better 


THE  NOX-NEUROXIC  DISEASES 


6^1 


than  a  long  description.  In  this  area  should  be  included  the  mucous 
membrane  'of  the  nose,  mouth,  tongue,  gums  and  inside  of  the  cheek  : 
also  the  conjunctiva  and  the  cornea.  On  account  of  the  uisensitive- 
Tiess  of  the  cornea,  winking  is  not  performed  as  systematically  as  it 
should  be  and  it  becomes  irritated  from  minute  particles  of  matter. 
The  secretion  of  tears  being  impaired  adds  to  this  misfortune.  Vision 
is  blurred  slightly.  Smell  and  taste  are  blunted  on  account  of  the  dry 
condition  of  the  mucous  membrane  of  the  nose  and  mouth.  Often  the 
-cheek  is  bitten  and  lacerated  internally  in  the  process  of  chewing. 

We  do  not  know  vet  just  exactly  the  nature  of  the  role  played 
l)y  the  trigeminal  nerve  in  the  matter  of  taste.  Alany  believe  that  the 
iibres  of  the  third  branch  which  subserve  the  function  of  taste  in  the 
anterior  two-thirds  of  the  tongue  are  wholly  from  the  glosso-pharyn- 

FIGURE  142. 


Cutaneous  area   of  the  head   supplied  by   the  trigeminal   nerve. 


seal,  albeit  thev  have  come  by  way  of  the  facial  and  chorda  tympani 
nerves.  This  being  so,  the  glosso-pharyngeal  nerve  is  the  nerve  of 
taste  for  the  whole  tongue.  However,  it  is  true  that  taste  depends 
largelv  upon  the  ordinary  sensory  and  trophic  condition  of  the  niu- 
cot^s  membrane,  and  in  maintaining  this  in  a  normal  state,  the  essential 
iibres  of  the  trifacial  nerve,  those  that  come  from  the  Gasserian  gan- 
glion, subserve  in  part  the  function  of  taste.  At  all  events  Sf^tory' 
disturbances  occur  in  the  anterior  two-thirds  of  the  tongue  when  the 
iifth  nerve  or  its  inferior  maxillary  or  lingual  branches  are  injured. 

Herpes  is  a  common  trigeminal  symptom.  Indeed  the  tiophic 
•symptoms  of  disease  of  this  nerve  or  its  branches  are  7°;^^  ^^^.^^^^^^ 
important.  In  neuroparalytic  keratitis  the  vision  is  badly  bl^ir  ed  the 
cornea  ulcerates;  perforation  takes  place;  the  whole  e>e  inflames 
(panophthalmitis^  This  is  a  pure  trophic  trouble  and  not  due  sole  > 
to  anesthesia  as  was  formerly  thought.     It  is  not  neuroparal>  tic  but 


652  THE  NON-NEURONIC  DISEASES 

nenritic  in  origin.  Ulceration  also  occurs,  as  a  trophic  symptom,  in 
the  cheek  and  nose.  The  teeth  loosen  and  fall  out,  though  this  is 
due  more  to  central  disease.  Some  authorities  believe  that  progressive 
facial  hemiatrophy  is  a  trophic  disease  of  the  trigeminal  nucleus. 

As  in  all  neuritic  palsies  these  are  flaccid  in  type,  the  temporal, 
masseter  and  pteragoid  muscles  atrophy  and  when  they  can  be  exam.- 
ined  the  electrical  reaction  of  degeneration  is  found.  The  jaw  re- 
flex, of  course,  is  absent.  In  unilateral  palsy  the  immobility  of  the 
jaw  is  not  so  noticeable.  If  the  patient  is  asked  to  press  the  teeth  to- 
gether and  then  still  more  compress  the  jaws,  it  will  be  noticed  that 
the  muscles  do  not  contract  on  the  paralyzed  side. 

Instead  of  signs  of  paralysis  there  may  be  signs  of  irritation. 
ParccsthesicE  then  are  in  the  lead  and  pains  and  excessive  secretion.. 
There  may  be  a  facial  spasm  and,  through  reflex  irritation,  coughing, 
sneezing,  vertigo,  etc. 

The  prognosis  of  course  depends  upon  the  nature  and  location  of 
the  lesion.  If  the  cause  of  the  inflammation  or  irritation  can  be  re- 
moved, recovery  may  be  expected. 

Treatment. — The  cause  must  be  removed  and  to  a  large  extent 
this  exhausts  the  treatment.  Syphilis  is  so  prolific  a  cause  that  antispe- 
cific  treatment  should  be  persevered  in,  even  if  immediate  results  are 
not  forthcoming.  I  have  had  good  results  from  such  a  mode  of  pro- 
cedure. The  eyes  should  always  be  protected.  For  pains,  analgesics 
and  electrotherapy  are  our  only  resources.  Surgery  may  accomplish 
much  if  the  indications  are  clear  enough.  It  is  questionable  whether 
the  risk  of  producing  trifacial  neuritis,  as  is  possible  in  the  injection 
of  perosmic  acid,  will  be  warranted  by  the  sufifering  sometimes  caused 
in  pure  trifacial  neuralgia.  The  latter  is  fearful  at  times,  but  the 
former  has  destroyed  vision  and  caused  facial  atrophy,  paralysis  and 
other  severe  manifestations. 

THE    FACIAL,    OR    SEVENTH    CRANIAL  NERVE. 

This  is  a  pure  motor  nerve,  whose  nucleus  is  in  the  floor  of  the 
fourth  ventricle  beneath  the  superior  fovea.  It  appears  at  the  upper 
part  of  the  medulla  in  the  groove  between  the  olivary  and  restiform 
bodies,  close  to  the  lower  edge  of  the  pons.  Outside  of  it  is  the  audi- 
tory nerve  with  a  strand,  the  pars  intermedia  of  Wrisberg,  arising  in  a 
nucleus  beneath  the  inferior  fovea  and  connecting  with  the  auditory. 
The  facial,  auditory,  and  pars  intermedia  all  enter  the  internal  auditory 
meatus  together.  At  the  bottom  of  the  meatus,  however,  the  facial 
parts  company  from  the  others  and  enters  the  aqueduct  of  Fallopius, 
following  the  windings  of  the  canal  through  the  temporal  bone  to  the 
stylo-mastoid  foramen.  In  the  canal  it  gives  ofif  two  important  branch- 
es, the  chorda  tympani,  which  seems  to  be  a  taste  nerve,  and  unites 
with  the  lingual  branch  of  the  fifth  to  innervate  the  anterior  two-thirds 
of  the  tongue,  and  the  branch  to  the  stapedius  musck.  After  its 
emergence  from  the  skull,  the  main  trunk  of  the  nerve  passes  down- 
wards and  forwards  through  the  parotid  gland  and  terminates  by 
dividing  just  behind   the  ramus  of  the  jaw   into  the   tcmporo-facial 


THE  NON-NEURONIC  DISEASES 


653 


above  and  the  temporo-ccrvical  below,  each  of  which  sends  numerous 
branches  to  the  side  of  the  head,  the  face  and  the  upper  part  of  the 
neck.  As  these  branches  inter-communicate  freely,  they  form  a  sort 
•of  a  plexus  which  is  often  called  the  pes  anserinus.  As  the  muscles 
to  which  these  filaments  go,  namely,  the  buccinator  and  all  those  of 
the  face  except  the  muscles  of  mastication,  play  so  prominent  a  role  in 
■expression,  the  facial  is  sometimes  called  the  "artist's  nerve." 

To  briefly  recapitulate,  the  facial  nerve  is  distributed  to  the  miis- 
■cles  of  the  scalp,  of  the  external  ear,  nose,  mouth,  eyelids  (excepting 
the  levator  palpebrse  superioris)  and  to  the  platysma.  It  also  supplies 
the  muscles  of  the  tympammi,  the  levator  palati  and     asygos     iiznilce 

FIGURE  143. 

— The  facial  nerve 
in  its  canal,  with  its  con- 
NECTING   BRANCHES,    &G.     (frOm 

Sappey,    after   HirscMeld  and 
Leveille).     ' 

The  mastoid  and  a  part  of  the 
petrous  bone  have  been  divided 
nearly  vertically,  and  the  canal  of 
the  facial  nerve  opened  in  its 
whole  extent  from  the  internal 
meattis  to  the  stylo-mastoid  fora- 
men ;  the  Vidian  canal  has  also 
been  opened  from  the  outside :  1, 
facial  nerve  in.  the  first  horizontal 
part  of  its  course  ;  2,  its  second 
jjart  turning  backwards ;  3,  its 
vertical  portion  ;  4,  the  nerve  at 
its  exit  from  the  stylo-mastoid 
foramen  ;  5,  geniculate  ganglion  ; 

6,  large  superficial  petrosal  nerve  ; 

7,  Spheno-palatine  ganglion  ;  8,  small  superficial  petrosal  nerve  ;  9,  chorda  tympani ; 
10,  posterior  auricular  branch  cut  short ;  11,  branch  to  the  digastric  muscle  ;  12,  branch 
to  the  stylo-hyoid  muscle  ;  13,  twig  uniting  with  the  glosso-pharyngeal  nerve  (Hand  15). 

(through  the  large  superficial  petrosal)  and  the  stylo-hyoid  and  the 
posterior  belly  of  the  digastric. 

It  is  well  to  remember  its  wide  inter-connection  with  other  nerves. 
It  is  thus  associated  with  the  fifth  nerve,  with  the  spheno-maxillary, 
submaxillary  and  otic  ganglia,  with  the  auditory,  the  glosso-pharyn- 
geal and  pneumogastric  nerves  (through  the  auricular  branch  of  the 
latter)  and  with  parts  of  the  sympathetic  and  spinal  nerves. 

Prosopoplegia,  or  facial  palsy,  is  the  most  common  of  the  nerve 
paralyses.  We  are  here  only  concerned  with  the  peripheral  type, 
though  the  disease  may  be  of  central  and  cortical  origin. 

Etiology. — Exposure  to  cold  is  the  time-honored  cause  of  Bell's 
palsy.  It  is  thus  sometimes  spoken  of  as  rheumatic  or  refrigeratory 
palsy.  It  often  follows  sleeping  beside  an  open  window,  working  in 
winter  on  a  derrick  with  the  head,  all  but  the  face,  completely  covered. 
Car-drivers,  expressmen,  and  persons  so  exposed  are  liable.  It  is  ac- 
knowledged that  cold  alone  can  produce  the  disease  in  healthy  individ- 
uals. However,  it  must  not  be  forgotten  that  in  a  very  large  number 
of  the  cases,  cold  only  acts  conjointly  with  some  underlying  infection. 


654  THE  XON-XEURONIC  DISEASES 

Lately  I  have  treated  a  syphilitic  sewing-girl  whose  face  became  par- 
alyzed on  one  side  after  sitting  in  a  cold  draught  of  air  blowing  in 
through  an  open  door.  It  follows,  local  infectious  processes  in  and 
about  the  temporal  bone.  Caries  and  otitis  media  and  tonsillar  angina 
have  started  it.  It  is  not  improbable  that  both  diseases  may  be  simul- 
taneous products  of  the  same  general  infection.  It  has  followed  thus, 
typhoid,  mumps,  and  influenza.  Syphilis  has  been  a  prolific  source  of 
the  trouble  in  my  observation,  notwithstanding  the  fact  that  some  au- 
thors say  that  of  all  the  nerves  of  the  body,  syphilis  respects  most  the 
facial.     It  occurs  in  diphtheria  and  the  puerperium. 

Diabetic  conditions  are  often  responsible  for  it ;  such  as  diabetes,, 
gout,  leukemia. 

Compression  paralysis  often  attacks  the  nerve  in  basal  gumma- 
tous meningitis.  This  is  a  common  cause  and  must  be  distinguished, 
by  other  signs  of  the  basal  disease,  from  the  syphilitic  neuritis  re- 
ferred to  above.  Other  forms  of  meningitis,  as  well  as  intracranial 
tumors,  aneurisms,  etc.,  may  compress  the  nerve  deleteriously.  Trau- 
mata must  not  be  omitted  from  its  etiology.  Not  infrequently  oper- 
ations about  the  ear  are  responsible  for  tlie  paralysis.  Bilateral  dis- 
ease may  occur  in  the  polyneuritides  and  a  diplegic  facial  paralysis 
may  be  the  symptom  of  pontile  and  medullar  disease,  such  as  tumor, 
hemorrhage,  embolism,  aneurism.  It  has  occurred  in  tetanus.  Pre- 
natal or  natal  damage  may  result  from  the  use  of  the  forceps.  I  once 
saw  a  severe  facial  palsy  of  this  sort.  This  is  called  congenital  facial 
paralysis  and  is  usually  bilateral.  Some  of  these  congenital  palsies 
are  undoubtedly  nuclear  in  origin,  as  also  are  some  of  the  diphtheritic 
cases.  In  many  instances  a  pronounced  neuropathic  state  of  the  con- 
stitution lurks  behind  it. 

Symptoms. — The  cardinal  symptom,  paralysis  of  the  face,  is  ob- 
vious enough.  In  fact,  it  is  so  obvious  that  the  diagnosis  of  facial 
palsy  does  not  confer  a  spark  of  credit  upon  the  practitioner.  Every 
newsboy  can  diagnose  facial  palsy  when  he  sees  it.  To  the  phvsi- 
cian  falls  the  duty  of  localizing  the  lesion,  and  therein  lies  the  cred- 
itable diagnosis. 

The  appearance  of  the  face  is  typical  and  striking.  On  the 
paralyzed  side  it  is  smooth,  dead  and  mask-like.  The  creases  of  the 
forehead  on  that  side  are  gone :  so  also  are  the  naso-labial  fold  and 
the  wrinkles  of  the  cheek  and  chin.  The  corner  of  the  mouth  droops, 
the  eye  is  almost  completely  open.  If  the  patient  attempts  to  whistle 
or  laugh  or  show  his  teeth,  or  draw  the  mouth  over  toward  the 
paralyzed  side,  the  paralysis  of  the  orbicularis  oris  is  especially  notice- 
able. 

If  he  is  asked  to  close  his  eyes,  the  well  side  closes  promptly  but 
the  affected  side  remains  open  or  the  upper  lid  moves  slowly  and  only 
slightly  towards  the  lower  lid. 

On  account  of  the  failure  of  the  buccinator  to  hold  the  bolus  or 
food  between  the  teeth,  chewing  is  difficult  and  in  bilateral  paralysis 
all  but  impossible.  Sometimes  a  slight  szcelling  of  the  face  accom- 
panies these  motor  manifestations.  Occasionally  for  several  davs  be- 
fore their  onset  there  will  be  fugitive  pains  in  the  ear,  face  or  neck. 


THE  XOX-XEL'RONIC  DISEASES  655 

The  asyiJiiiiefry  of  the  face  in  this  disease  is  the  pathognomonic 
feature.  The  eyes  water,  the  conjunctiva  bulges,  the  nose  inclines 
toward  the  well  side  and  saliva  tends  to  drool  from  the  mouth.  Upon 
attempted  movement  this  is  rendered  more  marked.  The  muscles  of 
the  ear  are  implicated,  also  the  platysma.  There  is  some  doubt  as  to 
the  implication  of  the  uvula  in  pure  peripheral  palsy.  Occasionally  the 
arch  of  the  palate  is  lower  on  one  side.  As  the  disease  involves  usu- 
ally that  part  of  the  nerve  in  the  aqueduct  of  Fallopius,  the  paralysis 
of  the  stapedius  causes  hyperacuity  of  the  hearing ;  and  of  the  chorda 
tympani,  disturbance  of  the  taste  in  the  anterior  two-thirds  of  the 
tongue.  The  latter  is  a  form  of  heiniageusia.  Rarely  it  may  be  total. 
Anosmia  may  occur  from  lessened  dilatation  of  the  nostril. 

Salivary  secretion  is  diminished  on  the  diseased  side.  This  is 
one  of  the  vasomotor  or  secretory  effects  of  the  nerve. 

The  tongue  is  not  implicated  as  that  is  under  the  control  of  the 
twelfth  nerve. 

Among  the  trophic  manifestations  of  facial  disease  are  oedema- 
tous  swelling  previously  mentioned,  the  herpetiform  eruptions  and  the 
degenerative  muscular  changes.  The  former  are  rare :  the  latter  com- 
mon. The  reaction  of  degeneration  is  an  important  symptom  as  it 
helps  to  determine  the  prognosis.  The  lid  reflexes  and  skin  reflexes 
are  lost,  of  course,  where  the  arc  involves,  on  the  motor  side,  the 
paralyzed  muscles. 

DiAGXosis. — The  most  important  point  of  the  diagnosis  is  the 
location  of  the  lesion.  The  disease  may  be  central  or  peripheral.  If 
it  is  peripheral  the  flaccidity  of  the  palsy,  the  muscular  atrophy,  the 
reaction  of  degeneration  and  the  loss  of  the  reflexes  will  go  far  to  de- 
termine it.  In  many  cases,  however,  the  paralysis  is  only  partial  and 
these  signs  are  not  pronounced  enough  to  form  a  positive  opinion  upon. 
The  distribution  of  the  paralysis  is  an  important  and  valuable 
means  in  differentiating  central  from  peripheral  facial  disease.  In 
peripheral  disease  the  whole  nerve  is  implicated  and  hence  the  upper 
and  lower  part  of  the  face  are  equally  affected.  In  central  disease  the 
upper  part  of  the  face  is  very  much  less  affected  than  the  lower.  This 
is  very  noticeable  in  hemorrhagic  apoplexy. 

The  path  from  the  facial  center  in  the  cerebral  cortex  to  the  facial 
nuclei  in  the  medulla  is  not  very  well  known,  though  we  believe  it 
joins  that  of  the  arm  and  leg  and  passes  down  through  the  internal 
capsule  of  the  pyramidal  tracts  in  the  crura  cerebri.  It  decussates. 
This  is  the  volitional  facial  tract.  When  the  lesion  is  anywhere  in 
this  part  of  the  tract,  the  upper  facial  is  intact  ( probably  because  of 
the  bilateral  cerebral  representation)  ;  the  reflexes  and  electrical  ex- 
citability are  normal.  The  muscles  tend  to  spasticity  and  there  is 
no  atrophy.  Usually  the  extremities  are  paralyzed  at  the  same  time. 
If  the  lesion  should  be  a  small  one  and  attack  this  upper  facial  path- 
way between  its  point  of  decussation  in  the  pons  and  its  termination 
in  the  nucleus,  the  paralysis  in  relation  to  the  face  and  limbs  will 
obviously  be  a  crossed  paralysis. 

The  localization  of  the  lesion  in  peripheral  disease  of  the  nerve  is 
often  important  and  usually  not  difficult.     Traumatic  causes  often  give 


656 


THE  NON-NEURONIC  DISEASES 


rise  to  disease  of  particular  branches.  A  knowledge  of  the  anatomy  of 
the  nerve  is  all  that  is  necessary  under  such  circumstances  to  settle 
which  branch  is  affected. 

It  is  difficult  at  times  to  differentiate  between  pontile  facial  palsy 
and  palsy  due  to  the  peripheral  trunk.  A  close  examination  will  usu- 
ally elicit  other  manifestations  of  the  disease  of  the  pons  under  such 
circumstances.  Other  nerves  may  be  involved,  especially  the  sixth 
and  sometimes  the  seventh. 

In  meningitis  and  other  basal  disease  implicating  the  facial  nerve, 
other  nerves  will  also  very  likely  be  included,  especially  the  auditory. 

FIGURE  144. 


Showing  the  facial  trunk  from  the  base  Of  the 
skull  to  the  pes  aiisennus.  N.f.,  facial  nerve,  F.st., 
stylomastoid  foramen  h'.a.p.,  posterior  auricular 
nerve  N.p.s.,  greater  sup.  petrosal  nerve  ,  N.e.c.p.l., 
communicating  nerve,  with  plex  tymp. ,  N.st ,  sta- 
pedius nerve,  Ch.l.,  chorda  tympani ,  N.a.,  acoustic 
nerve  .  G.^.,  gangl.  geniculi.    (After  Erb.) 

Of  course,  general  cerebral  symptoms  would  be  expected  also,  such  as 
pressure  headache,  vertigo,  vomiting,  possibly  papillitis. 

If  the  lesion  is  peripheral  to  the  point  where  the  chorda  tympani  is 
given  off,  and  central  to  that  where  the  tempore- facial  and  temporo- 
cervical  separate,  only  the  facial  muscles  will  be  paralyzed. 

If  the  lesion  is  in  the  aqueduct  of  Fallopius  the  chorda  tympani  and 
stapedius  branches  will  be  implicated  and  there  will  be  loss  of  the 
sense  of  taste  in  the  anterior  two-thirds  of  the  tongue  and  a  hypersensi- 
tiveness  of  the  hearing.  Erb's  diagram  helps  to  make  this  clear.  Vari- 
ations are  possible,  however. 

Prognosis. — Mild  cases  usually  get  well  in  three  or  four  weeks. 
Three  to  six  months  are  required  for  the  average  case.  Severe  cases 
do  not  get  well  undt;r  a  year  and  sometimes  they  remain  stationary. 


THE  NON-NEURONIC  DISEASES  657 

Of  course,  the  cause  and  nature  of  the  lesion  regulate  the  prog- 
nosis. If  the  cause  is  removable  early,  the  disease  will  disappear. 
Syphilitic  cases  are  very  hopeful.  Simple  refrigeratory  cases  are  favor- 
able. Severe  infectious  cases,  and  those  due  to  intracranial  neoplasms, 
aire  often  hopeless. 

The  degree  of  reaction  of  degeneration  is  a  most  valuable  indi- 
cator of  the  prognosis  and  probable  duration  of  the  disease.  If  this  is 
partial,  the  trouble  may  disappear  in  a  few  weeks.  If  this  is  complete, 
the  end  may  not  come  for  many  months  or  years  even.  Acute  cases  are 
better  than  the  slow,  chronic  and  progressive  cases. 

A  secondary  trouble  of  much  moment  are  the  contractures  that  oc- 
cur late  in  the  previously  paralyzed  muscles.  These  are  not  due  to 
electrical  treatment,  as  was  once  imagined.  They  are  due  to  the  irrita- 
tion of  the  nucleus  in  the  forcible  attempts  at  the  use  of  the  nerve,  or 
to  slight  secondary  nuclear  alterations. 

Sometimes  recovery  is  incomplete,  some  muscles  regaining  their 
power  and  others  remaining  palsied. 

Treatment. — The  first  indication  of  course  is  tO'  remove  the 
noxious  agent.  Infections,  like  rheumatism,  syphilis,  influenza,  must 
be  combated  along  known  lines.  Abscesses  must  be  drained.  Ear 
disease  should  be  treated.  A  general  and  local  antiphlogistic  treatment 
is  usually  in  order.  This  includes  purgation,  blood-letting,  warm  ap- 
plications beneath  the  ear,  vesication,  diaphoresis. 

When  active  inflammation  has  subsided,  electrical  treatment  is 
called  for  and  gives  most  happy  results.  The  galvanic  current  usually 
has  to  be  emplo3'ed  first.  The  anode  is  placed  on  the  sternum  or  other 
indifferent  spot,  while  the  cathode  is  placed  on  the  nerve  trunk  where 
it  emerges  from  the  stylo-mastoid  foramen.  For  two  or  three  minutes 
daily,  three  or  four  milliamperes  may  be  employed  in  a  slow,  alternating 
current.  Never  use  strong  currents,  also  be  careful  about  using  the 
faradic  current  in  severe  cases. 

Secondary  contractures  cannot  be  combated  by  any  known  means. 
Massage  may  help  some. 

THE   AUDITORY.    OR   EIGHTH    CRANIAL    NERVE. 

I'his  is  a  nerve  with  a  double  function,  both  sensory.  It  subserves 
hearing  and  the  space-sense.  It  arises  from  three  nuclei  in  the  floor  of 
the  fourth  ventricle  and  emerges  from  the  groove  between  the  pons 
and  the  medulla.  The  nerve  passes  with  the  facial  to  the  internal  audi- 
tory meatus.  In  the  meatus  it  separates  into  an  upper,  or  small,  and  a 
lower,  or  larger,  part.  The  upper  goes  to  the  utricle  and  the  ampullse 
of  the  superior  and  external  semicircular  canals.  The  lower  innervates 
the  organ  of  corti  in  the  cochlea,  sending  off  small  twigs  to  the  saccule 
and  the  posterior  semicircular  canal.  It  is  in  connection  with  the  pars 
intermedia  and  the  geniculate  ganglion  of  the  facial. 

Disease  of  this  nerve  does  not  occur  often  in  the  isolated  form. 
Middle  ear  disease  often  extends  to  the  terminal  branches  of  the  nerve 
in  the  labyrinth.  Meniere's  symptoms  are  thus  explained.  In  my  own 
opinion,  some  of  the  so-called  cases  of  Meniere's  disease  are  central 


658  THE  NON-NEURONIC  DISEASES 

troubles,  as  I  have  shown  elsewhere.  Caries,  periostitis,  tuuiors,  menin- 
gitis, infections,  cachexise  and  all  the  usual  causes  cited  in  connection 
with  facial  nerve  palsy  may  be  operative  here.  General  degenerative 
troubles,  like  tabes,  multiple  sclerosis,  alcohohc  neuritis,  may  include 
the  auditory  nerve.  Syphilis  I  have  seen  cause  trouble  in  it  many 
times.  This  was  probably  due  to  gummatous  meningitis.  Labyrinthine 
and  auditory  disease  cannot  always  be  differentiated,  which  is  one  of 
the  grounds  of  my  contention  that  Meniere's  syndrome  is  far  from  be- 
ing a  definite  disease,  hemorrhagic  or  otherwise.  Basal  disease  usually 
involves  the  facial  along  with,  or  more  often  apart  from,  the  auditory 
nerve. 

In  every  case  of  aural  vertigo,  of  tinnitus  and  of  disturbance  of 
hearing,  the  ear  should  be  thoroughly  examined.  Subjective  tinnitus 
and  subjective  deafness  may  occur  in  so  many  other  functional  and 
organic  diseases  that  the  implication  of  the  auditory  nerve  had  better 
be  made  by  exclusion. 

The  prognosis  and  treatment  of  auditory  paralysis  follow  the  usual 
principles. 

THE  GLOSSOPHARYNGEAL,  OR  NINTH  CRANIAL  NERVE. 

The  roots  of  this  nerve  are  traceable  back  to  a  nucleus  which  is 
closely  associated  with  that  of  the  vagus  nerve,  and  which  lies  in  the 
floor  of  the  fourth  ventricle  in  the  posterior  triangle  beneath  the  in- 
ferior fovea.  It  appears  at  the  upper  part  of  the  medulla,  in  the  groove 
between  the  olivary  and  restiform  bodies.  It  is  directed  outwards  to  the 
jugular  foramen.  Passing  through  this  in  company  with  the  pneu- 
mogastric  and  spinal  accessory,  it  presents  two  ganglia,  the  jiigular  and 
the  petrous.  The  nerve  lies  between  the  internal  carotid  artery  and  the 
jugular  vein.  It  courses  down  over  the  artery  and  beneath  the  styloid 
process  and  the  muscles  connected  with  it,  to  the  hinder  border  of  the 
stylo-pharyngeus.  Crossing  the  outer  surface  of  this  muscle  and  pass- 
ing beneath  the  hypoglossus,  it  ends  in  a  number  of  branches  to  the 
posterior  part  of  the  tongue.  It  supplies  the  mucous  membranes  of  the 
tongue,  pharynx  and  middle  ear,  as  well  as  one  muscle,  the  stylo- 
pharyngeus.  It  is  connected  with  the  inferior  maxillary  division  of  the 
fifth  nerve  (through  the  otic  ganglion),  the  facial,  the  pneumogastric 
(its  trunk  and  branches)  and  the  sympathetic. 

This  is  regarded  as  preeminently  a  nerve  of  taste.  We  know  so 
little  about  it,  however,  that  nothmg  can  be  said  positively  in  regard  to 
its  physiology  or  pathology.  It  has  motor  fibres,  as  we  have  seen,  and 
it  certainly  conducts  sensations  of  simple  touch.  The  nerve  may  be 
implicated,  like  any  other  cranial  nerve,  with  tumors,  traumata,  aneu- 
rism, neighboring  inflammation.  Thrombosis  of  the  jugular  vein  and 
periphlebitis  may  affect  it.  It  is  subject  to  degeneration  as  a  part  of 
a  most  extensive  process. 

Its  paralysis  causes  ancesthesia,  ageusia  in  the  posterior  third  of  the 
tongue  and  palate  and  dysphagia.  Diphtheria  causes  som.e  of  these 
symptoms. 


THE  NON-NEURONIC  DISEASES  659 

THE  PNEUMOGASTRIC,  OR  TENTH  CRANIAL  NERVE. 

The  roots  of  this  nerve  can  be  followed  back  to  the  trigomim  vagi 
in  the  floor  of  the  fourth  ventricle.  The  nucleus  ambiguus  is  believed  to 
be  the  origin  of  the  motor  strands.  The  sensory  roots  represent  the  cen- 
tral processes  of  the  neurones  whose  cell-bodies  lie  in  the  ganglion  of 
the  root  and  of  the  trunk.  These  processes  enter  the  medulla  and  de- 
scend with  those  of  the  glosso-pharyngeal  root,  arborizing  around  cells 
which  make  up  the  so-called  vagus,  sensory  nucleus.  It  is  very  probable 
that  these  cells  of  the  terminal  nuclei  of  this  and  the  ninth  nerve  are  but 
homologues  of  those  making  up  the  vesicular  column  of  Clarke.  Both 
the  motor  and  sensory  fibres  of  this  nerve  are  distributed  to  viscera 
chiefly. 

The  roots  appear  in  the  groove  between  the  olivary  and  restiform 
bodies.  This  nerve  has  the  largest  course  of  any  of  the  cranial  nerves, 
reaching  from  the  neck  to  the  upper  part  of  the  abdomen.  It  passes 
outward  from  the  medulla,  attains  the  jugular  foramen,  presents  two 
ganglia,  is  joined  by  the  accessory  part  of  the  spinal  accessory  nerve 
and  finally  passes  on  down  the  neck  and  thorax  and  abdomen  dis- 
tributing branches  to  the  lungs,  the  heart  and  the  other  viscera. 

In  the  jugular  foramen,  a  branch  is  given  to  the  dura  mater  and 
one  to  the  ear.  In  the  neck  the  pharnyx,  larynx  and  the  heart  are  sup- 
plied. In  the  thorax,  branches  are  furnished  to  the  heart,  the  lungs 
and  the  oesophagus.  In  the  abdomen  the  terminal  branches  are  given 
to  the  stomach,  the  liver  and  other  organs.  Motio'n,  sensation,  secretion 
and  vasomotor  action  are  all  under  the  influence  of  the  vagus. 

A  primary  neuritis  of  this  nerve  is  very  rare,  if  it  occurs  at  all. 
Disease  of  any  other  structure  along  its  course  may  damage  it 
in  that  neighborhood,  however,  and  in  this  way  the  nerve  is  not  in- 
frequently afl^ected.  Primary  inflammation  of  the  nerve  has  been  ob- 
served in  rheumatism,  alcoholism,  diphtheria,  typhoid,  pneumonia, 
scarlatina,  malaria,  cholera,  influenza.  Under  these  circumstances  it 
has  usually  constituted  a  part  of  a  polyneuritis.  I  recently  saw  it 
affected  in  chronic  lead-poisoning  to  a  dangerous  degree.  Arsenic 
will  injure  it.     Morphine  and  atropine  may  intoxicate  it. 

It  is  usually  implicated  in  bulbar  disease.  Disease  at  the  base  of 
the  skull  constitutes  an  important  factor  in  etiology.  This  includes 
caries,  exostoses,  tumors,  aneurisms,  hemorrhages,  meningitis  with 
exudates. 

Numerous  are  the  vascular  troubles  that  disturb  it,  such  as  arterio- 
sclerosis, thrombosis  of  the  transverse  sinus,  jugular  thrombosis  and 
phlebitis.  Mediastinal  tumors,  suppuration,  tuberculous  glands,  peri- 
carditis, and  wounds  and  operations  in  the  neck  and  thorax  must  all 
be  sometimes  reckoned  with. 

Not  only  are  vagus  symptoms  associated  with  tabes  and  multiple 
sclerosis  but  they  also  appear  in  hysteria  and  other  neuroses. 

Symptoms. — A  total  vagus  paralysis  may  occur  from  basal  dis- 
ease, but  it  is  not  common.  Other  cranial  nerves  are  usually  implicated 
at  the  same  time.  The  eleventh,  ninth  and  twelfth  are  thus  usually 
included. 


660  THE  NON-NEURONIC  DISEASES 

The  symptoms  of  vagus  palsy  usually  assume  characteristics  in 
accordance  with  the  particular  location  of  the  lesion.  Phonation  is 
affected  and  the  palate,  larynx  and  fauces  are  seen  to  be  paralyzed. 
On  account  of  the  condition  of  the  palate  the  speech,  of  course,  is  nasal. 
Dysphagia  is  present.  The  respiration  is  disturbed.  Rarely  there 
has  been  anaesthesia  of  the  pharynx  and  larynx. 

Acceleration  of  the  heart  action  is  an  old  and  well-known  symp- 
tom. The  inhibitory  control  of  the  nerve  over  the  heart  is  one  of  the 
ancient  teachings  of  physiology.  In  unilateral  lesions  the  heart  has 
been  seen  to  be  retarded.  Irritative  lesions  may  exaggerate  the  in- 
hibition and  so  retard  the  cardiac  phenomena. 

Respiratory  disturbance,  bulimia,  vomiting,  absence  of  hunger 
and  thirst,  pain  in  the  stomach  and  diabetic  manifestations  are  all  to 
be  attributed  to  vagus  trouble  sometimes.  The  respiratory  implication 
results  usually  in  what  is  called  aspiration  pneumonia,  or  hypostatic 
congestion  of  the  lungs. 

Laryngeal  paralysis  is  especially  signilicant.  It  may  occur  alone 
or  as  a  part  of  a  general  vagus  palsy.  These  cases  belong  to  laryngol- 
ogy. I  have  under  my  care  a  syphilitic  with  complete  paralysis  of  the 
right  vocal  cord.  Spasmodic  coughing,  embarrassed  breathing  and 
alteration  of  the  voice  are  all  among  the  symptoms.  In  bilateral  palsy, 
there  is  complete  aphonia,  inspiratory  stridor  and  dyspnoea.  This  oc- 
cus  in  diseases  of  the  medulla  usually  and  not  infrequently  in  hysteria. 
I  saw  it  lately  as  a  neurosis  following  a  lightning  stroke.  As  a  neurosis 
phonation  is  much  more  affected  than  respiration,  whereas  in  organic 
disease  respiration  is  dangerously  involved  along  with  the  loss  of 
voice.  The  reason  is  obvious  for  respiration  is  a  function  much  farther 
removed  from  the  volitional  cerebral  functions  than  is  phonation. 

Paroxysmal  tachycardia,  asthma  nervosum  and  partial  paralysis 
of  phonation  may  all  be  observed. 

Treatment. — Seach  for  and  remove  the  cause.  Syphilis  especially 
must  be  attended  to.  ^  Alcohol,  tobacco  and  other  toxins  must  be  re- 
moved. Lead  should  be  eliminated  in  the  usual  way  with  baths,  purga- 
tives and  the  iodides.     Supporting  diet  must  be  urged. 

Electrical  treatment  has  not  proved  of  much  benefit  in  my  hands, 
though  it  is  well  always  to  try  it.  External  applications  are  better  than 
■direct  applications  in  the  larynx. 

There  is  a  massage  of  the  larynx. 

Tracheotomy  may  have  to  be  resorted  to  in  some  dangerous  cir- 
cumstances. 

THE  ACCESSORIUS,  OF  ELEVENTH  CRANIAL  NERVE. 

A  part  of  this  nerve,  the  accessory,  belongs  practically  to  the  vagus 
system  and  physiologically  cannot  be  separated  from  it.  The  spmal  part 
of  the  nerve  supplies  the  sferno-niastoid  and  trapesins  muscles.  Some 
of  the  cervical  nerves  assist  in  partially  innervating  these  muscles  so 
that  paralysis  of  the  eleventh  nerve  does  not  eventuate  always  in  the 
complete  destruction  of  their  function.  The  control  of  the  sterno- 
mastoid  is  almost  completely  a  function  of  the  eleventh  nerve.     The 


THE  NON-NEURONIC  DISEASES  66l 

trapezius  is  in  its  clavicular  portion  quite  a  little  subject  to  the  acces- 
sorius  nerve. 

Disease  of  the  cervical  cord  and  spinal  roots  may  affect  the  nerve. 
Also  is  it  liable  to  damage  from  carious  vertebrae  here,  from  exostoses, 
abscesses,  tuberculous  and  syphilitic  conditions,  tumors  and  menin- 
gitic  exudations.  Compression  may  occur  from  trouble  in  the  fora- 
men magnum.  The  nerve  may  be  primarily  inflamed  and  this  neuritis 
may  be  unilateral  or  bilateral. 

The  chief  symptoms  of  disease  in  this  nerve  are  complete  paraly- 
sis of  the  sterno-mastoid  muscle,  partial  paralysis  in  the  trapezius.  The 
latter  does  not  produce  much  of  a  deformity.  The  former  causes  one 
form  of  torticollis  or  wryneck.  The  chin  cannot  be  moved  back  towards 
the  side  of  the  diseased  muscle.  When  both  sterno-mastoids  are 
affected,  the  head  falls  back  upon  the  shoulders. 

Prognosis  and  treatment  need  no  special  comment  as  they  follow 
the  ordinary  principles  for  peripheral  neuritic  disease. 

THE    HYPOGLOSSAL,    OR    TWELFTH    CRANIAL    NERVE. 

This  is  a  pure  motor  nerve ;  springs  from  a^  nucleus  in  the  medulla 
that  corresponds  with  the  upward  extension  of  the  anterior  horn  of  the 
cord ;  and  in  some  of  the  lower  animals  is  a  pure  spinal  nerve.  It  ap- 
pears at  the  side  of  the  medulla  between  the  pyramid  and  olivary  body. 
It  supplies,  alone  or  in  conjunction  with  branches  from  some  spinal 
nerves,  all  the  muscles  connected  with  the  hyoid  bone,  including  the 
tongue,  but  excepting  the  digastric,  stylo-hyoid,  mylo-hyoid  and  the 
middle  constrictor  of  the  pharynx.  It  stimulates  also  the  sterno-thyroid 
muscle.  It  is  in  connection  with  the  pneumogastric,  lingual,  upper 
three  cervical  nerves,  and  the  sympathetic. 

The  nerve  is  more  often  damaged  within  its  cerebral  and  medullary 
course  than  outside.  It  occurs  in  association  with  cerebral  hemiplegia, 
the  tract  connecting  the  cortical  center  for  the  tongue  with  the  hypo- 
glossal nucleus  in  the  medulla  running  along  through  the  internal  cap- 
sule and  crus  with  the  tract  for  the  extremities.  In  this  hemiplegic 
form  of  the  parlysis,  of  couse,  there  is  no  muscular  atrophy. 

Bilateral  or  unilateral  atrophic  paralysis  of  the  tongue  is  usually 
a  medulla  disease. 

Peripheral  damage  to  the  nerve  may  be  caused  by  favorably 
located  tumors,  meningitic  exudations,  bone  disease,  basal  hemorrhage, 
aneurisms  of  the  verebral  artery  and  dislocations  of  the  upper  cervical 
vertebrae.  It  has  accompanied  hydatid  cysts.  Cervical  traumata  and 
tumors  may  injuriously  compress  the  nerve.  Rarely  there  may  be  an 
isolated  neuritis,  following  an  infection  of  some  sort,  such  as  scarlatina. 

It  may  be  associated  with  tabes,  disseminated  sclerosis,  syringo- 
myelia, facial  hemiatrophy  and  disease  of  other  cranial  nerves. 

If  the  palsy  is  bilateral  the  tongue  lies  dead  and  limp  on  the  floor 
of  the  mouth.  If  it  is  unilateral  the  tip  of  the  tongue  inclines  toward 
the  normal  side  but  upon  protrusion  of  it,  the  whole  tongue  moves 
toward  the  paralyzed  side.  The  root  of  the  tongue,  according  to 
Gowers,  is  a  little  higher  on  the  paralyzed  than  on  the  sound  side.     The 


662  THE  NON-NEURONIC  DISEASES 

raphe  is  arched,  with  the  concavity  toward  the  paralyzed  side.  The 
deviation  is  one  of  the  residts  of  the  atrophy  in  the  genioglossus 
muscle. 

This  paralysis,  like  all  neuritic  peripheral  palsies,  is  accompanied 
by  muscular  atrophy,  flaccidity,  fibrillary  tremor,  incomplete  reaction 
of  degeneration  and  reflex  alteration. 

The  speech,  mastication,  deglutition  are  not  very  much  embar- 
rassed when  the  palsy  is  unilateral.  When  it  is  bilateral  they  may  be 
very  markedly  disturbed,  such  trouble  being"  usually  of  medullary 
origin. 

The  prognosis  is  favorable  in  syphilitic,  traumatic  and  rheumatic 
cases.     Other  cases  are  relatively  unfavorable. 

The  treatment  should  be  carried  out  along  the  lines  indicated  un- 
der the  head  of  neuritis  and  the  other  cranial  nerves. 


PART  I 


Non-Neuronic  Diseases  of  the  Brain, 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN.  CERE- 
BRAL LOCALIZATION.  CRANIO-CEREBRAL  TOPOG- 
RAPHY.    SYMPTOMS    OF    DISEASE    OF    THE    BRAIN. 

Anatomy. — As  I  have  shown  under  the  head  of  the  anatomy  of 
the  spinal  cord,  it  is  unfortunate  that  the  gross  and  artificial  division 
of  the  cerebrospinal  axis  mto  the  brain  and  cord  has  become  so  estab- 
lished in  the  minds  of  the  profession.  It  is  not  a  physiological  divis- 
ion and  for  the  proper  conception  of  nervous  diseases,  the  physiology 
of  the  nervous  system  is  a  matter  of  infinitely  greater  importance  than 
is  its  mere  anatomy.  I  am  convinced  that  miich  of  the  commonly  ex- 
pressed difficulty  in  the  understanding  of  nervous  diseases,  is  due  to 
the  fact  that  anatomy  and  physiology  have  not  hitherto  taught  the 
structure  of  the  nervous  system  in  the  same  way.  The  former  has 
used,  and  unfortunately  still  uses,  coarse,  artificial  lines  of  division,  a 
misleading  nomenclature  and  an  irrelevant  method  of  description.  The 
student  has  always  to  revise  his  anatomical  lore  as  soon  as  he  begins 
to  delve  into  the  physiology  of  the  nervous  system.  If  he  is  lucky  in 
forgetting  much  of  his  anatomy  and  relearning  it  upon  a  physiological 
basis,  he  will  have  no  trouble  in  understanding  the  diseases  of  the 
nervous  system.  If,  however,  he  is  a  busy  practitioner,  who  acquired 
his  anatomical  knowledge  long  ago  and  who  now  has  no  time  to  fol- 
low up  the  latest  physiological  discoveries,  he  will  not  understand  the 
diseases  of  the  nervous  system.  He  will  constantly  find  them  a  puzzle 
and  a  mystery.  These  diseases  represent  physiological  and  anatomico- 
physiological  changes  and  not  merely  anatomical  abnormalities.     The 


THE  NOX-XEUROXIC  DISEASES  663 

only  salvation  for  the  old  graduate  is  to  forget  his  old  anatomical 
studies  and  relearn  the  structure  of  the  nervous  system  upon  the  mod- 
ern physiological  basis.  He  must  learn  tiiat  cerebrum,  medulla  and 
cord,  for  instance,  are  not  separate  organs,  having  their  own  duties 
to  perform ;  for  they  all  work  together  and  in  unison  as  one  great 
organ.  A  still  better  way  to  put  it  would  be  that  these  names  merely 
indicate  a  certain  general  locality  in  wdiich  are  found  some  of  the 
serial  deposits  of  gray  matter  that  make  up  the  whole  apparatus  and 
from  whose  cells  processes  run  back  and  forth  from  one  to  the  other. 
The  brain,  so-called,  consists  merely  of  that  particular  set  of  ganglionic 
masses  that  happen  to  be  inside  of  the  skull.  Neither  anatomically  nor 
functionally  does  the  skull  limit  them,  however.  They  are  as  much 
in  touch  with  the  cord,  anatomically  and  physiologically,  and  the  cord  is 
as  much  in  touch  with  them  as  one  lobe  of  the  liver  is  with  another 
lobe  of  the  liver.  Xay,  more,  they  are  in  closer  touch  than  are  the 
hepatic  lobes,  for  cerebral  elements  actually  reach  down  (pyramidal 
tracts)  and  become  a  part  of  the  cord,  and  spinal  elements  (direct 
cerebellar  tracts,  for  instance,)  extend  up  and  become  parts  of  the 
brain. 

In  using  the  old  nomenclature  and  the  old  anatomical  divisions  and 
subdivisions  of  the  nervous  system,  I  do  so  in  deference  to  the  long- 
grounded  conception  of  the  nervous  system  still  held  throughout  the 
profession,  and  because  it  would  be  too  radical  to  all  at  once  cease 
using  convenient  names  simply  because  they  happen  to  convey  erro- 
neous physiological  ideas.  Some  day  we  will  speak  everywhere  and 
tmder  all  circumstances  of  the  cerebrospinal  axis  as  a  single  organ, 
just  as  we  now  do  of  the  liver.  There  will  grow  up  in  our  minds  the 
truth  that  this  is  a  composite  organ  with  one  universal  function  through- 
out all  of  its  parts,  just  as  is  the  case  with  the  liver.  We 
will  realize  that  essentially  the  cells  (neurones)  of  one  part  of  this 
organ  do  not  functionate  per  se  difterently  from  the  cells  (neurones) 
of  another  part.  We  will  be  reconciled  to  the  startling  fact  that  the 
apparent  differences  between  the  functions  of  these  widely  separated 
neurones  or  constituent  cells  of  the  cerebrospinal  organ  are  due  merely 
to  the  dift'erences  between  the  end-organs  to  which  they  respctively 
happen  to  be  attached.  Certain  brain  cells  see,  let  us  say,  and  the 
cord  cells  do  not  see.  because  the  former  are  attached  to  a  particularly 
differentiated  end-organ  of  epiblastic  origin,  the  eye,  that  is  different 
from  any  end-organ  with  which  the  cord  happens  to  be  attached.  The 
cells  themselves,  both  anatomically  and  physiologically,  however,  are 
from  all  evidence,  exactly  the  same.  This  fact  must  be  kept  well  in 
mind  in  our  studies  of  the  physiology  of  the  brain  or  any  other  part 
of  the  nervous  system. 

With  the  understanding,  therefore,  that  old  names  are  used  lor 
mere  rough  topographical  purposes,  and  not  in  any  sense  as  convey- 
ing a  correct  idea  of  the  anatomico-physiological  structure  of  the  nerv- 
ous system,  as  we  now  know  it,  I  will  take  up  the  anatomy  and  phys- 
iology of  the  brain. 

The  brain,  or  encephalon,  is  all  of  that  part  of  the  nervous  sys- 
tem that  lies  above  the  foramen  magnum  in  the  occipital   bone  and 


664  THE  NON-NEURONIC  DISEASES 

which  fills  the  great  cranial  cavity.  Conventionally  it  is  said  to  be 
attached  to  the  spinal  cord  at  the  foramen  magnum.  It  is  a  large, 
ovoid,  convoluted  mass,  smooth  and  covered  with  membranes.  Turn- 
ing it  upside  down  we  see  that  we  can  divide  it  conveniently,  for 
topographical  purposes,  into  four  sub-niasses,  the  cerebnini,  the  cere- 
bellum, the  pons  Varolii,  and  the  medulla  oblongata. 

The  weight  of  the  brain  is  a  matter  of  some  importance.  For  the 
majority  of  males  it  ranges  between  1,300  and  1,450  grammes.  The 
female  brain  weighs  a  trifle  less.  The  heaviest  brain  that  has  been 
put  upon  record  was  that  of  Bismarck.  It  was  calculated  to  have 
weighed  over  1,867  grammes.  Brain  weight  not  only  varies  in  ac- 
cordance with  the  sex  but  with  the  intelligence,  the  age  and  the  race 
as  well. 

The  question  of  the  relationship  between  brain  weight  and  intel- 
ligence has  long  been  debated.  Intelligence  is  an  elastic  term.  There 
are  men  of  a  high  degree  of  intelligence  in  one  direction,  but  of  dense 
ignorance  in  another.  Both  with  or  without  cultivation,  intelligence 
may  mean  something  very  difl^erent  between  two  men.  The  only  real 
standard  of  intelligence  that  we  could  adopt  would  be  one  that  en- 
compassed all  knowledge  and  all  mentality.  That  is  never  seen  and 
hence  our  definitions  of  intelligence  are  always  partial.  It  is  a  fact 
that  in  a  few  instances  of  special  lines  of  mental  cultivation,  correspond- 
ing parts  of  the  brain  have  shown  some  special  development.  Gam- 
betta  was  a  great  orator.  His  speech  center  in  the  brain  was  said  to 
have  been  uncommonly  developed.  The  visual  centers  in  the  occipital 
lobe  have  been  found  well  developed  in  artists.  These  suggestive  facts 
taken  in  conjunction  with  the  truth  that  men  of  marked  intellectuality 
and  that  certain  superior  races  have  had  heavier  brains  than  others,  one 
is  almost  inclined  to  believe  that  brain  weight  has  a  great  deal  to  do 
with  intelligence.  Cuvier's  brain  weighed  1,830  grammes;  Byron's, 
1,807;  Kant's,  1,650;  Schiller's,  1,630;  and  Dantes'.  1.420.  English,. 
Scotch  and  German  brains  are  heavier  than  those  of  the  Russians, 
French  and  Italians.  Some  of  the  smallest  brains  found  are  among 
the  primitive  African  and  Australian  races.  The  negro  brain  averages 
about  1,250  grammes.  Perls  and  Edinger  have  worked  at  the  prob- 
lem from  another  side  and  obtained  similarly  suggestive  results.  They 
noticed  that  many  men  of  eminence  in  the  intellectual  sphere  give 
evidence  of  having  had  hydrocephalus  which  had  healed  in  childhood. 
Such  was  probably  the  case  with  Rubenstein,  Cuvier,  Walter  Scott 
and  others.  It  is  suggested  that  this  favored  brain  expansion  with 
possible  increase  in  weight  and  size.  Of  course,  it  is  understood  in 
this  that  mere  bigness  of  brain  does  not  create  intelligence  by  any 
means.  One  of  the  finest  and  largest  brains  I  ever  removed  at  a  post 
mortem  was  from  a  man  who  scarcely  had  his  equal  for  ignorance  and 
stupidity.  It  is  inferred  merely  that  largeness  of  brain  furnishes  a 
large  capacity  for  intelligence  if  it  is  exercised. 

All  brains  that  weigh  less  than  1,130  grammes  in  man,  or  990  in 
woman,  are  spoken  of  as  microcephalic;  all  that  weigh  over  1,490 
in  man,  or  1,345  in  woman,  are  referred  to  as  me galo cephalic. 

At  birth  the  brain  weighs  about  -^2"/  grammes.     Up  to  four  years 


THE  XON-XEUROXIC  DISEASES 


66  = 


of  age  it  grows  very  rapidly.  From  four  to  seven,  its  growth  is  slower. 
From  the  latter  age  to  twenty  its  increase  in  size  is  very  slow.  Then 
it  remains  stationary.  At  45  and  50,  in  men  and  women  respectively, 
it  begins  to  lose  in  weight  but  very  slowly.  At  eighty  it  has  lost  about 
120  grammes.  The  relation  of  the  brain  to  the  body  development,  of 
course,  must  be  alwa}s  taken  into  count.  The  relative  weight  is  about 
2  per  cent. 

The  Meiiibraiies  of  the  Brain. — There  are  three  membranes  that 
cover  the  brain,  namely,  the  dura  mater,  the  arachnoid,  and  the  pia 
mater. 

The  dura  mater  is  an  inelastic  and  dense  structure,  composed  of 

FIGURE  145. 


ritjcm  spinal,  int. 

The  blood-vessels  of  the  dura  mater.   Lateral  view.    (After  Heit2mann.) 

white  fibrous  and  yellow  elastic  tissue  and  is  lined  on  its  under  svir- 
face  with  flat  endothelial  cells  It  consists  of  two  layers.  The  outer 
layer  is  the  nutrient  endosteum  and  is  attached  more  tightly  to  the 
bones  at  the  base  of  the  skull  than  at  the  vertex.  Through  the  cranial 
sutures  and  various  foramina  it  becomes  continuous  with  the  perios- 
teum on  the  outside  of  the  skull. 

The  inner  layer  separates  from  the  outer  to  form  the  sheaths  of 
the  cranial  nerves  and  the  great  venous  sinuses.  ^Moreover  it  sends 
down  between  the  main  divisions  of  the  brain  the  great  septa  called 
processes. 

The  falx  cerebri  and  the  falx  cerebelli  are  vertical  curtains  that 
hang  in  the  great  longitudinal  fissure  and  separate  the  two  halves  of 
the  brain.  Another  curtain  is  the  tentorium  cerebelli  which  passes 
horizontally  forward  into  the  transverse  fissure  and  separates  the  pos- 
terior part  of  the  cerebrum  from  the  cerebellum. 


666 


THE  NON-NEURONIC  DISEASES 


The  bony  attachments  of  the  falx  cerebri  are  the  crusta  galU  in 
front  and  the  internal  occipital  protuberance  behind.  It  is  also  fastened 
to  the  upper  surface  of  the  tentorium,  along  the  occipital  crest  and  to 
the  posterior  border  of  the  foramen  magnum.  In  the  upper  convex 
and  lower  free  borders  of  this  falx  are  the  superior  and  inferior  longi- 
tudinal sinuses,  the  superior  extending  from  the  foramen  caecum  back 
to  the  torcular  Herophili  at  the  internal  occipital  protuberance,  and  the 
inferior  uniting  with  the  common  vein  of  Galen,  or  vena  cerebri  magna, 
and  becoming  the  sinus  rectus  that  courses  through  the  tentorium  to 
the  torcular. 

The  attachments  of  the  falx  cerebelli  are  the  inferior  surface  of 

FIGURE  146. 


The  blood-vessels  of  the  dura  mater.    Bird's-eye  view.    (After  Heitzmann.) 

the  tentorium  and  the  occipital  crest  to  the  posterior  edge  of  the  fora- 
men magnum.  Through  this  septum  runs  the  occipital  sinus  or  si)iuses 
from  the  foramen  magnum  upwards  and  backwards  to  the  torcular. 

The  fastenings  of  the  tentorium  are  the  internal  occipital  pro- 
tuberance, the  petrous  bone  and  the  clinoid  processes  of  the  sphenoid. 
Through  a  large  notch  the  brain  stem  is  transmitted.  At  its  sides  are 
the  lateral  sinuses.  These  run  from  the  torcular,  along  the  horizon- 
tal arms  of  the  occipital  crucial  ridge  to  the  petrous  bone  where  the 
corresponding  superior  petrosal  sinuses  enter  them  and  finally  turn 
downward  through  the  sigmoid  fossa,  uniting  with  the  inferior  petro- 
sal sinuses  in  the  jugular  foramina. 

The  pituitary  fossa  is  specially  covered  by  a  portion  of  the  dura 
called  the  diaphragm  sellcc. 


THE  XOX-XEUROXIC  DISEASES  667 

It  will  be  observed  that  the  various  parts  of  the  brain  are  bv 
these  dural  septa  encased  in  membranous  boxes,  as  it  were.  This  pro- 
tects the  brain  from  sudden  jars.  It  also  limits  and  directs  the  course 
of  hemorrhagic  and  purulent  collections  that  may  form  in  them  or 
enter  from  without. 

In  addition  to  the  sinuses  that  have  already  been  mentioned,  notice 
must  be  taken  of  the  circular  sinus  around  the  sella  turcica,  the  two 
cavernous  sinuses  on  eitlier  side  and  joined  by  the  circular,  and  the 
transverse  or  basilar  sinus  that  unites  the  inferior  petrosal  sinuses. 

The  dura  receives  its  blood  supply  from  the  anterior  and  poste- 
rior ethmoidal  bra»5ches  of  the  ophthalmic,  from  the  anterior  menin- 
geal of  the  internal  carotid,  the  great  and  small  meningeals,  from  the 
internal  maxillary,  the  meningeal  branches  of  the  ascending  pharyngeal 
and  occipital,  and  the  posterior  meningeal  branch  of  the  vertebral.  The 
important  arter}-  is  the  middle  meningeal  from  the  external  carotid. 

The  veins  are  numerous  and  connect  with  those  of  the  cranium. 

The  dura  is  the  only  cerebral  membrane  that  has  a  }ierre  supply. 
There  are  branches  from  the  sympathetic  that  accompany  the  arteries. 
There  are  also  branches  from  the  trochlear,  the  ophthalmic,  the  Gasse- 
rian  ganglion,  and  the  tenth  and  twelfth.  The  motor  branches  of  the 
nerves  innervate  the  arteries. 

The  arachnoid  is  a  loose  membrane,  delicate  and  lace-like.  The 
inner  surface  is  so  attached  to  the  pia  mater  by  trabeculse  that  there 
are  a  lot  of  inter-communicating  subarachnoidal  spaces  filled  with  cere- 
brospinal fluid.  On  the  outer  surface  are  the  enlarged  villi,  known 
as  Pacchionian  bodies,  or  granulationes  arachnoideales,  that  project 
within  and  along  the  superior  longittidinal  sinus  and  that  probably 
serve  as  an  outlet  for  the  subarachnoid  fluid  into  the  sinus.  The  mem- 
brane follows  the  inner  surface  of  the  dura  and  does  not  dip  into  the 
sulci  with  the  pia.  The  posterior  subarachnoid  space  communicates 
with  the  fourth  ventricle  through  the  foramen  of  Magendie  and  the 
foramina  of  Key  and  Retzius.  The  arachnoid  is  without  vessels  and 
nerves. 

The  pia  mater  is  a  highly  vascular  membrane  consisting  of  a  net- 
work of  arteries  and  veins  held  together  by  fibro-elastic  areolar  tissue. 
Outwardly  its  epithelium  lines  the  subarachnoid  trabeculse  and  spaces. 
These  spaces  are  very  large  at  the  base  of  the  brain.  The  pia  hugs 
closely  the  surface  of  the  brain  and  sends  septa  and  bloodvessels  vertic- 
ally into  the  brain  substance.  It  dips  down  everywhere  into  the  sulci 
and  it  forms  investing  sheaths  to  the  cranial  nerves.  Bet\\"een  the 
fornix  and  the  interbrain  it  enters  the  choroid  fissure  and  ultimately 
becomes  the  velum  interpositum  and  part  of  the  tela  choroidea  ven- 
triculi  tertii.  Between  the  medulla  and  cerebellum  it  is  inserted  over 
the  fourth  ventricle  and  helps  to  form  the  posterior  choroid  tela  which 
is  perforated  by  the  foramina  of  Magendie,  Key  and  Retzius. 

The  anterior,  middle  and  posterior  cerebral  arteries,  the  anterior 
and  posterior  inferior  cerebellar  and  the  superior  cerebellar  all  sup- 
ply the  pia.  Its  venous  supplv  is  also  abundant.  The  veins  all  empty 
into  the  sinuses  and  are  the  venae  Galeni,  choroid  plexuses  of  the  ven- 
tricles and  the  cerebral  veins.     The  sympathetic,  of  course,  innervates 


668 


THE  NON-NEURONIC  DISEASES 


it,  as  well  as  the  third,  fifth,  sixth,  seventh,  ninth,  tenth  and  eleventh 
cranial  nerves. 

General  Anatomy  of  the  Brain. — A  brief  study  of  the  embryo- 
logical  development  of  the  brain  makes  clear  certain  facts  that  it  is 
well  to  understand  before  going  on  with  a  discussion  of  its  anatomical 
structure. 

By  the  "fifteenth  day  after  conception,  the  neural  tube  resulting 
from  the  infolding  of  the  epiblast,  is  complete,  except  for  a  short  dis- 
tance posteriorly.  In  that  portion  which  is  to  become  the  encephalon, 
or  brain,  later  on,   two  constrictions  take  place  which  divide  it   into. 


FIGURE  147. 


Epilhalamlia  (Corpus  pineale) 


Motathalamus  (Corpora  geniculata) 


Corpora  quadrigemina 


Pedunculns  cerebri 


RhineDcephalon 

Corpus  atrlatum' 
Sulcus  bypotbalamicns  [Monro! 

Chiasms  opticum 


Cerebellum 
Fossa  rhomboidea 


Brain  of  the  human  embryo  five  weeks  old.     Right  half  viewed  from  the  lett. 
(After  His.) 

three  primary  brain  vesicles.  Behind  the  third  vesicle,  the  tube  con- 
tinues small  and  constitutes  the  later  spinal  cord.  The  brain  vesicles 
develop  rapidly  and  again  break  up  into  subdivisions.  A  constriction 
appears  in  the  anterior  and  posterior  vesicles.  Thus  ultimately  there 
are  five  vesicles.  These  with  their  surrounding  elements  are  named 
from  before  backwards,  the  Prosencephalon,  or  Telencephalon ;  the 
Thalamencephalon,  or  Diencephalon ;  the  Mesencephalon ;  the  Meten- 
cephalon ;  and  the  Myelencephalon. 

As  development  goes  on  the  various  parts  of  the  brain  assume 
their  adult  appearance  in  these  vesicular  areas  and  the  interconnected 
cavity  within  them  becomes  the  ventricles.  The  adtilt  ventricles  consist 
of  the  tzvo  lateral,  the  third,  fourth  and  fifth;  with  the  foramina  of 
Monroe  connecting,  y-shape,  the  two  lateral  with  the  third,  and  the 
aqueduct  of  Sylvius  the  third  with  the  fourth. 


THE  XOX-NEUROXIC  DISEASES 


669 


Along  the  sides  of  these  ventricles  can  be  traced  the  groove  or 
line  of  Monroe  which,  according  to  ^linot,  is  of  great  significance  in 

FIGURE  148. 


iJL. 


Embryonal  Development  of  the  Brain. 
A— Brain  and  Spinal  Cord  at  the  Third  :Month. 
B— Base  of  the  Brain  at  the  Fourth  jSIonth. 
C— ]Median  surface  of  the  Brain  at  the  Fourth  Month. 

D— Outer   surface   of  a   Cerebral   Hemisphere  at   the   Fifth   :\Ionth.      (After 
Jakob.) 

showing  the  developmental  separation  between  the  dorsal  or  receiving 
zone  of  the  cerebrospinal  organ  and  the  ventral  or  emissive  zone.     In 


670 


THE  NON-XEUROXIC  DISEASES 


the  former  are  small  nerve  cells  whose  jDrocesses  never  pass  out  of  the 
central  nervous  apparatus  to  form  nerves.  In  the  latter  are  the  large 
cells  whose  processes  do  pass  out  to  hecome  nerves.  The  sensory 
nerve  paths  which  are  received  by  the  dorsal  zone  are  the  processes 
of  the  cells  in  the  cranial  nerve  ganglia  and  posterior  spinal  ganglia 
which  are  developed  out  of  the  original  neural  crests  and  not  directly 
from  that  part  of  the  neural  tube  from  which  the  brain  and  cord  de- 
velop. 

FIGURE  149. 


FRONTAL  lOBE 


PAHIETAL  LOBE 

POSTH  DIVISION  OP 
YLVIAN    FISSURE 


TEMPO  RO-SPbE(t 


OCCIPITAL  LOBE 


(After  Gray.) 

The  parts  around  the  vesicles  are  not  all  equally  elaborated  in 
the  adult  brain.  For  instance,  the  prosencephelon  in  man  becomes 
enormously  developed  into  the  cerebral  cortex.  The  diencephalon  is 
rather  poorly  developed  and  the  olfactory  projections  (erroneously 
called  nerves)  are  actualh"  atrophied.  In  some  lower  animals  the  olfac- 
tory bulbs  are  larger  than  the  cerebral  hemispheres.  The  mesen- 
cephalon is  a  rudimentary  organ.  The  metencephalon  is  wxll  elabor- 
ated, whereas  the  myelencephalon  is  again  relatively  undeveloped. 

Three  great  flexures  occur  in  the  cephalic  part  of  the  neural  tube, 
two  ventral  and  one  dorsal,  which  further  help  to  disguise  the  primi- 


THE  XOX-XEURONIC  DISEASES 


671 


tive  origin  of  the  brain  and  cord  of  the  adidt.  The  mesencephahc 
ventral  flexure  is  a  very  early  one  and  at  about  the  twenty-eighth  day 
amounts  to  nearly  180  degrees.  The  thalamencephalon  is  thus  brought 
almost  into  contact  with  the  epencephalon.  A  cervical,  ventral  flexure 
occurs  where  the  last  vesicle  joins  the  spinal  cord.  It  represents  the 
bending  of  the  head  upon  the  body  of  the  embryo  and  at  about  the 
fourth  week  it  amounts  to  90  degrees.  There  is  finally  a  late  dorsal 
flexure,   sometimes  called  the  metencephalic,  at  the  point  where   the 


FIGURE  150. 

View 
of  the  corpds 
callos0ji  fr03i 
ABOVE  (from 
Sappey  after  Fo- 
viUe).      i 

The  upper  sur- 
face of  the  corpus 
callosum  has  been 
fully  exposed  by 
separating  the  ce- 
rebral hemispheres 
and  throwing  them, 
to  the  side  ;  the  gy- 
rus fornicatus  has 
been  partly  de- 
tached, and  the 
transverse  fibres  cf 
the  corpus  callo- 
sum traced  for 
some  distance  into 
the  cerebral  medul- 
lary substance. 

l,the  upper  sur- 
face of  the  corpus 
callosum ;  2,  me- 
dian furrow  or 
raphe ;  3,  longitu- 
dinal strice  bound- 
ing the  furrow ; 
4,  swelling  formed 
by  the  transverse 

bands  as  they  pass  into  the  cerebrum,  arching  over  the  side  of  the  lateral  ventricle  ;  5, 
anterior  extremity  or  knee  of  the  corpus  callosum  ;  6,  posterior  extremity  ;  7,  anterior, 
and  8,  posterior  fibres  proceeding  from  the  corpus  callosum  into  the  frontal  and  occipital 
lobes  respectively  ;  9,  margin  of  the  swelling  ;  10,  anterior  part  of  the  gyrus  fornicatus  ; 
11,  fissure  between  the  corpus  callosum  and  this  convolution  opened  out ;  outside  12,  is 
the  termination  of  the  calloso-marginal  fissure,  and  before  13  is  the  parieto-occipital 
fissure;  13,  upper  surface  of  the  cerebellum 

fourth  and  fifth  vesicles  approximate.  By  the  eighth  week  it  amounts 
to  i8o  degrees  and  thus  causes  the  dorsal  part  of  the  cerebellum  to 
partially  rest  upon  the  medulla  oblongata.  The  cervical  and  meten- 
cephalic flexures  are  temporary ;  the  mesencephalic  is  permanent. 

This  is  all  the  result  of  the  working  of  the  laws  of  evolution  and 
in  large  part  represents  the  principle  of  adaptation  to  environment.  The 
value  of  this  lies  in  the  fact  that  we  can  thus  unravel  the  complicated 
architecture  and  functions  of  the  adult  human  brain  by  the  compara- 
tive study  of  the  lowxr  and  less  developed  brains  of  the  animal  world. 


(^^2  THE  NON-XEURONIC  DISEASES 

The  marvelous  harmony  and  consistency  of  nature  are  thus  not  only 
realized  in  the  primitive  tracings  of  the  highest  expression  of  vital  de- 
velopment, the  human  brain,  but  the  value  of  all  morphological  and 
biological  studies  is  enormously  enhanced. 

I  will  now  resume  the  general  anatomical  description  of  the  en- 
cephalon.  The  following  ganglionic  deposits  and  their  connecting  pro- 
cesses are  to  be  passed  in  review : 

I.  Cerebrum   (Prosencephalon)  consisting  of 

a.  Hemispheres    (Telencephalon), 

Their  cortex  and  centrum  ovale, 

Corpus   callosum. 

Fornix, 

Commissura  hippocampi,  and 

Anterior  commissure. 

b.  Interbrain   (Diencephalon  ) , 
Lamina  cinerea, 

Tuber  cinereum  and  infundibulum, 
Pituitary  body  or  hypophysis  cerebri. 
Corpora  albicantia. 
Optic  thalami, 

[Middle  and  posterior  commissure. 
Pineal  body  or  epiphysis  cerebri, 
External  geniculate  bodies. 
Optic  tracts  and  commissure. 

II.  ISIidbrain,  Crus"  Cerebri  or  Pedunculus  Cerebri 
Crustse    ( ^Mesencephalon ) , 

Substantia  nigra. 

Tegmentum, 

Corpora  quadrigemina. 

Internal  geniculate  bodies. 

III.  Hindbrain   (Metencephalon), 

Pons  Varolii, 
Cerebellum. 

IV.  Afterbrain    (^Myelencephalon), 

]vledulla  oblongata. 

Most  of  these  parts  are  shown  in  the  accompanying  diagrams.  For 
a  further  general  anatomical  description  of  them  the  reader  is  referred 
to  works  upon  anatomy. 

Lohes,  Convolutions,  Fissures  and  Sulci  of  the  Brain. — It  is  im- 
portant for  topographical  purposes  that  the  surface  of  the  brain  be 
mapped  out  in  areas  and  named.  The  fissures  and  sulci  serve  as  most 
convenient  lines  of  division.  The  accompanying  maps  of  the  brain 
will  assist  the  reader  and  save  a  long  description. 

The  surface  of  the  brain  is  called  the  cortex.  It  is  seen  to  be 
divided  into  a  great  many  subdivisions,  as  though  it  were  made  up  of 
a  mass  of  worms,  "by  large  and  small  fissures.  The  fissures  are  re- 
ferred to  as  primary  and  secondary.  They  represent  infoldings  of  the 
cortex,  allowing  thus  of  a  great  area  to  be  packed  away  in  a  small 


THE  XOX-XEUROXIC  DISEASES 


673 


space.  This  is  a  condition  of  comparative  intelligence  and  evolution- 
ary development,  for  primitive  brains  are  deficient  m  fissuration.  The 
higher  in  the  scale  of  life  the  animal  is  the  greater  the  amount  of 
convohiting  is  there  of  the  brain  surface.  The  fissures  and  sulci  corre- 
spond with  the  developmental  rearrangement,  therefore,  of  various 
ganglionic  deposits  in  the  brain  to  accommodate  them  to  the  narrow 
capacity  of  the  skull.  This  is  virtually  true  of  all  of  them,  but  as  some 
of  them  seem  to  be  older  and  more   fundamental,   more   permanent, 


FIGURE  151. 

Lobus  irontalis 


Corpus  callosnm  (cnt  throngh) 


Cnis  fomicis 


Caput  nuclei  caudati 


Nucleus  lentifonnis 
.,  Stria  termiuaUa 


Pars  centralis 
ventricuU 
lateralis 

Comu  inferius 
Tentricoli 
lateralis 


Cauda  nuclei 

Plexus  chorioi- 

deus  ventriculi 

lateralis 


Fissura  calcanna  "^^^^  Splenium  corporis  callosi 

Lobua  occipiiali 

Lateral    ventricle,    openedj  viewed  from  above. 
{After   Spalteholz.) 


than  others,  we  speak  of  them  as  the  primary  fissures,  and  the  others 
as  the  secondary. 

The  primary  fissures  of  the  brain  are : 

The  Longitudinal,  between  the  two  hemispheres. 

The  Transverse,  or  choroidal,  extending  in  betweeen  the  cerebrum 
and  cerebehum. 

The  Rolandic,  on  the  upper  mid-surface  of  the  cerebrum.  This 
is  a  most  important  localizing  fissure  from  the  surgical  point  of  view. 


674 


THE  NON-NEURONIC  DISEASES 


The  Sylvian,  in  the  mid-lateral  area,  and  important  on  account 
of  the  middle  meningeal  artery  that  passes  up  along  it. 

The  Parieto-occipital,  on  the  posterior  internal  surface  of  the 
hemisphere  chiefly. 

The  Calcarine  and  Parietal  fissures  are  by  some  classified  as  pri- 
mary. 

Five  great  general  divisions  of  the  surface  of  the  brain  are  out- 


FIGURE  152. 


Corpus  callosum  (out  through) 
Cavum  septl  pellucidi 


Lamioa  septi  pellucidi 
Corpus  striatum 


CoUimDa  fomi 

(pars  libera)     "■ 


Recessus  triangular: 


Lamina  affi 

Taenia  chorioidea 
Ventriculus 
tertius 
Stria  medull: 
Commissura 
posterior  [cerebri) 
Habenulii 


Corpus  pineale 


Corp  I 
quadrigi 


Lobus  temporalis 


Digitationes 
-hippocampi 

Corou  inferlua 
vcntricuU  lat*iraliB 

Uncus 
Igyri  hippo'-ampi] 
Gyrus  hipfocampi 

EmlneDtia 
--'coUateraJis 
Fascia  denta^a 
'   hippocampi 
_    Fimbria 
hippocampi 
Taenia  fimbriae 


-Hlppofi 


Trigonum  collaterale 


Fissura  calcari 


Trigonum  habenulae 
Commissura  habenularum 


Cerebellum  /  |    Lobus  occipitali; 

Third    ventricle,    opened,  viewed  from  above. 
(After   Spalteholz.) 

lined  by  these  fissures.  Above  the  Sylvian  and  in  front  of  the  Rolan- 
dic  fissure  is  the  Frontal  Lobe.  Above  the  Sylvian  and  behind  the 
Rolandic  is  the  Parietal  Lobe.  Below  the  horizontal  limb  of  the  Syl- 
vian fissure  lies  the  Temporal  or  Temporo-sphenoidal  Lobe.  Behind 
the  Parieto-occipital  is  the  Oecipital  Lobe,  If  the  Sylvian  fissure  be 
separated,  a  cortical  area  will  be  found  lying  at  the  bottom  of  it.  This 
is  the  Central  Lobe  or  Island  of  Reil,  and  contains  the  great  central 
ganglia.  To  these  are  sometimes  added  the  Limbic  Lobe,  on  the  mesial 
surface  of  the  hemisphere  just  above  the  corpus  callosum,  and  the 
Olfactory  Lobe  or  Bulb  which  is  so  much  atrophied  in  man. 


THE  NON-NEURONIC  DISEASES 


67: 


These  lobes  are  a^ain  subdivided  into  lobules  and  convolutions  by 

^'^  'o^tll^l^^^S^e  Frontal  Lobe  -  two  horizontal  and 
one  vertical  sulcus,  thus  forming  a  superior^  middle  and  mfenor  con- 
volution and  behind  them  the  precentral  or  a.c.;^m.  c.n^ral  convolu- 
don      The  part  of  the  lobe  that  is  immediately  behmd  the  short,  ver- 

FIGURE  153- 


Scheinatic    representation    of    the    cerebrum    viewed    from    above. 


tical  limb  of  the  Sylvian  fissure  is  known  as  the  operculum.    The  mesial 

^rus  in  front  of  that.    The  basal  surface  is  grooved  for  the  olfactory 
"""' The  Parietal  Lobe  includes  on  the  outer  surface  the  postcentral 


676 


THE  NON-NEURONIC  DISEASES 


or  posterior  ascending  convolution  and  the  upper  and  lower  lobules, 
separated  by  the  interparietal  sulcus,  which  is  long,  arched  and  fre- 
quently interrupted.  The  convolution  of  the  inferior  lobule  that  sur- 
rounds the  posterior  end  of  the  horizontal  limb  of  the  fissure  of  Syl- 
vius is  known  as  the  supra-marginal.  That  which  surrounds  the  pos- 
terior end  in  like  manner  of  the  superior  temporal  fissure  is  called  the 
angular  gyrus.  The  forward  end  of  the  interparietal  fissure  is  the 
inferior  retrocentral,  and  the  hinder  end  the  anterior  occipital.  So  im- 
portant are  the  ascending  convolutions  on  either  side  of  the  fissure  of 
Rolando,  that  we  are  beginning  to  put  them  together  and  call  them 
the  central  lobule.  This  must  not  be  confounded  with  the  central  lobe, 
or  Island  of  Reil.    On  the  median  surface  of  the  hemisphere  the  parietal 

FIGURE  154- 


Schematic  representation  of  the  right  cerebral   hemisphere. 


lobe  runs  over  into  the  precuneus  just  above  the  parieto-occipital  fis- 
sure. The  precuneus  is  continued  forward  as  the  gyrus  fornkatus, 
which  lies  just  above  the  corpus  callosum  and  curves  around  the  knee 
in  front,  to  terminate  in  the  subcallossal  gyrus.  Above  the  fornicate 
gyrus  is  the  calloso-marginal  sulcus. 

On  the  exterior  surface  of  the  Occipital  Lobe  we  find  the  supe- 
rior, middle  and  inferior  gyri,  the  first  being  separated  from  the 
parietal  lobe  by  the  anterior  occipital  sulcus  and  from  the  second  occip- 
ital convolution  by  the  lateral  occipital  sulcus.  On  the  median  sur- 
face the  cuneus  is  an  important  lobule,  wedge-shaped,  and  lying  be- 
tween the  parieto-occipital  above  and  the  calcarine  fissure  below.  On 
the  under  surface  of  this  lobe  is  the  end  of  the  gyrus  hippocampi, 
separated  from  the  occipito-temporal  gyrus  by  the  occipito-teniporal 
■fissure.     The  gyrus  hippocampi  also  appears  on  th£  median  surface  of 


THE  NON-NEURONIC  DISEASES 


677 


the  hemisphere  just  beneath  the  dentate  gyrus  and  is  continued  back- 
ward into  the  lingual  gyrus. 

The  Temporal  Lobe  is  divided  into  superior,  middle  and 
inferior  convolutions  by  superior  and  inferior  temporal  sulci. 
On  the  mesial  surface  of  the  brain  the  middle  tem- 
poral gyrus  seems  to  run  back  into  the  gyrus  fusiformis.  The  front 
part  of  the  temporal  lobe  on  the  median  surface  is  known  as  the  uncus, 
or  gyrus  imcinatus. 

CRANIO-CEREBRAL  TOPOGRAPHY. 

For  the  guidance  of  the  surgeon,  it  is  obviously  necessary  that 
the   relationship   of  the   underlying  fissures  and  convolutions   of  the 

FIGURE  155. 


Schematic  representation  of  the  right  cerebral   hemisphere,  viewed  from  the 
left. 

brain  to  the  various  parts  of  the  outside  of  the  skull  should  be  known. 
Broca,  long  ago,  attempted  to  determine  this  by  boring  small  holes 
through  the  skull,  inserting  pegs,  then  carefully  removing  the  calva- 
rium  and  noting  the  parts  of  the  brain  that  were  damaged.  Turner 
adopted  the  method  of  removing  small  parts  of  the  bone  and  observ- 
ing the  fissures  and  convolutions  that  appeared  below.  To  Heft'tler 
and  Bischoff,  Fere,  Seguin  and  others  are  we  indebted  for  very  ac- 
curate knowledge  as  to  this  relationship  between  the  brain  and  the 
sutures  and  other  points  on  the  skull. 

The  fissures  that  it  is  especially  desirable  to  know  about  in  this 
respect  are  the  Rolandic,  Sylvian  and  Pafieto-occipital.  The  accom- 
panying diagram  shows  the  relationship. 

For  surgical  purposes,  however,  the  marks  on  the  skull  are  not 
always  pronounced  enough  to  serve  as  guides,  hence  other  methods 


678 


THE  XON-XEURONIC  DISEASES 


have  been  devised  by  Thane,  Seguin,  Horsley,  Dana,  Reid  and  Fraser. 
These  methods  are  based  upon  exact  measures,  here  and  there,  from 
definite  and  fixed  points  of  prominence. 

All  one  needs  is  a  steel,  pliable  tape  measure  and  a  blue  pencil 
or  brush  with  iodine  on  it.  The  head,  of  course,  must  be  shaved.  The 
innumerable  instruments  like  the  cyrtometer,  encephalometer,  may  be 
dispensed  with. 

FIGURE  156. 


Schematic  representation  cf  the  base  of  the  cerebrum. 

To  locate  the  fissure  of  Rolando,  the  distance  from  the  glabella 
to  the  inion  has  to  be  measured.  About  two  centimeters  behind  the 
middle  point  on  this  line,  or  more  accurately  55.7  per  cent,  of  the 
whole  line  measured  back  from  the  glabella,  will  be  found  the  upper 
end  of  the  fissure.  In  adult  men  this  point  generally  measures  about 
48  mm.  behind  the  bregma,  in  women  45,  and  in  children  from  30  to 
42,  according  to  age.  A  line  running  downward  and  forward,  at  an 
angle  of  67  degrees  with  the  sagittal  line,  will  correspond  with  the 
upper  two-thirds  of  the  fissure.  The  lower  third  is  a  trifle  more  vertical. 


THE  NON-NEURON IC  DISEASES 


679 


The  end  of  the  fissure  below  will  just  about  touch  a  line  drawn  from 
the  stephanion  to  the  asterion. 

Bennet  and  Godlee's  method  for  determining  the  Rolandic  fissure 
is  somewhat  different  and  is  based  upon  the  views  of  Reid,  largely.  A 
vertical  line  is  erected  from  the  anterior  border  of  the  external  audi- 
tory meatus.  Measuring  about  two  inches  back  of  the  point  where 
this  line  cuts  the  glabella-inion-sagittal  line,  a  parallel  line  is  drawn 
vertically   downward   again   and   beside    the   posterior   border   of   the 

FIGURE  157. 


5f2£ 


Lamia 


Uhzll 


lucort 


Outline  skktch   of  the    skull,    with    the   position   of   some  of    the 
principal  cerebral  sulci  marked  upon  it  ^ 

Sy,  Sylvian  fissure;  Sy.a.,  Sy.p.,  its  anterior  and  posterior  limbs  ;  /.i?.,  furrow  of 
Rolando  ;  tr.fr. f.,  transverse  frontal  furrow  ;  i.par.f.,  intraparietal  furrow;  p.o.,  position 
of  the  parieto-occipital  fissure;  par.j.  parallel  furrow;  m.t.s.f.,  middle  temporo- 
sphenoidal  furrow. 

(Modified  from  Thane.) 

mastoid  process.  Where  the  posterior  line  touches  the  sagittal  the 
tipper  end  of  the  fissure  is  found.  Its  lower  end  corresponds  Avith  a 
point  on  the  anterior  vertical  line  about  two  inches  above  the  upper 
border  of  the  external  auditory  meatus. 

After  the  Rolandic  fissure  has  thus  been  determined,  it  is  an  easy 
matter  to  establish  the  relative  position  of  the  central  convolutions  and 
their  particular  motor  areas. 

The  fissure  of  Sylvius,  running  horizontally,  lies  usually  just  a 
little  above  the  parieto-squamous  suture.  A  line  following  the  external 
orbital  process,  the  parieto-squamous  suture  and  the  ^  parietal 
eminence  will  pretty  nearly  outline  its  course.  The  fissure  is  higher 
up  and  more  oblique  in  children.    The  point  of  union  between  the  ver- 


680  THE  NON-NEURONIC  DISEASES 

tical  and  horizontal  limbs  of  this  fissure  is,  according  to  Merkel,  about 
four  or  four  and  a  half  centimeters  above  the  middle  of  the  zygomatic 
arch. 

The  parieto-occipital  fissure  is  determined  b}'  first  finding  the 
lambda,  marking  a  point  3  mm.  in  front  of  it,  drawing  a  line  at  right 
angles  to  the  sagittal  through  this  point,  and  then  measuring  about 
2.5  cm.  on  this  line  either  side  of  the  sagittal  point. 

The  frontal  lobe  lies  almost  entirely  behind  the  frontal  bone. 

Behind  the  parietal  will  be  found  the  central  convolutions 
the  parietal  lobe  and  a  part  of  the  occipital  lobe.  The  parietal  boss  con- 
ceals the  supra-Diarginal  gyrus.  The  greater  part  of  the  temporal  lobe 
is  behind  the  temporal  bone. 

Ofttimes  it  is  desired  to  reach  the  ventricles.  Usually  there  are 
several  ways  of  doing  this.  Keen  recommends  the  lateral  route. 
Draw  a  base  line  through  the  lower  border  of  the  orbit  and  the  ex- 
ternal auditory  meatus.  At  a  point  on  this  line  1^:4  inches  behind  the 
meatus  erect  a  vertical  line.  A  point  on  this  vertical  line  i}^  inches 
above  the  base  line  is  where  the  trocar  may  be  introduced.  The  in- 
strument should  be  plunged,  after  trephining,  of  course,  into  the  brain 
in  the  direction  of  a  point  2^  or  3  inches  vertically  above  the  oppo- 
site external  auditory  meatus.  From  2  to  2  V4  inches  in  the  ventricle 
will  be  penetrated. 

The  Minute  Structure  of  the  Brain. — I  have  enumerated  the 
main  anatomical  parts  of  the  brain.  It  is  now  necessary  to  discuss 
its  minute  structure.  Like  all  other  parts  of  the  nervous  system,  this 
consists  of  a  network  of  neurones,  supported  by  sustentacular  tissue 
consisting  of  neuroglia,  connective  tissue,  bloodvessels,  lymphatics  and 
ependymal  epithelium. 

The  brain  differs  from  the  cord  not  in  the  character  of  its  ele- 
ments but  merely  in  the  arrangement  of  them  and  the  relative  quantity 
of  gray  to  white  matter.  The  neurones  are  the  same  kind  of  neu- 
rones ;  are  bunched  together  in  the  same  way ;  have  various  sized 
processes ;  and  are  distributed  in  relation  to  one  another  in  contiguous 
series  in  the  same  way.  It  hardly  needs  to  be  said  that  the  susten- 
tacular elements  are  exactly  the  same  as  those  found  outside  of  the 
cranium.  It  is  obvious,  therefore,  that  little  need  be  said  upon  the 
constituent  elements  of  the  brain  beyond  what  has  already  been  said 
in  the  chapters  devoted  to  the  neurone  and  the  neuronic  architecture. 
Some  consideration  must  be  given,  however,  to  the  arrangement  of 
these  constituent  elements  in  the  encephalic  mass. 

As  in  the  cord,  so  here  we  find  gray  and  white  matter.  The  gray 
matter  is  spread  out  on  the  surface  in  the  form  of  the  cortex  and  de- 
posited here  and  there  in  clumps  or  bilateral  masses  all  through  the  en- 
cephalon.  The  white  matter  appears  in  a  large  area  just  beneath  the 
cortex  and  in  streaks  and  radii  here  and  there  between  the  masses  of 
gray  matter,  and  between  the  bram  and  the  parts  of  the  nervous  sys- 
tem outside  of  the  head.  It  is  very  clear  then  that  we  have  ganglia 
here,  just  as  we  have  in  the  cord,  consisting  of  little  accumulations  of 
neurone  bodies  in  special  spots  and  bundles  of  neuraxones  making 
up  the  pathways  along  which  impulses  of  all  sorts  travel  between  dif- 


THE  NON-NEURONIC  DISEASES  68l 

ferent  parts  of  the  brain  and  between  the  brain  and  the  rest  of  the 
nervous  system. 

At  a  first  glance  we  discover  that  the  brain  contains  the  ioillowing 
deposits  of  gray  matter  or  gangHonic  collections  of  cells — viz.,  cerebral 
cortex,  corpora  striata,  olfactory  lobes,  optic  thalami,  corpora  genicu- 
lata,  corpora  albicantia,  Luy's  body,  corpora  c[uadrigemina,  red  nuclei, 
substantia  nigra,  cerebellar  cortex,  cerebellar  nuclei,  pontile  nuclei, 
olivary  bodies,  nodal  nuclei  and  the  cranial  nuclei. 

The  processes  of  the  cell  bodies  which  enter  into  the  composition 
of  these  ganglionic  masses  make  up  three  great  groups  of  tracts  which 

FIGURE  158. 


Diagram  to  illustrate   the  association,  commissural,  and  projection  tracts   of 
the  brain. 


constitute  the  white  ^natter.  They  are  the  association  tracts,  the 
commissural  tracts  and  the  projection  tracts. 

It  now  behooves  us  to  analyze  these  ganglia  and  tracts  a  little  more 
in  detail.  I  would  again  urge  the  reader  to  note  the  great  similarity,  so 
far  in  our  account,  of  the  brain  with  the  spinal  cord. 

Cortex. — If  the  much  infolded  cerebral  cortex  were  spread  out 
smooth,  as  you  would  smooth  out  a  handkerchief,  it  would  be  a  thin 
sheet  of  gray  matter,  with  an  area  of  about  three  hundred  square  inches, 
and  a  fairly  uniform  thickness  of  about  one-tenth  or  one-twelfth  of  an 
inch.  Therefore  the  convolutions,  which,  by  the  way,  correspond  at 
the  seventh  month  with  thO'Se  of  the  adult  baboon,  are  seen,  when  the 


682 


THE  NON-NEURONIC  DISEASES 


brain  is  sliced  transversely,  to  have  a  narrow  gray  border  following 
all  of  their  changes  and  detours.  Running  through  the  middle  of  this 
gray  lx)rder,  parallel  to  its  edges,  is  a  fine  white  line.    In  the  vicinity  of 


P^'<  t#S 


FIGURE  159- 


^•.■^f-^  ' 


'if^- 


HUMAN  CEREBRAL  CORTEX. 


^1:^^^-^^^ 


1.  Central  convolution.     A,   medullary  substance;   b,  layer  of  spindle  cells;  c,   radial  bundles; 

d,  giant  pyramidal  cells;   e,   large  pyramidal  cells;   f,   stratum  of  Baillarger;   g,   small 
pyramidal  cells;   h,  tangential   fibres;   i,  pia  mater. 

2.  Occipital    lobe.      A,    medullary    substance;    b,    layer    of    spindle    cells;     c,    inner    granular 

layer;    d,   layer  of   large   pyramidal   cells;   e,   outer   granular   layer;    f,    layer   of   Vicq 
d'Azyr;   g,  small   pyramidal   cells;   h,  tangential  fibres. 

3.  Cornii    ammonis.      A,    ependyma    of    lateral    ventricle;    b,    medullary    layer    of    alveus;    c, 

layer    of    spindle    cells;    d,    large    pyramidal    cells;    e,    stratum    radiatum;    f,    layer   of 
lacunae;    g,   small  pyramidal   cells;    h,   tangential  fibres. 

4.  Fascia  dentata  Tarini.     A,  spindle  cells  and  nerve-fibres;  b,  large  pyramidal  cells;   c,   stra- 

tum  granulosum    (small   pyramidal    cells). 

(After   Benda.) 

the  calcarine  fissure  it  is  .so  distinct  that  it  can  be  seen  with  the  naked 
eye.  It  is  here  spoken  of  as  the  white  line  of  \^icq  d'Azyr.  Under  the 
microscope,  here  and  in  other  convolutions,  a  second  inner  and  finer 


THE  NON-NEURONIC  DISEASES  683 

line  can  be  seen.  It  is  known  as  the  i)i}ier  line  of  Baillarger.  These 
lines  at  once  demonstrate  to  us  that  the  cortical  gray  substance  is  ar- 
ranged in  layers.  With  a  high  power  of  the  microscope  it  is  observed 
that  the  gray  lines  represent  the  massing  of  cell-bodies,  whereas  the 
white  striae  are  caused  by  the  predominence  of  their  processes.  Five 
or  seven  different  layers  of  cells  have  thus  been  differentiated  in  the 
cortex,  and  the  effort  is  being  made  to  assign  to  them  respectively  par- 
ticular functions.  At  the  edge  of  the  cortex,  just  beneath  the  pia  mater, 
is  a  layer  of  neuroglia  with  only  a  few  small  neuronic  cells  in  it.  A 
^reat  mass  of  fibres  run  through  it  parallel  with  the  surface,  for  which 
reason  they  are  spoken  of  as  the  tangential  fibres.  Just  below  the  tan- 
gential fibres  are  the  strice  of  Bechterew  and  Kaes. 

Next  below  this  come  the  small  pyramidal  cells,  making  up  the 
nmhigiious  layer  of  Andriezen  and  the  second  general  layer,  counting 
the  layer  of  tangential  fibres  as  the  first.  The  striae  of  Bechterew  and 
Kaes  make  up  the  upper  half  of  the  second  or  ambiguous  layer.  Nu- 
merous small  round  cells  mingle  with  the  small  pyramidal  cells  of  this 
layer. 

Between  the  second  and  the  third  layers  there  is  a  superradiarv 
network.  The  third  layer  is  a  ver}-  broad  one,  presents  in  its  middle 
the  appearance  known  as  the  striae  of  Baillarger,  and  is  commonly  called 
the  large  pyramidal  cell  layer.  These  cells  are  the  largest  in  the 
cerebral  cortex,  are  most  abundant  in  the  Rolandic  area,  and  being 
triangular  or  pyramidal  in  shape,  have  their  apices  pointing  in  the 
direction  of  the  tangential  layer  and  send  off  from  their  bases  great 
long  neuraxones  which  run  to  the  lowest  depths  of  the  cortex  and  out 
into  the  underlying  white  substance.  From  the  apices  project  upwards 
long  dendrites  and  from  the  sides  shorter  dendrites.  The  cells  increase 
in  size  as  we  proceed  downward  in  this  layer,  until  we  meet  with  the 
very  largest  of  them  at  the  bottom.  Between  this  large  pyramidal 
layer  and  the  next,  or  fourth  layer  is  an  interradiary  network. 

In  the  upper  part  of  the  fourth  layer  the  cells  suddenly  appear 
small  and  spindle-shaped  and  hence  the  layer  has  been  spoken  of  as  the 
spindle  cell  layer,  or  layer  of  polymorphous  cells.  The  lower  part  of 
this  layer  assumes  a  markedly  fibrous  appearance  and  has  been  recog- 
nized as  being  made  up  of  Meynert's  intra-cortical  association  fibres. 

Immediately  beneath  the  last  and  fourth  layer  comes  the  white 
substance  of  the  brain,  made  up  largely  here  of  the  subcortical  asso- 
ciation fibres. 

To  recapitulate,  then,  the  cerebral  cortex  from  without  inward  is 
seen  to  be  made  up  of  the  four  great  layers,  the  tangential,  the  small 
pyramidal,  the  large  pyramidal  and  the  spindle-celled.  The  other  layers 
mentioned  are  mere  subdivisions  of  these.  Neurones  and  sustentacular 
tissue  are  the  constituents.  Nothing  need  be  said  further  of  these  than 
what  has  already  been  mentioned. 

The  large  cells  seem  to  be  emissive  or  motor  in  function  and  are 
most  abundant  in  the  motor  areas  ;  the  small  cells  are  probably  receptive 
or  sensory  and  are  found  more  numerous  in  the  sensory  areas.  This, 
of  course,  produces  variations  of  a  secondary  sort  in  the  appearance 
of  the  cortex.     It  is  well,  however,  to  keep  in  mind  its  more  or  less 


684 


THE  NON-NEURONIC  DISEASES 

FIGURE  1 60. 


ft -IT 


U2 


A%l 


}W 


n 


-/^ 


III 


,x 


Tangential  fibres. 


Striae  of  Bechterew  and  d» 
Kaes. 


Superradiary  network  (of  the. 
/      second  and  third  layers). 


Striae  of  Baillarger. 


^\r, 


:y<.i 


K' 


Interradlary  network  Cof  the 
third  and  fourth  layers). 


Meynert's  intracortical 
association  fibres. 


Subcortical  association 
fibres. 


Schematic   diagram   of   the   different   layers    of  the   cerebral    cortex.      (After 
Ramon  y  Cajal.) 


THE  XOX-NEUROXIC  DISEASES  685 

uniform  four-layer  appearance  and  not  to  confuse  one's  self  with  too 
fine  a  secondary  subdivision  of  it.  The  directions  in  which  the  cells 
lie,  their  shapes  and  the  minute  course  of  their  processes  are  morpho- 
logical facts  that  as  yet  have  no  special  clinical  significance. 

The  primary  fissures  in  the  cerebral  cortex  average  a  little  less 
than  an  inch  (20  to  23  mm.)  in  depth.  The  total  area  of  the  cortex, 
according  to  Donaldson's  careful  estimation,  is  2,352  sq.  cm.  Of  this 
the  frontal  lobe  has  41  per  cent. ;  the  parietal  21  per  cent. ;  the  tem- 
poral 2J  per  cent. ;  the  occipital  10  per  cent. ;  and  the  island  of  Reil 
I  per  cent.  It  is  roughly  estimated  that  the  total  area  of  gray  matter 
in  the  sulci  is  about  twice  that  on  the  surface.  After  correcting,  by 
recent  data,  the  errors  of  judgment  of  Hammaberg,  Meynert,  Wagner 
and  Donaldson,  and  supplying  what  they  had  obviously  omitted, 
Thompson  has  estimated  the  number  of  cells  in  the  cortex  to  be  9200 
millions.  This  is  about  0.23  per  cent,  of  the  number  of  cells,  by 
Francke's  estimation,  in  the  whole  human  body.  This  is  undoubtedly 
the  most  accurate  calculation  of  these  marv^elous  elements  that  has 
ever  been  made.  This  enormous  number  of  functional  nerve  cells 
makes  up  only  1.37  per  cent,  of  the  total  volume  of  the  cortex. 

These  cells  varv-  considerably  in  size.  The  small  pyramidal  and 
spinal  cells  measure  from  1-1200  to  1-600  of  an  inch.  There  are  many 
small  round  cells  no  larger  than  1-2500  in.  In  the  central  and  para- 
central convolutions  may  be  seen  the  huge  giant  cells  of  Betz,  which 
attain  the  size  of  1-500  to  1-200  in.  in  diameter.  These  various  t3'pes 
of  cells  are  believed  to  have  distinctive  functions.  In  the  second  and 
granule  layers  are  the  small  receiving  cells. 

The  spindle  cells  and  cells  of  Cajal,  nestling  partly  in  the  first  and 
partly  in  the  fourth  layer,  are  believed  to  be  associative  and  coordinat- 
ing in  function.  Tlie  large  pyramidal  cells  in  the  third  layer  are  almost 
certainly  emissive  cells.  They  resemble  the  large  motor  cells  in  the 
anterior  liorns  of  the  cord.  They  are  seen  most  abimdantly  in  the 
motor  areas  of  the  cortex,  whereas  the  smaller  cells  predominate  in  the 
sensory  areas.  A  curious  feature  of  these  large,  deeply-seated,  pyra- 
midal cells  is  that  their  dendrites  extend  upwards  a  long  distance  and 
end  in  the  tangential  layer  in  dense,  profuse  ramifications.  From  these 
small,  terminal  branches  a  series  of  minute  secondary  twigs,  each  end- 
ing in  a  little  knob,  project  laterally.  The  opportunity  is  thus  afforded 
for  countless  possible  combinations  betw^een  the  dendrites  of  the  cells, 
such  as  a  speculative  psychologist  would  have  never  dared  to  imagine. 

The  fibres  of  the  cortex  I  have  already  indicated  as  the  tangential 
and  the  striae  of  Baillarger  and  the  striae  of  Bechterew  and  Kaes.  To 
these  should  be  added  the  superradiary,  the  interradiary  layers  and  the 
intercortical  and  subcortical  association  fibres.  They  of  course  are  all 
neuraxones  from  their  respective  cells.  There  are  transverse  or  rather 
vertical  fibres  that  come  in  from  the  sensory  projection  system  and 
carry  afferent  impulses  or  pass  out  and  earn'  efiferent  impulses.  The 
association  fibres  are  both  long  and  short  and  represent  the  processes 
of  the  cells  reaching  over  to  arborize  around  the  cells  in  the  next  con- 
volution or  more  remote  parts  of  the  cortex.  The  short  fibres  pass 
around  under  the  fissures,  while  the  long  run  in  all  imaginable  direc- 


686 


THE  NON-NEURONIC  DISEASES 


tions  through  the  white  centrum  semiovale.  The  projection  processes 
that  pass  in  and  out  of  the  cortex  are  arranged  in  httle  bundles  in  such 
a  way  as  to  give  the  latter  a  columnar  appearance. 

Olfactory  Lobes. — These  are  parts  of  the  brain  and  in  structure 


FIGURE  i6i. 
Ti 


. — Section  across  the  hippocampus  major,  dentate  fissure,  dentate  fascia 
AND  fimbria  (after  Henle). 

Gh,  part  of  the  gyms  hippocampi  or  uncinate  convolution  ;  Fd,  fascia  dentata  or 
flentate  convolution  ;  between  them  is  the  dentate  fissure  ;  Fi,  fimbria,  composed  of 
longitudinal  fibres  here  cut  across  ;  1,  2,  medullary  centre  of  the  hippocampal  gyrus  pro- 
longed around  the  hippocampus,  H,  as  the  so-called  alveus,  into  the  fimbria  ;  3,  layer  of 
large  pyramidal  cells ;  4,  stratum  radiatum  ;  5,  stratum  laciniosiim  ;  6,  superficial 
medullary  lamina,  involuted  around  the  dentate  fissure  ;  **,  termination  of  this  lamina, 
the  fibres  here  running  longitudinally  ;  7,  superficial  neuroglia,  of  the  fascia  dentata  ; 
*,  stratum  granulosunj. 

reveal  the  typical  cortical  arrangement  of  the  neurones.  They  have 
been  termed  the  rhinencephalon  and  are  developed  from  a  secondary 
division  of  the  first  cerebral  vesicle.  The  olfactory  apparatus  is  a  much 
atrophied  affair  in  man.     It  includes,  when  traced  from  before  back- 


THE  NON-NEURONIC  DISEASES 


687 


wards,  the  olfactory  bulb  with  its  peripheral  processes,  the  olfactory 
tracts  and  their  lateral  roots,  with  the  gray  root  or  trigonum  between 
them,  the  hippocampal  convolution,  cornua  ammonis,  part  of  the  con- 
volution of  the  corpus  callosum,  the  nerves  of  Lancisi  and  the  anterior 
commissure.  In  addition  to  all  this  there  are  connections  between  the 
olfactory  apparatus  and  the  interbrain. 

FIGURE  162. 


Cortex  of  the  olfactory  bulb  of  the  rabbit,  showing  the  olfactory  fibres,  the 
stratum  glomerulosum.  the  bipolar  granule-cells,  the  layer  of  large  pyramidal 
cells,  the  external  granular  layer,  the  radial  fibres,  the  internal  granular  layer  and 
the  medullary  layer,  from  above  downwards.     (After  Benda.) 

The  inedulla  olfactorius,  constituting"  the  olfactory  field,  arises 
for  the  most  part  from  the  bulbus.  One  tract,  the  olfactory  bundle  to 
the  cornua  a.mmonis  ,has  been  outlined.  Another  tract  from  the  olfac- 
tory field  runs  backward  and  can  be  followed  into  the  region  of  the 
corpora  albicantia.  It  passes  through  the  ventral  regions  of  the  cor- 
pora striati,  but  receives  no  fibres  from  them.     Some  of  these  fibres 


688 


THE  NON-NEURONIC  DISEASES 


even  go  so  far  back  as  the  region  of  the  uiterpeduncular  gangha,  per- 
haps even  into  the  fillet. 

A  third  tract  starts  from  the  lateral  parts  of  the  medi-illa  olfac- 
torius  of  the  olfactor}-  field  and  passes  through  the  anterior  part  of 
the  thalami.  It  then  reaches  the  inner  surface  of  the  ventricle  and  as 
the  taeniae  thalami  ultimately  reaches  the  ganglia  habenulse.  Thus  as 
a  large  complex  of  ganglia  and  bundles,  running  through  the  greater 
part  of  the  brain,  the  olfactory  fibres  are  to  be  traced  as  far  as  into  the 
cerebral  cortex  on  the  one  hand,  and  as  far  as  the  ganglion  habenulse, 
and  possibly  the  corpus  mamillare,  on  the  other.  Other  ganglia  of  the 
midbrain  and  interbrain  stand  in  close  connection  with  these  ganglia. 

What  are  called  the  olfactory  nerves  are  the  central  processes  of 

FIGURE  163. 


—Nervous  mechanism  of  the  olfactory  apparatus,  a,  bipolar  cells  of  the  olfactory 
apparatus  (Max  Schultze's  olfactorial  ceUs)  ;  b,  olfactory  glomeruli  ;  c,  mitral  cells  ; 
D,  granule  of  white  layer  ;  e,  external  root  of  the  olfactory  tract  ;  f,  grey  matter  of 
the  sphenoidal  region  of  the  cortex  ;  a,  small  cell  of  the  mitral  layer ;  b,  basket  of  a 
glomerulus  ;  c,  spiny  basket  of  a  granule  ;  e,  collateral  of  the  axis-cylinder  process  of 
a  mitral  cell ;  /,  collaterals  terminating  in  the  molecular  layer  of  the  frontal  and 
sphenoidal  convolutions  ;  ff,  superficial  triangular  cells  of  the  cortex  :  h,  supporting 
epithelium  cells  of  the  olfactory  mucous  membrane.    (Ramon  y  Cajal.) 

the  sense  cells  of  the  olfactory  mucous  membrane  in  the  nose.  Passing 
through  the  cribriform  plate,  these  processes  decussate  repeatedly  after 
arriving  at  the  ventral  surface  of  the  bulb.  The  arborization  of  each 
process  intermingles  with  the  thick  branches  of  a  dendritic  process  from 
a  cell  above  and  thus  forms  the  complex  roundish  olfactory  glomerulus. 
The  cell  above  gives  off  other  processes  of  like  nature,  but  only  this  one 
enters  into  relation  with  the  peripheral  cell  in  the  glomerulus.  Thus 
the  pathway  of  smell  impulses  is  seen  to  consist  of  a  peripheral  or  pri- 
mary neurone  and  a  central  or  secondary  neurone.  Other  cells  have 
been  seen,  however,  in  the  cortex  of  the  olfactory  bulb,  but  their  nature 
is  still  somewhat  doubtful.  These  types  of  granular  cells,  marked  a,  b, 
c,  are  observed  in  the  accompanying  figure  lying  between  the  cells  first 
described  and  the  layer  of  meduUated  fibres. 

It  will  be  observed  that  this  illustration  of  the  cortex  of  the  bulb 
bears  a  most  striking  resemblance,  upside  down,  to  the  cortex  of  the 
cerebrum.     The  layer  of  mitral  cells,   called   so  on   account  of  their 


THE  NON-NEURONIC  DISEASES 


689 


shape,  send  up  their  neuraxones  to  become  part  of  the  olfactory  tract. 
The  granular  cells  have  no  axis  cylinders,  resemble  the  spongioblast 
cells  of  the  retina  and  are  merely  associative  in  function.  The  neu- 
raxones of  the  olfactory  tract  have  been  traced,  as  described  above,  into 
the  olfactory  field  of  the  brain. 

Corpora  Striata. — These  are  two  important  basal  ganglia  which, 
with  the  optic  thalami,  are  second  only  to  the  cortex.  They  not  only 
modify  impulses  that  pass  through  them,  but  they  probably  originate 

FIGURE  164. 


Lobus  frontalis 


Commiasura  anle 
Pars  tecta  colomnae  fori 

Caput  nuclei  cauditi 


Pars  frontalis  capsulae  mternm 
Pntanien 


Globus  pallid 


\is  corporis  callosi 
Cormi  anteniis  ventriculi  lateralis 
Cppiit  nuclei  caudati 

Pars  libera  coluiniiae  fornic 


Fascjciihis 
thalamomatuillarls 
[Vicq  d'AzyiiJ 
"Kucleus  hypothaianiicus 
(Corpus  Luysl| 
Pars  occipitalis 
capsulae  irtterna^        ^ 
Fasciculus  retro- 
flexus  [MeynertiJ  ^ 

Nucleus  ruber 

tegmenti  -  ~ 

Stratum  gri^eum 

centrals  t--^ 

Corpus  geol-  

•culatiim  mediale         " — — - 
r 
Pulvlnar  -     ^ — 

Corpora    |;=:^-. 

qnadrlgemlna 


[Gratioleti] 

Calcar  avLs 


I/**" 


Z- 


^Globus  pallidus)'"""'* 
^  Tap'iiila  externa 

<  Iau3trum 

Insula 

Fascicnhis 

-thalaniomaniillaria 

(Vicq  d'A7.yri] 

Niiclens"  \ 

niediaha    I     .    ,      , 
.,     J         >  ihalaml 

^  lateralis  j 
"^        -Niiclens  habenulat 


parietooccipital'' 
Sulcus  corporis  callosi 
lODgitudiualia  lateralis 


Horizontal  section  through  the  brain,  viewed  from  above.     In  the  left  half  of 
the  picture,  the  plane  of  section  is  about  i  cm  deeper  than  it  is  in  the  right  half. 
(After  Spalteholz.) 

subconscious  impulses  that  play  an  important  role  in  mentalization. 
Each  striate  body  is  divided  into  a  caudate  nucleus  and  a  lenticular 
nucleus.  Between  the  two  nuclei  dorsally  run  the  great  projection 
sensory  and  motor  pathways  to  and  from  the  cortex.  This  is  the  in- 
ternal capsule,  wherein  a  great  mass  of  fibres  from  widely  separated 
parts  of  the  cortex  are  closely  brought  together.  To  the  outer  side  of 
tiie  corpus  is  the  external  capsule  and  beyond  that  a  long  thin  strip  of 
:gray  matter  known  as  the  claustrum. 


690 


THE  NON-NEURONIC  DISEASES 


The  internal  capsule  is  a  part  of  the  brain  that  the  clinician  must 
keep  always  clear  in  his  memory.  As  so  many  functional  systems  con- 
verge here,  a  small  lesion  may  cause  a  wide  distribution  of  sympto 
matic  manifestations.  The  arrangement  of  the  pathways  through  it  is 
relatively  constant,  so  that  if  the  lesion  be  small  enough  to  affect  but 
one  of  them  we  could  theoretically  definitely  localize  it.  Just  behind 
the  genu  or  knee  of  the  internal  capsule  course  the  great  motor  or 
pyramidal  tracts  from  the  cortex  to  the  cord.  In  front  of  these,  and 
therefore  at  just  about  the  knee,  are  the  facial  and  hypoglossal  fibres. 
Behind  the  pyramidal  tracts,  in  what  is  called  the  tegmental  radiation, 
pass  the  sensory  fibres  with  the  pathway  from  the  occipital  to  the 
beginning  of  the  optic  nerve  most  posteriorly.    The  other  special  sense 

FIGURE  165. 


Stria  loDgitudinalis  uiediati 

Stria  longitudinalis  lateral 
i  corporis  callosi 


Caada  nQclei  caadat 
Stria  terniiiialis 
Vena  temuDalis 
Corpus  fomi' 
Stratum  zonale  thalami 
LamiDa  medutlaris  thalanii 
Nucleus  auterior  tbalami 
Nucleus  lateralis  thaJanii     — 

Nucleus  tuediaUfl  thalami  — 

Fa.sciculn9  thalamo- 
manjillaris  [Vicq  d'Azyri 
Massa  intermedia 

Capsula  interna  j 

Nucleus  lentiform 

Hypothalai 
Pedunculus  cerebri 
Tractus  opticus 

Nuclei  corpo: 


Lamina  chorioidLa 

epitbelialfs 

Pars  centralis 

ventriculi  lateralis 

Plexus  chorioideus 

uli  lateralis 

ventriculi 


Plexua  chorioideus 

ventriculi  tertii 
Tienia  thalami 


Frontal  section  through  the  middle  of  the  third  ventricle.      (After  Spalteholz.) 

paths  are  shown  clinically  as  probably  also  passing  through  this  part 
of  the  capsule. 

The  caudate  nucleus  is  anatomically  divided  into  the  head  in  front 
and  the  tail  behind.  The  tail  curves  round  the  brain  stem  and  can  be 
traced  almost  to  the  inferior  horn  of  the  lateral  ventricle.  The  head 
of  the  nucleus  is  related  to  the  gray  matter  of  the  anterior  perforated 
space.-  The  nucleus  is  in  continuation  with  the  amygdalum  of  the 
cortex  in  the  temporal  lobe,  the  claustrum  and  the  outer  part  of  the 
lenticular  nucleus. 

The.  lenticular  nucleus  is  also  in  relation  with  the  anterior  per- 
forated space.  It  is  significantly  divided  into  the  pntamen,  or  outer 
portion,  and  the  globus  pallidus,  or  inner  part.  The  putamen  and 
caudate  nucleus  enter  into  the  formation  of  the  fibre  system  of  the 
corpus  striatum  and  thus  constitute  a  rudimentary  but  biologically 
very  ancient  part  of  the  central  nervous  system.  By  a  few  association 
fibres  the  corpus  striatum  is  connected  with  the  cortex  above.  By  an 
abundant  set  of  fibres  which  originate  in  its  own  cells  it  is  brought 


THE  NON-NEURONIC  DISEASES 


691 


into  physiological  association  with  various  parts  of  its  own  substance 
and  with  parts  below  it.  The  cortical  fibres  that  pass  directly  through! 
it  have  been  already  referred  to  in  the  description  of  the  internal  cap-- 
sule.  The  nucleus  is  in  intimate  connection  with  the  corpus  sub-- 
thalamicum,  optic  thalamus,  inferior  olivary  bodies  and  cerebellum  andl 
cranial  nerve  nuclei  in  the  medulla.  The  putamen-caudate-nucleusis 
also  in  close  union,  by  means  of  connecting  fibres,  with  the  globus  palli- 
dus.     The  cells  in  this  part  of  the  brain  measure  from  1-1800  to  1-500 


FIGURE  166. 


[Vicq  d'A/yrii 
Massa 


Nucleus 
ypothalamicua. 
[Corpus  Luysi|,, 
Siibstanlia 
nigra 


Vertical  section  through  the  brain 
the  cerebrum,  a  second  cut  was  made 
view  somewhat  farther  dorsalward. 


,  viewed  from  m  front.  In  the  left  half  of 
parallel  to  the  first  and  a  plane  presented  to 
(After  Spalteholz.) 


in.  in  diamieter.     Some  of  them  are  ver}^  large  and  are  found  in  the: 
lenticular  nucleus. 

Optic  Thalami. — These  are  two  large  collections  of  nuclei  that  are" 
on  either  side  of  the  third  ventricle.  They  are  connected  by  the  middle: 
gray  commissi  ire.  They  form  part  of  the  walls  of  the  lateral  ventricles.. 
As  constituting  the  greater  part  of  the  interbrain,  the  thalami  lie  just 
behind  the  cerebrum.  Their  constituent  nuclei  are  not  sharply  sep- 
arated from  one  another.  They  are  referred  to  as  the  mesial,  lateral 
and  anterior  nuclei.  The  pulvinar  is  the  entire  posterior  part  of  the: 
thalamus  and,  like  a  tumor,  projects  into  the  ventricle.  On  the  mediani 
border  is  the  ganglion  habemdce.  Lying  against  the  ventral  and  ex- 
ternal surface  of  the  pulvinar  and  projecting  far  into  its  substance  is; 


692 


THE  XOX-XEUROXIC  DISEASES 


the  peculiar  grayish  lateral  geniculate  body.  It  gives  origin  to  many 
fibres  of  the  optic  tract.  The  thalamus  is  in  connection  with  the  corpus 
subthalamicnm,  the  red  iiucleits  and  the  corpora  albicautia  beneath  it 
and  with  the  geiuculate  bodies  postero-external  to  it.  The  corpora 
quadrigemina  are  also  in  connection  with  it. 

The  cells  of  the  optic  thalami  are  multipolar,  rather  large,  and 
loosely  grouped  together.  There  is  also  a  stellate,  small  cell.  The 
associative  Golgi  type  of  cell  is  also  found.  The  neuraxones  from 
these  cells  pass  up  to  the  cortex.  In  it  are  also  the  terminal  arboriza- 
tions of  neuraxones  of  cells  lying  in  the  cortex  above  and  in  the  sensory 
cranial  and  spinal  nuclei  below.  The  associative  cells  serve  as  the 
connecting  links  between  these  af^'erent  and  efferent  paths  that  meet 
in  the  thalamus.  Its  anatomy  indicates  that  this  ganglion  is  a  most 
important  way  station  between  a  great  mass  of  inpouring  and  out- 


FIGURE  16 


—Scheme  of  the  retinal  elements.  A,  cones  of  the  fovea  centralis  ;  B,  granules 
(nuclei)  of  these  cones ;  C,  synapse  between  the  cones  and  bipolar  cells  in  external 
molecular  layer ;  D,  synapse  between  the  bipolar  and  ganglion  cells  in  the  internal 
molecular  layer ;  a  and  h,  rods  and  cones  in  other  regions  of  the  retina  ;  c,  bipolar  cell 
destined  f6t  the  cones ;  d,  bipolar  cell  destined  for  the  rods  ;  E,  e,  ganglion  cells  ; 
/,  spongioblast;  g,  efferent  'fibre  (;  trophic;,  originating  from  the  cell  ;«,  in  geniculate 
body ;  h,  optic  nerve ;  i,  terminal  arborisations  of  optic  nerve  fibres  in  geniculate 
body;  j,  fibres  from  the  cells  of  geniculate  body  on  the  way  to  cerebral  cortex. 
(E.  y  Cajal.) 

going  impulses.  It  is  preeminently  and  first  of  all  a  great  "receiving 
station"  for  fibres  from  the  cortex  and  for  fibres  from  the  corpus 
striatum.  In  proportion  to  its  great  mass,  it  sends  an  exceeding  small 
number  of  fibres  downward. 

Optic  Tracts. — As  these  are  not  nen^es,  but  actual  tracts  of  the 
brain,  it  will  be  appropriate  to  speak  of  them  in  this  place.  The  retinal 
cells,  like  the  olfacton,-  cells  and  the  spinal  sensory  cells  in  the  posterior 
ganglia,  send  their  central  processes  in  to  unite  with  the  next  set  of 
neurones. 

The  retina  is  a  purely  nervous  structure  and  is  made  up  of  three 
layers,  which  are  subdivided  into  six.  The  three  primary  layers  are 
those  of  the  visual  cells,  the  bipolar  cells  and  the  ganglion  cells.  Each 
of  these  layers  is  divided  into  two  again,  as  follows,  layer  of  rods  and 
cones  and  external  granular  layer,  external  molecular  and  internal 
granular  layer,  internal  molecular  and  ganglionic  layer.  The  neu- 
raxones of  this  last  layer  of  cells  become  the  optic  tracts,  each  tract 
containing  about  500,000  of  them.    The  rods  and  cones  are  mereh'  the 


THE  NON-NEURONIC  DISEASES 


693 


highly  difterentiated  peripheral  processes  of  the  bipolar  cells  that  make 
up  the  external  granular  la3:er.  The  central  processes  of  these  remark- 
able peripheral  neurones  pass  inward  to  come  into  apposition,  by  means 

FIGURE  168. 


CUNEUS 


'SU  A\- 


— Diagram  of  visual  paths.  (From  Vialet,  modified.)  OP.  N.,  Optic  nerve 
OP.  C,  Optic  chiasm.  OP.  T..  Optic  tract.  OP.  R.,  Optic  radiations.  GEN.,  Genic- 
ulate body.  THO..  Optic  thalamus.  0.  QU.,  Corpora  quadrigemina.  '  C.  C.  Corpus 
callosum.  V.  S.,  Visual  speech  centre.  A.  S.,  Auditory  speech  centre.  M.  S.,  Motor 
speech  centre.  A  lesion  at  1  causes  blindness  of  that  eye ;  at  2,  bi-temporal  hemia- 
nopia ;  at  3,  nasal  hemianopia.  Symmetrical  lesions  at  3  and  3'  would  cause  bi-nasal 
hemianopia;  at  4,  hemianopia  of  both  eyes,  with  hemianopic  pupillary  inaction;  at 
5  and  6,  hemianopia  of  both  eyes,  pupillary  reflexes  normal ;  at  7,  amblyopia,  espe- 
cially of  opposite  eye ;  at  8,  on  left  side,  word-blindness. 

of  their  arborizations,  with  the  second  bipolar-cell  layer,  whose  proc- 
esses have  more  or  less  of  a  horizontal  direction.  The  ganglionic  layer 
contains  large  horizontal  cells,  which  are,  according  to  Cajal,   spon- 


694 


THE  NON-NEURONIC  DISEASES 


gioblas'ts.  There  are  in  the  retina  the  terminal  arborizations  of  cells 
embedded  in  the  optic  thalami,  corpora  geniculata  and  anterior  corpora 
quadrigemina.  These  neurones,  of  course,  carry  the  impulses  from  the 
primary  optic  centers  to  the  retina,  whereas  the  previous  cells  carry 
Xhe  impulses  to  the  optic  centers  from  the  retina. 

The  optic  tracts  partly  decussate  in  the  optic  chiasm  and  then 
•curve  backwards  around  the  crura  to  divide  into  the  lateral  and  mesial 
root  and   ultimately  terminate  in   arborizations  in   the   primary   optic 

FIGURE  169. 


— Section  THROuon  the    superior  part  of  one  of  the  superior  corpora 

QTJADRXGEMINA    AND    THE    ADJACENT    PART    OF    THE  OPTIC    THALAMUS  (after  Meyn^rt). 

s,  aqueduct  of  Sylvius  ;  gr,  grey  matter  of  the  aqueduct;  c.q.s,  quadrigeminal 
eminence,  consisting  of  :  I,  stratum  lemnisci  ;  0,  stratum  opticum  ;  c,  stratum  cinereum  ; 
Th,  thalamus  (pulvinar)  ;  c.g.i,  c.g.e,  internal  and  external  geniculate  bodies  ;  br.s, 
ir.i,  superior  and  inferior  brachia  ;  /,  fillet;  p. I,  posterior  longitudinal  bundle; 
r,  raphe ;  III,  third  nerve ;  n.  Ill,  its  nucleus ;  l.p.p,  posterior  perforated  space  ; 
s.n,  substantia  nigra  ;  above  this  is  the  tegmentum  with  its  nucleus,  the  latter  being 
indicated  by  the  circular  area  ;  cr,  crusta  ;  11,  optic  tract :  M,  medullary  centre  of 
the  hemisphere;  n.c,  nucleus  caudatus;  st,  stria  terniinalis. 


centers — namely,  the  pulvinar,  the  external  geniculate  bodies  and  the 
.anterior  corpora  quadrigemina.  In  the  latter  nuclei  these  optic  fibres 
•are  brought  into  association  with  the  oculomotor  nerve,  and  thus  is 
•explained  the  reflexes  of  the  eye.  Moreover,  these  primary  optic  cen- 
.ters  are  in  connection  with  other  cranial  nerve  nuclei  in  the  medulla. 
The  processes  of  the  cells  of  tliese  primary  optic  centers  pass 
thirough  the  extreme  posterior  part  of  the  internal  capsule  and  con- 
tinuing on  as  the  optic  radiations  of  Gratiolet  ultimately  termnate  in 
the  cortex  of  the  occipital  lobe,  chiefly  the  cuneus.  By  reason  of  the 
partial  decussation  of  the  tract  at  the  chiasm,  the  temporal  half  of  each 
retina  is  connected  with  the  occipital  lobe  of  the  same  side,  the  nasal 
llalf  with  the  lobe  of  the  opposite  side.     This  is  shown  in  the  accom- 


THE  NON-XEURONIC  DISEASES 


695 


panying  diagram  from  Malet.  The  fibres  that  connect  the  two  tracts 
behind,  running  as  a  commissure  between  the  primar}-  nuclei,  are  not 
shown  because  they  are  of  no  significance  cHnically  so  far  as  we  know. 

Regio  Suhthalamica. — This  is  a  very  compHcated  region  just  be- 
neath the  optic  thalami  and  contains  a  number  of  small  grayish  ganglia 
whose  functions  we  do  not  know  much  about.  The  nucleus  tegmenti, 
or  red  nucleus  of  the  tegmentum,  is  highly  vascular  and  rich  in  cells. 
External  to  this  lies  the  lenticular-shaped  Luys'  body  or  corpus  sub- 
thalamicum.     It  has  a  few  cells,  but  rather  abundant  plexus  of  fibres. 

Somewhat  mesial  to  Luys'  body  is  the  substantia  nigra  of  Somer- 
ing,  an  accumulation  of  grayish  pigmented  cells  of  rather  large  size. 
Dorsal  to  the  substantia  nigra  is  the  tegmentum,  or  sensory  part  of  the 

FIGURE  170. 


Ti-ac-t 


fro  a"<o  -To  nil  I  c 

Transverse  section  through  the  corpora  quadrigemina  and  cerebral  peduncles ; 
diagrammatically  represented,  to  show  the  relative  positions  of  the  prominent 
tracts. 


cerebral  peduncles,  while  ventral  to  it  is  the  pes  or  motor  part  con- 
taining the  great  fibre  system  of  the  motor  cortex  and  capsule.  As 
far  as  the  end  of  the  midbrain  can  the  substantia  nigra  be  demon- 
strated above  the  pes.  In  it  terminates  the  last  remnant  of  the  fibre 
system  from  the  corpus  striatum. 

From  the  posterior  part  of  the  red  nucleris  a  fibre  system  can  be 
traced  to  the  opposite  half  of  the  cerebellum.  This  is  an  important 
tract,  the  tractus  tegmento-cerebellaris. 

Corpora  Quadrigemina. — These  are  four  tubercles  just  behind  and 
beneath  the  optic  thalami,  two  in  front  and  two  behind.  Beneath  them 
is  the  third  ventricle  and  the  upper  end  of  the  aqueduct  of  Sylvius.  On 
top  of  them  rests  the  epiphysis  cerebri  or  pineal  gland,  which  in  some 
low  forms  of  life  has  all  the  appearance  of  an  atrophied  primitive  eye. 
It  is  sometimes  called  the  conariuui.    It  contains  solid  epithelial  tubules, 


696 


THE  NON-NEURONIC  DISEASES 


an  abundant  blood-supply  and  the  so-called  brain-sand.  This  remark- 
able structure  in  several  selachians  and  in  many  reptiles  passes  through 
a  hole  in  the  skull  to  a  sense  organ  under  the  skin.  In  this  organ  we 
can  see  a  cornea,  a  lens,  a  retina,  and  below  this  a  pigmental  layer.  In 
the  higher  forms  of  life  it  has  become  useless  and  withdrawn  into  the 
head. 

Immediately  in  front  of  the  pineal  gland  is  the  ganglion  habcnnlcc, 
which  appears  to  receive  fibres  from  the  olfactory  field  by  way  of  the 
tccnia  thalami. 

From  the  anterior  corpora  quadrigemina  arise  part  of  the  optic 
nerves.     Thus  we  see  three  ganglia  in  this  immediate  neighborhood 


FIGURE  171. 


Nucleus  arciiat 


Stratum  zonalc  thalanil 
Piilvlnar 


Stratum  griseum  collicuH  Buperiorl: 
corporum  qiiadrlgeminonim 

Stratum  zouale 


Commissura  posterior 
(cerebri] 
Stratum  gnseum 
centrale 
Aquaeductus 
cerebri  (Sylvii] 
Forniatio  reticuli 
(Nucleus  latx?ralls  superior) 

Nucleus  n.  oculomotoni 


N.  ^culoijiotorius 


t*eduDculus  cerebri 


Substantia  nigra 

Section  at  the  level  of  the  root  of  the  oculomotorius  nerve.     (After  Spalteholz.) 

serving  as  the  origin  of  the  optic  nerves — namely,  the  pulvinar,  the 
anterior  corpora  quadrigemina  and  the  external  geniculate  bodies. 
They  all  receive  fibres  from  the  occipital  lobe  which  come  by  way  of 
the  optic  radiations  and  the  posterior  part  of  the  internal  capsule. 
These  are  the  fibres  oi  Gratiolet. 

The  posterior  quadrigeminal  bodies  receive  fibres  from  the  tem- 
poral lobe.  The  great  development  of  these  posterior  bodies  in  whales 
leads  to  the  supposition  that  they  have  something  to  doi  with  the  audi- 
tory nerve,  by  way  of  the  nucleus  acusticus.  The  maintenance  of  equi- 
librium, it  must  be  remembered,  is  one  of  the  functions  probably  of  the 
semicircular  canals. 

The  anterior  lobes  of  the  quadrigeminal  bodies  picsent  a  micro- 
scopic appearance  resembling  layers  of  the  cortical  type,  ctccording  to 
Spitzka.  Outside  are  optic  tract  fibres,  then  a  thin  layer  of  small 
nerve-cells,  then  again  some  optic  fibres  and  finally  a  layer  of  a  few 
large  cells.     The  posterior  lobes  are  less  striking  in  appearance  and 


THE  NON-NEURONIC  DISEASES 


697 


merely  contain  some  small  cells  and  one  nucleus  filled  with  a  network 
of  fine  fibres.  The  two  posterior  ganglia  are  connected  by  fibres  that 
pass  over  the  aqueduct  of  Sylvius. 

Beneath  the  corpora  quadrigemina  are  the  peduncles  of  the  brain, 
the  aqueduct  of  Sylvius  separating  the  corpora  from^  the  latter.  I 
have  already  spoken  of  the  substantia  nigra  lying  in  the  middle  and 
stretching  transversely  across  each  peduncle.  The  part  above  the 
substantia  is  the  tegmenttnv.;    that  below  is  the  pes  pedunculi.     The 


FIGURE  172. 


Corpora  quadrigemina  (coUiculus  superior) 

Corpus  Pulvinar  \ 

geniculaium  mediale  \  \ 

Radix  medialiB 


lotorii 
Nucleus  n.  troehlearis 
'^'    troehlearis 
Radi: 


:scenclens 


land 


'pbali. 

nucleus   radicis 
descendentis 
-.'  trigemini 

Nucleus  moto- 

,  txig'e- 
miiii 


Portio  major  1 

unor     /  fi^""'"* 

- ^^=^     i    radicis 

lui  [internum]/ n-  facialis 
uleus  n    abducentis 
Pars  ]»nma  radicis  n  facialis 
Nucleus 
II.  facialis 
N'.  facialis 


N.  vagus 

\ N.  glosso- 

iiclei  motorii  pharyngeus 

nn.  glossopharyngei  et  vagi  (nucleus  ambi- 
guus  [lateral]  and  nucleus  dorsalis  [medial]) 
Nucleus  n.  hypoglo 


Nucleus  alae 

and  nucl' 
Ganglion 


Diagrammatic  representation  of  the  nuclei   of  origin  of  the  motor,  and  the 
primar}^  terminal  nuclei  of  the  sensory  cerebral  nerves.     (After  Held.) 

substantia  seems  to  be  in  part  the  termination  posteriorly,  in  the 
stratum  intermedium,  of  the  fibre-system  of  the  striate  body.  The 
real  function  of  the  gray  matter  we  know  nothing-  about.  The  tegmen- 
tum is  the  great  sensory  tract  and  contains  the  decussating*  fibres  of  the 
anterior  cerebellar  peduncle  which  connect  upon  opposite  sides  the 
cerebelhtm  and  the  red  nucleus  of  the  tegmentum. 

The  pes  pediincidi,  below  the  substantia  nigra,  contains  the  great 
efferent  system-fibres  from  the  cortex.  According  to  Dejerine,  the 
fibres  in  the  outer  fifth  of  it  arise  from  the  middle  part  of  the  temporal 
lobe.  The  median  fifth  fibres  come  from  the  operculum.  The  middle 
three-fifths  of  the  pes  contain  fibres  from  the  posterior  portion  of  the 


698 


THE  XOX-XEUROXIC  DISEASES 


frontal  lobe  and  the  central  convolutions.  This  is  the  pyramidal  tract, 
or  tractus  cortico-spinalis. 

Behind  the  quadrigemlnal  bodies,  in  the  central  gray  matter,  ap- 
pear the  first  of  the  cranial  nerve  nuclei — namely,  the  collection  of 
cells  along  side  of  the  aqueduct  of  S}lvius,  that  give  rise  to  the  oculo- 
motorius  nerve.  These  nuclei  deserve  special  consideration  as  local- 
ization symptoms  in  connection  with  them  are  often  vers^  definite. 

Cranial  Nerve  Nuclei. — ^These  nuclei  or  ganglionic  masses  are  in 
all  respects  the  homologues  of  the  anterior  horns  of  the  spinal  cord. 

FIGURE  173. 


Anterior  median  d'mall-  .i  Ml»Cl.'-   ^._'^.1-jZ..''-^   I  -VV^      "^^i-^'lSi!  I 


ceUed)  nucleus 


Edinger-Westphal' 8  nucleus 
[median  and  lateral  groups) 


Lateral  (large-celled)  ,'_ 
nculomolor  nucleus  '\ 


Vcmimut 


Mixed  trochlear  oculo- 
rnotor  nttcleus 


Trochlear  nucleus 


Trochlearnerve 
Post,  longitudiiwl  fascicidus 


Trochlear  decussation  in  the  L-tlwn 


Grouping  of  the  nuclei  of  the  oculomotor  region.     Schematlcborizontal  section. 
(After  Slemerling.) 

They  give  origin  to  motor  cranial  nerves  or  to  the  motor  strands  of  the 
cranial  nerves  and,  like  the  spinal  motor  cells,  preside  over  their  nutri- 
tion. They  are  to  be  found  along  the  aqueduct  of  Sylvius,  in  the  floor 
of  the  fourth  ventricle  and  in  the  deeper  parts  of  the  pons  and  medulla. 
It  may  appropriately  be  mentioned  in  this  connection  that  the 
ganglia  on  the  sensory  cranial  nen-es  are  the  homologues  of  the  gan- 
glia on  the  posterior  spinal  nerve  roots.  In  the  development  of  the 
cephalic  portion  of  the  neural  crest  in  the  embryo  there  appear  five 
pairs  of  ganglia,  which  gradually  shift  their  position  totthe  ventral  side 
of  the  brain.  They  are  the  jugular,  petrosal,  geniculate,  auditory  and 
Gasserian  ganglia.  From  them  originate  the  sensory  parts  of  the 
pneumogastric.   the   glosso-pharyngeal   and   facial   nerves,   all   of   the 


THE  NON-NEURONIC  DISEASES  699 

auditory,  and  sensory  part  of  the  trifacial.  In  all  of  these  ganglia, 
except  the  auditory,  the  cells  become  unipolar.  The  single  process  di- 
vides T-like  into  peripheral  and  central  fibres,  just  as  they  do  in  the 
posterior  spinal  ganglia.  The  central  process  assumes  all  the  appear- 
ances of  a  neuraxone ;  the  peripheral  that  of  a  modified  dendrite.  The 
auditory  ganglion  moves  backward  to  a  point  behind  the  geniculate 
ganglion.  Its  dendrites  nm  outward  to  their  termination  in  the 
acoustic  apparatus  of  the  ear.  Its  axones  penetrate  the  medulla.  The 
central  axones  of  the  other  ganglia  give  off  numerous  collaterals,  enter 
the  brain  and  divide  T-like.  They  pass  up  and  down  and  arborize 
•chiefly  in  the  terminal  nuclei  of  the  respective  nerves,  some  of  them, 
the  excito-reflex  fibres,  terminating  in  the  nuclei  of  the  motor  nerves. 

The  similarity  between  the  cranial  nerves  and  the  spinal  nerves  is 
thus  made  obvious  and  the  contention  upheld  that  the  brain  in  a  large 
measure,  at  least,  is  but  a  highly  developed  and  much  rearranged  por- 
tion of  the  serial  ganglia  that  constitute  the  entire  cerebro-spinal  axis. 

Nucleus  of  the  Motor-Oculi  Nerve. — This  nucleus  lies  in  the  floor 
of  the  aqueduct  of  Sylvius.  It  consists  of  a  number  of  subsidiary 
nuclei  that  supply  the  different  muscles  that  rotate  the  eye  ball,  that 
contract  the  pupil  and  that  elevate  the  lid.  The  nucleus  is  connected 
writh  those  of  the  fourth  and  sixth  cranial  nerves  behind,  it  by  means 
of  fibres  running  in  the  posterior  longitudinal  bundle.  It  is  also  con- 
nected with  the  optic  nerve,  but  just  how  is  still  a  matter  of  dispute. 
Some  authors  state  that  the  ocular  facial  nerve  strands  arise  in  the 
distal  part  of  the  nuclear  area  of  the  third  nerve,  though  this  is  contra- 
dicted by  Schiff,  Cassirer,  Siemerling  and  others.  In  the  third  or 
•oculomotor  nucleus  the  subsidiary  nuclei  are  arranged  somewhat  thus 
antero-posteriorly. 

Median  Line. 
Sphincter  iridis.     Musculus  ciliaris. 
Levator  palpebme.     Rectus  internus. 
Rectus  superior.     Rectus  inferior. 
Obliquus  inferior. 

The  neuraxones  from  these  little  groups  of  cells  enter  the  third 
■cranial  nerve  and  terminate  in  the  correspondingly  named  muscles. 
The  same  may  be  said  of  the  nuclei  of  the  fourth  and  sixth  cranial 
nerves  lying  still  farther  posteriorly  and  sending  their  stimulation  re- 
spectively to  the  superior  oblique  and  external  rectus  muscles  of  the 
■eye.     Note  that  the  sixth  fibres  do  not  decussate ;    all  the  others  do. 

The  posterior  longitudinal  fasciculus,  that  I  said  a  moment  ago 
-connected  the  various  subsidiary-  parts  of  the  third  nucleus,  also  in  all 
probability  connect  all  of  the  cranial  nuclei.  It  extends  much  farther 
forward  than  the  third  nucleus.  In  all  vertebrates  it  extends  from  the 
interbrain  to  the  region  of  the  anterior  columns  of  the  spinal  cord,  and 
is  thus  one  of  the  fundamental  features  of  the  brain.  In  a  way  it  be- 
longs to  the  pyramidaL system. 

Trigeminal  Nucleus. — Tlie  sensory  Hhres  of  the  fifth  cranial  nerve 
arise,  as  I  have  stated,  from  the  Gasserian  ganglion  resting  on  the 
petrous  part  of  the  temporal  bone.    The  central  ends  of  these  neurones 


700 


THE  NON-NEURONIC  DISEASES 


ramify  in  the  sensory  nucleus  of  the  preoblongata.  They  divide,  just 
hke  the  central  ends  of  the  spinal  sensory  neurones  do  in  the  columns 
of  Burdach,  into  a  descending  branch,  which  forms  the  spinal  or  long- 
root  of  the  trigeminus,  and  an  ascending  branch.  The  collaterals  from 
these  up-and-down  branches  arborize  and  ramify  in.  the  neighboring 
gray  matter,  which  is  continuous  with  the  spinal  substantia  gelatinosa 
and  surround  the  cells  therein  found.  It  is  believed  that  collaterals  also 
extend  to  the  facial  and  other  cranial  nerve  nuclei.  The  pontile  por- 
tion of  the  nucleus,  according  to  Kolliker,  is  only  the  beginning  of  the 
gray  matter.  It  is  thus  made  plain  how  the  components  of  the  fifth 
nerve  represent  the  sensory  correspondents  of  the  third,  fourth,  sixths 

FIGURE  174. 


IV  z 


— Sections  through  the  origin  op  the  foorth  nUrve  (Stilling).     ~ 

A,  transverse  section  at  the  place^of  emergence  of  the  nerve-fibres.  B,  oblique  section 
carried  along  the  course  of  the  bundles  from  the  nucleus  of  origin  to  the  place  of  emer- 
gence. ,  Aq,  Sylvian  aqueduct,  with  its  surrounding  grey  matter  ;  IV,  the  nerve-bundles 
emerging  ;  IV',  decussation  of  the  nerves  of  the  two  sides  ;  IV",  a  round  bundle  passing 
downwards  by  the  side  of  the  aqueduct  to  emerge  a  little  lower  down  j  71,  IV,  nucleus  of 
the  fourth  nerve.  /,  fillet;  s.  c.  j).,  superior  cerebellar  peduncle;  cl.V.,  descending 
root  of  the  fifth  nerve  ;  pi,  posterior  longitudinal  bundle ;  r,  raphe. 


inotor  branch  of  the  fifth,  the  seventh  and  the  twelfth  nerves.  Insteact 
of  remaining  separated  as  they  are  in  the  cord  below,  the  sensory 
paths  have  here  all  become  amalgamated  intoi  the  fifth  nerve,  while  the- 
motor  correspondents  still  remain  separated. 

It  is  believed  from  recent  investigation  that  the  proximal  part  of 
the  trigeminal  root  fibres  correspond  to  the  third  branch  of  the  nerve, 
while  the  distal  part  corresponds  to  the  first. 

The  motor  root  springs,  of  course,  from  the  large-cell  motor  nu- 
cleus. There  is  also  a  cerebral  root  to  this  nerve,  called  the  mesen- 
cephalic, because  it  has  its  origin  in  the  pregeminal  region  just  in  front 
of  the  aqueduct  of  Sylvius.     This  is  probably  a  motor  root. 

Facial  Nucleus. — This  is  a  large-cell  nucleus,  hoanologous  tO'  the 
anterior  horn  of  the  cord,  and  lies  mesially  to  the  spinal  trigeminal  in 
the  lower  part  of  the  pons.  After  joining,  the  processes  from  its  cells 
curve  in  a  bundle  around  the  sixth  nucleus  and  then  continue  obliquely 
outward  and  downward  between  the  facial  nucleus  and  the  trigeminal 
root.    The  two  facial  nuclei  are  connected  by  commissural  fibres. 

The  nerve  of  Wrisherg  has  its  origin  apparently  from  the  ganglion 


THE  NOX-NEUROXIC  DISEASES 


701 


:g-eniculi  and  is  thus  a  part  of  the  sensory  glosso-pharyngeal  root.  By 
this  nerve  the  chorda  tympani  becomes  united  with  the  glosso-pharyn- 
^eal  nerve  or  the  sohtary  fascicuhis.  Thus  is  explained  the  visceral 
iunction  of  the  facial  nerve  as  seen  in  the  taste  phenomena  related  to 
the  chorda  tympani. 

The  facial  nucleus  belongs  to  the  series  of  the  motor  nuclei  of 
the  ninth,  tenth  and  eleventh  nerves,  which  represent  the  upward 
prolongation  of  the  lateral  and  anterior  gray  matter  of  the  cord.     The 

FIGURE  176. 


Strac    lld.m 


Stc.ac, 


Str.acf 


aOS- 


Earcf 


Cross-section  through  the  medulla  at  the  height  of  the  entrance  of  the  acousiic     (Enlargement 
■  X.)     VIII^,  ventral  acoustic  nucleus;    VIII-,  dorsal  acoustic  nucleus;   A'. C,  cochlear  nerve; 
Pc,  cerebellar  peduncle  (restiform  body) ;  E.d.  VIII,  descending  acoustic  root ;  Str.ac,  acoustic  stria ; 
■CO,  cerebello-olivary  fibres,  etc.     (After  Kolliker.) 

nucleus  receives  a  cortical  stimulus  by  way  of  the  fibres  that  course 
down  through  the  anterior  part  of  the  posterior  limb  or  knee  of  the 
internal  capsule.  These  fibres  lie  in  the  crusta  to  the  inner  side  of  the 
pyramidal  tract.     They  decussate  before  reaching  the  nucleus. 


702 


THE  NON-NEURONIC  DISEASES 


THE  XOX-XEUROXIC  DISEASES 


703 


Auditory  Nuclei. — Innervating  the  cochlea  and  semicircular  canals 
of  the  internal  ear,  the  auditory  nerve  contains  fibres  that  subserve 
different  functions — namely,  hearing-  and  space-sense  appreciation,  and 
hence  has  two  sets  of  nuclei;  The  nerve  enters  the  medulla  by  the 
two  roots,  lateral  or  posterior  and  median  or  anterior.  These  roots 
are  connected  with  three  nuclei.  The  cochlear  root  processes  terminate 
and  arborize  in  the  acccssorius,  or  ventral  acoustic  nucleus  and  acoustic 
tubercle  that  lie  in  the  substance  of  the  lateral  root  and  between  it  and 


FIGURE  177. 


Nucleus  n. 
bularis  superior 

[Flechsig,  Bechtere^ 

Nucleus  D.  Testibula]_ 

medialis  [Schwalb€ 


Nucleus  arcuatu-i 
Pjrarois  [mcdullae  qblongatacf 

Section    through    the    middle   of    the    cerebellum    and    through    the    medulla 
oblongata.     (After  Flechsig  and  Held.) 


the  median  root.  The}'  are  the  pathway  of  the  auditory  impressions  and 
arise  in  the  spiral  ganglion  of  the  cochlea.  They  probably  connect 
somewhat  also  with  the  other  ganglia  or  nuclei.  The  vestibular  root 
processes  originate  in  the  ganglion  scarpae  of  the  labyrinth  and  instead 
of  hearing,  have  the  function  of  sending  coordinating  impulses  to  the 
central  organ,  particularly  the  cerebellum.  Their  central  arborizations 
are  in  the  dorsal  central  inner  nucleus  or  chief  nucleus  and  the  large 
cell  nucleus  of  Dieter  and  the  continuation  of  this  in  the  vestibular 


704  THE  NON-NEURONIC  DISEASES 

nucleus  of  Bechterew.  This  vestibular  pathway  is  not  only  continued 
up  into  tlie  cerebellum,  but  it  seems  to  run  down  towards  the  spine  in 
a  tract  which  is  a  continuation  of  the  funiculus  cuneatus  (Burdach's 
column).  It  is  known  as  the  descending  acoustic  root.  The  acoustic 
stricc  seen  running  across  the  floor  of  the  fourth  ventricle  is  a  sensory 
tract  from  the  acoustic  tubercle  that  decussates  in  the  raphe  and  con- 
tinues on  into  the  lateral  lemniscus. 

The  accessory   nucleus   sends    its   cell  processes   up   through   the 
lateral  lemniscus  to  the  posterior  corpora  quadrigemina  and  so  on  to 

FIGURE  178. 


Posterior  view  of  the  medulla  oblongata,  the  fourth  ventricle  and  the  severed 
cerebellum,  i,  fourth  ventricle;  2,  strise  acusticee;  3,  posterior  cerebellar  pedun- 
cle; 4,  fasciculus  gracilis;  5,  anterior  cerebellar  peduncle;  6,  fillet;  7,  middle  cere- 
bellar peduncle;  8,  corpora  quadrigemina.     (Aflier  Ilirschfeld  and  Leveille.) 

the  first  and  second  temporal  convolutions.  Some  fibres  pass  directly 
through  the  lemniscus  and  tegmentum  to  the  temporal  lobe  without 
going  to  the  posterior  corpora  quadrigemina.  This  nucleus  connects 
also  with  the  superior  olivary  bodies,  with  other  cranial  nuclei,  and  by 
way  of  the  acoustic  stria:  with  the  formatio  reticularis,  sensory  tract, 
posterior  corpora  quadrigemina  and  temporal  cortical  area. 

The  Dieter's  and  chief  nuclei  send  their  processes  to  the  direct 
sensory  cerebellar  tract  and  thence  to  the  red  nucleus  of  the  tegmentum 
and  the  emboliform  and  globose  nuclei  of  the  cerebellum. 

Vago-glosso-pharyngeal  Nucleus. — The  nuclei  of  the  ninth  and 
tenth  cranial  nerves  cannot  well  be  separated.  The  sensory  branches 
have  the  cell  bodies  of  their  neurones  nesting  in  their  respective 
ganglia  on  the  roots.  From  thence  the  central  processes  enter  the 
brain,  divide  T-like  and  send  one  branch  downward  and  the  other 
upward.  The  dowmward  branches  constitute  what  used  to  be  called  the 
ascending  root  of  these  nerves.  They  give  off  collaterals.  This  so- 
called  ascending  root  is  the  solitary  bundle  or  fasciculus.  It  receives 
the  central  terminations  of  the  neurones  in  the  root  ganglia  (jugular, 


THE   XOX-XEURONIC  DISEASES 


7^h 


petrosal,  plexiform,  etc.)  of  the  vagus  and  glosso-pharyngeal  nerves. 
It  sends  its  o\\ti  processes  on  up  into  the  brain.  The  motor  branches 
of  these  nerv^es  arise  from  one  common  nucleus,  the  micleus  ambiguus. 

The  accessory  branch  of  the  eleventh  or  spinal  accessor v  nerve 
arises  from  the  nucleus  ambiguus.  The  nucleus  is  probably  homo- 
logous in  some  respects  to  the  column  of  Clarke.  The  motor  branch 
of  the  spinal  accessory  nervx  arises  from  a  group  of  cells  in  the  an- 
terior horns  of  the  cervical  coid  reaching  from  the  first  nearly  to  the 
sixth  cervical  segment.  Its  representation  in  the  upper  three  segments, 
how^ever,  is  the  most  important. 

Hypoglossal  Xvcleus. — This  nucleus  is  the  homologue  of  the  an- 


FIGURE  179 


II. 


Section  of  cerebellar  cortex,  stained  by  Golgi's  method;  i.  taken  across  the 
lamina;  11.  in  the  direction  of  the  lamina;  a,  outer  or  molecular  layer;  b,  inner  or 
granular  layer  ;  c,  white  matter,  a,  Cell  of  Purkinje  ;  b,  small  cells  of  inner  layer  ;  c, 
dendrons-oi  these  cells  ;  d,  axis-cyUnder  process  of  one  of  these  cells  becoming  longitu- 
dinal in  the  outer  layer  ;  e,  bifurcation  of  one  of  these  ;  g,  a  similar  cell  lying  in  the 
■white  matter.     (Bamon  y  Cajal.) 


terior  horns  of  the  cord  and  of  the  nuclei  of  the  third,  fourth  and  sixth 
Tien^es.  It  lies  near  the  raphe  in  the  lower  part  of  the  floor  of  the 
fourth  ventricle.  Its  ceils  are  large  and  it  has  a  rich  network.  In 
some  lower  animals  the  hypoglossal  is  a  pure  spinal  nerve. 

There  are  some  minor  nodal  nuclei  and  other  small  deposits  of 
gray  matter  in  addition  to  these  to  be  found  in  the  after-brain  or 
medulla. 

The  Olivary  Bodies  are  two  large  ganglia  lying  on  either  side  of 
the  after-brain.  They  connect  with  the  cerebellum,  but  of  their  func- 
tions we  know  nothing. 

Cerebellum. — The  cerebellum  lies  beneath  the  posterior  part  of 
the  cerebrum;  consists  of  a  middle  and  two  lateral  lobes;  and  is  con- 
nected with  the  cerebrum  above  and  the  cord  below.  The  two  sides  of 
the  cerebellum  are  united  by  pontile  fibres.  In  general  structure  it  is 
not  verv  unlike  the  cerebrum.     The  vermis,  or  middle  lobe,  and  the 


7o6 


THE   XON-XEURONTC   DISEASES 


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THE   NON-NEURONIC  DISEASES 


707 


hemispheres  are  divided  into  lobes  and  lobules  and  fantasticallv  named,- 
The  gray  matter  or  cortical  layer  on  its  surface  is  so  minutely  and. 
peculiarly  folded  that  with  its  intervening  white  matter  it  gives  the- 
appearance  of  an  arbor  vitcc.  In  the  center  of  the  white  substance  is; 
the  convoluted  nucleus  called  the  corpus  dentatuni,  or  ciliary  body. 
Other  nuclei  are  the  cuiboliforju,  fastigium  and  globosus. 

Cerebellar  Cortex. — This  is  a  remarkable  arrangement  of  neu- 
rones. With  the  low  power  of  magnification  it  can  be  seen  that  there 
are  three  distinct  layers;  externally  the  sona  molecularis,  internally 
the  zona  granulosa,  and  between  the  two  the  layer  of  the  large  cells 

FIGURE  181. 


Capsola  externa         /  ^< 
Cap3ula  interna 


N    cochlear] 
Nucleus  n.  cochleans  ventrahs 
Tubcrculum  acusl 


Illustration  to  show  the   course  of  some  of  the  more   prominent   conduction- 
paths  in  the  brain.     (After  Held.) 

of  Purkinje.  '^Tliese  cells  of  Purkinje  are  among  the  largest  in  tfre^ 
nervous  system,  measuring  from  1-800  to  1-600  of  an  iach.  They  pos- 
sess also  large  round  nuclei.  Each,  cell  sends  a  neuraxone  down  into-' 
the  zona  granulosa,  on  the  way  giving  off  collaterals  that  bend  around, 
pass  upward  and  break  up  into  branches,  around  the  cell-body.  The 
dendritic  processes  are  enormousl}^  profuse  and  extend  up  toward  and 
almost  to  the  edge  of  the  cerebellum.  The  prof  useness  of  the  dendritic: 
elaboration  is  best  seen  in  a  section  made  in  the  sagittal  plane. 

Among  the  profuse  dendritic  branches  are  mingled  thick  fibres  or 


7o8 


THE   XOX-XEURONIC  DISEASES 


unknown  orig-in.  though  they  apparently  have  come  in  from  the  white 
substance  crossing  the  zona  granulosa.  Among  them  are  other,  small, 
stellate  cells,  which  send  their  processes  here  and  there  parallel  to  the 
surface  of  the  cortex  and  down  to  the  bodies  of  the  Purkinje  cells, 
which  they  surrooind  with  their  terminal  arborizations  in  such  a  basket- 
like way  that  they  have  been  called  basket-cells.  These  smaller  cells 
that  obviously  have  given  the  name  molecular  layer  to  this  outermost 

FIGURE  182. 


Illustration  to  show  the  ci.air>e  'A  the  pyramidal  tract  and  of  the  cerebro- 
pontile  paths ;  the  termination  of  the  auditory  conduction  path  and  the  indirect 
continuation  of  the  medial  lemniscus  and  the  brachium  conjunctivum  from  the 
lateral  nucleus  of  the  thalamus.     (After  Held.) 


part  of  the  cortex  serve  well  as  inter-communicating  elements  between 
the  individual  Purkinje  cells. 

The  granular  layer  is  made  up  chiefly  of  small  polygonal  cells  with 
large  nuclei,  measuring  about  1-5000  inch  in  diameter.  They  have 
short  dendrites  with  clubbed  extremities  and  a  neuraxone.  The  latter 
passes  up  to  the  molecular  layer,  where  it  divides  into  two  branches 
which  run  transversely  to  the  axis  of  the  body  of  the  cell.  There  are 
in   the  granular  layer  also  cells  of  the  Golgi   type,   large,   with   axis 


THE  XO.y-XEURONIC  DISEASES 


709 


cylinders   that    divide   and    subdivide    and    end    in   a.  finely    ramifying 
plexus. 

The  fibre  systems  of  the  cerebellum,  like  those  of  the  cerebrum, 
are  tangential  and  radiating.  The  complicated  arrangement  of  the  ele- 
ments of  the  cerebellar  cortex  and  their  character  suggest  the  possi- 
bility of  an  enormous   number  of  combinations.     Hence  it  reveals   a 

FIGCRE  183. 


Illustration  to  show  the  position  of  the  pyramidal  tract,  the  secondary  optic 
radiation,  the  fronto-pontile  path,  the  temporo-pontile  path,  the  auditory  con- 
duction path,  the  primary  optic  radiation,  the  medial  lemniscus,  the  brachium 
conjunctivum,  the  lateral  areas  of  the  formatio  reticularis,  and  the  cortical  path 
from  the  lateral  nucleus  of  the  thalamus.     (After  Held.) 

marvelous  condition  for  bringing  together  and  coordinating  and  har- 
monizing the  activities  of  a  great  many  diverse  elements.  The  large 
cells  being  so  comparatively  less  numerous  than  the  small,  we  see 
that  the  cerebellum  is  a  great  receiving  or  way  station  for  impulses 
traveling  between  the  brain  and  the  periphery.  It  adjusts  nerve  im- 
pulses and  coordinates  their  further  distribution. 


yiO  THE   XOX-NEURONIC  DISEASES 

The  Conducting  Tracts  of  the  Brain. — In  the  brain,  as  in  the  cord, 
the  same  laws  in  regard  to  the  degeneration  of  the  neurones  when 
separated  from  their  nutritive  centers  in  the  cells  hold  true.  By  this 
means  the  tracts  of  the  brain  and  the  tracts  between  the  brain  and 
cord  have  been  largely  traced.  In  our  study  oi  the  minute  anatomy 
of  the  brain  most  all  of  these  tracts  have  been  mentioned.  It  may  be 
well  to  briefly  recapitulate  them  here.  The  reader  is  also  referred  to 
the  chapters  on  the  neuronic  architecture  and  on  the  anatomy  and 
physiology  of  the  cord. 

The  calculation  has  been  made  that  onl}-  about  one-third  of  the 
brain  cortex  is  involved  in  the  projection  tracts.  The  remaining  two- 
thirds  do  not  send  processes  out  to  or  receive  processes  directly  from 
the  periphery.  Tliis  two-thirds  is  intimately  inter-connected  by  asso- 
ciation, commissural  and  other  intercalated  tracts. 

The  motor  projection  tracts  start  from  the  cells  of  the  central  con- 
volutions of  the  cortex  and  pass  down  through  the  internal  capsule  to 
the  various  cranial  nuclei  and  anterior  cornua  of  the  spinal  cord,  as 
lias  been  previously  explained.  It  is  throughout  a  crossed  tract,  though 
the  crossing  does  not  occur  at  the  same  place  for  all  parts  of  it.  The 
parts  that  pass  to  the  cranial  nuclei  we  cannot  trace  as  clearly  as 
some  other  parts,  but  we  believe  they  decussate  just  before  they  reach 
the  respective  nuclei.  Of  the  remainder  of  the  tract,  nine-tenths  of  it 
decussates  in  the  pyramidal  decussation  of  the  medulla,  and  one-tenth 
crosses  over  lower  down  in  the  anterior  commissure  of  the  cord. 

The  sensory  projection  tracts  are  more  complicated  and  less  well 
known  than  the  motor.  Those  of  the  posterior  columns  of  the  cord 
terminate  in  the  nuclei  of  the  medulla  found  at  the  top  of  these 
columns.  Thence  the  tract  continues  across  to  the  other  side  in  the 
lemniscus  or  fillet  decussation  (internal  arciform  fibres,  midolivary 
strata,  chief  lemnisctis),  and  so  on  up  to  the  cortex  directly  or  after 
interruption  in  the  optic  thalamus,  or  possibly  also  in  the  lenticular  nu- 
cleus. Another  sensory  pathway  is  the  antero-lateral,  Gowers'  column, 
the  chief  lemniscus  of  the  medulla  and  cortex  directly  or  after  interrup- 
tion. It  terminates  in  the  central  convolutions,  parietal  areas  and  gyrus 
fomicatus. 

The  tracts  from  the  soisory  cranial  nerve  nuclei,  the  nucleo-cor- 
tical  tracts,  are  very  little  known.  They  decussate  in  the  raphe  or 
perhaps  pass  through  the  chief  lemniscus. 

Many  are  the  ways  in  which  sensory  impulses  reach  the  brain,  and 
for  aught  we  know,  there  may  be  more  intermediary  neurones  than 
liave  so  far  been  described  in  each  tract. 

The  cerebellar  tracts,  the  visual  tracts  and  others  have  all  been 
.sufficiently  noted  when  describing  the  cerebellum,  optic  nerves,  etc. 

CIRCULATION  OF  THE  BRAIN. 

Before  passing  on  to  the  consideration  of  the  physiology  of  the 
"brain,  some  note  must  be  taken  of  its  circulation.  Including  the  scalp, 
the  skull  and  the  dura  mater,  the  head  and  its  contents  are  furnished 
with  blood  by  way  of  the  external  and  internal  carotids  and  the  verte- 
bral arteries,  the  latter  fcrming  the  basilar  arterv. 


f  THE   NOX-NEURONIC  DISEASES  7II 

The  external  carotid  supplies  the  outside  of  the  head,  sending  into 
the  interior  of  the  cranium  onl_v  meningeal  arteries.  Tliese  meningeal 
branches  include  the  inferior  meningeal,  the  posterior  meningeal,  the 
middle  and  small  meningeals. 

Of  all  the  meningeal  arteries  the  middle  meningeal  is  the  most 
important,  because  it  is  the  largest,  is  most  direct  in  its  communication 
between  the  outside  and  inside  of  the  skull,  and  its  area  of  distribution 
is  related  to  parts  of  the  brain  of  great  functional  significance.  The 
blood  returning  from  the  meninges  empties  into  the  diploic  veins  and 
thence  passes  to  the  lower  occipital  and  lateral  sinuses.  The  venae 
comites  carry  some  of  it. 

The  internal  carotid  has  no  branches  in  the  neck.  It  supplies  the 
interior  of  the  cranium  by  means  of  its  anterior  meningeal  branches, 
anterior  and  middle  cerebral,  posterior  comniunicating  and  anterior 
choroid  branches. 

The  basilar  artery  terminates  in  the  posterior  cerebral,  anterior, 
superior  and  inferior  cerebellar  and  posterior  meningeal  branches. 

The  inter-communication  of  tiie  branches  of  the  internal  carotid 
in  front  and  the  basilar  behind  fonns  at  the  base  of  the  brain  a  remark- 
able anastomosis  known  as  the  circle  of  Willis.  This  circle  of  Willis 
is  really  a  heptagon  and  reaches  from  a  point  in  the  longitudinal  fissure 
in  front  of  the  optic  chiasmi  back  to  the  edge  of  the  pons  Varolii.  It 
measures  about  an  inch  in  width  and  is  an  inch  and  a  half  antero-pos- 
teriorly.  Its  front  limitation  is  formed  of  the  anterior  cerebral  arteries 
that  have  just  left  the  internal  carotids  and  that  are  united  by  the 
transverse  anterior  commtinicating  artery.  Its  lateral  boundaries  are 
made  up  of  the  posterior  comniunicating  arteries  which  form  an  anas- 
tomosis between  the  internal  carotids  and  the  posterior  cerebral  arteries 
which  bound  the  circle  behind.  This  circle  of  Willis  supplies  especially 
the  midbrain  and  the  basal  structures.  The  midbrain  receives  blood 
also  from  the  superior  cerebellar  arteries. 

The  cerebral  cortex  and  white  substance,  together  with  the  pia 
mater,  receive  their  vascular  supply  from  the  large  distal  branches  of 
the  cerebral  arteries.  The  internal  ganglia  and  interbrain  are  fur- 
nished by  the  small  proximal  branches.  It  is  both  convenient  and 
physiological,  therefore,  to  discuss  the  blood  supply  of  the  cerebrum 
under  the  heads  of  the  cortical  system  and  the  ganglionic  system.  The 
choroid  system  should  also  be  taken  into  special  account. 

Cortical  System. — Entering  the  front  lower  part  of  the  longitudinal 
fissure,  after  winding  around  the  genu  of  the  corpus  callosum,  the 
anterior  cerebral  arteries  pass  backward  along  the  mesial  surface  of  the 
hemispheres  as  far  as  the  parieto-occipital  fissure.  From  each  artery 
spring  the  anterior  internal  frontal,  supplying  the  internal  orbital  con- 
volution, olfactory  bulb,  superior  frontal  and  anterior  half  of  the  mid- 
dle frontal  convolutions;  the  middle  internal  frontal  supplying  the 
corpus  callosum,  the  g}^rus  fornicatus,  marginal  gyrus  and  upper  end 
of  the  ascending  frontal  convolution  ;  and  the  posterior  internal  frontal, 
supplying  the  quadrate  lobule  and  part  of  the  superior  parietal  convo- 
lution. 

In  the  Sylvian  fissure  runs  a  most  important  artery,  the  middle 


712 


THE  XOX-XEUROXIC  DISEASES 


cerebral.  This  has  four  branches.  Of  these  the  external  and  inferior 
frontal  furnish  blood  to  the  anterior  and  posterior  orbital  and  third 
frontal  convolutions;  the  ascending  frontal  and  ascending  parietal 
carry  it  to  the  convolutions  of  the  same  name ;  and  the  parieto-temporal 
supplies  it  to  the  supra-marginal,  angular,  superior  and  middle  temporal 
gyri. 

FIGURE  184. 


The  arteries  at  the  base  of  the  brain.  (After  Monakow.)  Acera,  anterior  cerebral  artery 
Ccma,  anterior  communicating  artery ;  AFSy,  artery  of  the  Sylvian  fissure  ;  Alent,  lenticular  arterj- . 
1-5,  the  cortical  chief  branches  of  the  Sylvian  artery  ;  cp,  posterior  communicating  arterj-  Acha 
anterior  choroid  artery ;  2,  lateral  branches  of  the  posterior  communicating  artery';  Acp,  posterior 
cerebral  artery  ;  Abas,  basilar  arterj- ;  At,  temporal  artery  ;  Aocc,  occipital  artery  ,  A  cer  sap,  superior 
cerebellar  artery  ;  A  cer  med,  median  cerebellar  artery  ;  A  cer  inf,  inferior  cerebellar  artery  ,  Spa. 
anterior  spinal  artery. 

Three  cortical  branches  spring  from  the  posterior  cerebral  arteries 
and  cover  the  tentorial  area  of  the  brain.  The  occipital  goes  to  the 
cuneus  and  cortex  of  the  occipital  lobe ;  the  uncinate  supplies  the  un- 
cinate convolution  (the  hippocampal  and  lingual  areas)  ;  and  the  tem- 
poro-sphenoidal  carries  its  blood  to  the  fourth,  third  and  part  of  the 
second  temporal  gyri. 


THE  XOX-XEUROXIC  DISEASES 


713 


Ganglionic  System. — This  system  is  constituted  of  the  small  ar- 
teries of  the  circle  of  Willis  and  cerebral  arteries.  Generally  six  groups 
of  vessels  are  recognized.  Some  of  these  are  of  immense  importance 
to  the  pathologist  and  clinician. 

The  antero-median  ganglionic  arteries  originate  in  the  anterior 
cerebrals  and  the  anterior  communicating.  They  penetrate  the  lamina 
cinerea  and  a  few  of  them  supply  the  head  of  the  caudate  nucleus  and 
anterior  wall  of  the  third  ventricle. 

FIGURE  185. 
re 


MI.S, 


Lateral  view  of  the  right  hemisphere  showiDg  the  area  supplied  by  the  middle  cerebral  artery. 
(After  Monakow.)  Art.F.S.,  artery  of  the  Sylvian  fossa;  I-V,  the  five  chief  branches  of  this 
artery;  Fc,  central  fissure;  FS,  Syhian  fossa;  OP.,  interparietal  fissure;  t,  first  temporal  fissure; 
-fi--f3.  first,  second,  and  third  frontal  convolutions  ;  Sif,  supramarginal  gyrus  ;  Ang,  angular  gyrus ; 
O1-O3,  first,  second,  and  third  occipital  convolutions.  The  dotted  line  shows  the  area  supplied  by 
the  Sylvian  artery. 


The  antero-lateral  ganglionic  arteries,  making  up  the  second  and 
third  groups,  arise  from  the  middle  cerebrals  just  outside  of  the  circle 
of  Willis.  They  penetrate  the  anterior  perforated  space  and  carry 
blood  to  the  corpora  striata,  internal  capsules  and  optic  thalami.  The 
lenticulo-striafe  artery  of  this  group,  that  supplies  the  entire  striate 
body,  is  sometimes  called,  on  account  of  the  frequency  of  its  rupture, 
the  artery  of  cerebral  hemorrhage. 

The  postero-median  ganglionic  arteries  are  branches  of  the  pos- 
terior cerebral  and  posterior  communicating  arteries.  The  inter- 
peduncular structures  and  crustse  receive  their  blood  from  them  and 
after  piercing  the  posterior  perforated  lamina  they  supply  the  walls  of 
the  third  ventricle  and  the  mesial  parts  of  the  optic  thalami. 


714  THE   XOX-NEURONIC  DISEASES 

The  fifth  and  sixth  groups  are  made  up  of  the  postcro-lateral 
ganglionic  arteries.  They  spring  from  tlie  posterior  cerebral  arteries 
after  the  latter  have  wound  around  the  crura  and  are  distributed  to  the 
posterior  parts  of  th^  optic  thalami,  the  corpora  quadrigemina  and  the 
corpora  geniculata. 

These  ganglionic  arteries  do  not  anastomose  with  one  another  or 
with  other  cortical  arteries  .  They  belong  to  the  Cohnheim  type  of 
terminal  arteries.  On  account  of  the  relatively  poor  blood  supply  of 
the  brain  between  the  cortical  and  ganglionic  systemis,  this  area  is  par- 
ticularly liable  to  encephalomalacia. 

The  choroid  arteries  are  three  in  number.  The  anterior  choroids 
spring  from  the  internal  carotids,  enter  the  apices  of  the  descending 
horn  of  the  lateral  ventricles  and  supply  the  inferior  two-thirds  of 
the  choroid  plexus,  part  of  the  velum  interpositum,  the  hippocampus 
major  and  corpus  fimbriatum.  The  postero-Iateral  choroids  originate 
in  the  posterior  cerebrals  and  are  distributed  to  the  upper  third  of  the 
choroid  plexus  of  the  lateral  ventricles  and  to  the  velum  interpositum. 
The  postero-niedial  choroids  also  start  from  the  cerebral  arteries  and 
supply  the  choroid  plexuses  of  the  third  ventricle  and  its  velum  inter- 
positum. The  velum  interpositum  also  receives  branches  from  the 
superior  cerebellar  arteries. 

Veins. — The  vena  cerebri  magna,  common  vein  of  Galen,  collects 
the  blood  from  the  velum  interpositum,  the  lateral  and  the  third  ven- 
tricles. The  superior  cerebral,  medial  cerebral  and  inferior  cerebral 
veins  drain  the  surface  of  the  brain  and  empty  into  the  neighboring 
sinuses.  It  may  be  of  some  clinical  importance  to  note  that  the  in- 
ferior cerebral  veins,  on  the  tentorial  surface  of  the  brain,  empty  into 
the  petrosal  sinuses  against  the  current. 

Lymphatics  are  not  found  in  the  brain  or  cord,  but  there  are 
perivascular  lymph  spaces. 

The  pons  Varolii,  medulla  oblongata  and  cerebellum  are  supplied 
by  terminal  branches  wholly  from  the  vertebral  and  basilar  arteries. 
They  are  called  nuclear  and  radicular  arteries  and  need  no  special  de- 
scription. The  hypoglossal  nerve  root  is  furnished  with  blood  by  the 
anterior  spinal  artery ;  the  other  cranial  nerve  roots  get  their  supply 
from  branches  of  the  vertebrals.  The  olives  and  pyramids  are  supplied 
from  either  the  vertebrals  or  the  anterior  spinals.  The  restiform 
bodies  get  their  supph'  from  the  inferior  cerebellars,  which  also  send 
branches  to  the  roots  of  the  vagus,  accessorius,  spinal  root  of  the 
trigeminus  and  the  reticular  field  generally. 

PHYSIOLOGY  OF  THE  BRAIN  AND  CEREBIML  LOCALIZA- 
TION. 

The  credit  for  the  earliest  suggestion  that  the  brain  is  a  composite 
rather  than  a  single  organ  is  usually  given  to  the  phrenologist,  Gall 
(1758-1828),  whose  work  Sur  les  Fonctions  dn  Cervcau  et  siir  Cellcs 
de  Chacune  de  ses  Parties  appeared  in  1825.  M.  Farabeuf,  the  dis- 
tinguished anatomist  of  Paris,  has  discovered,  however,  a  work  by 
Joseph  Baader,  a  professor  at  Freiburg-im-Bresgau  from  1746  to  1750, 


THE  NON-NEURONIC  DISEASES 


715 


in  which  it  is  clearly  intimated  that  tlie  sensory  and  motor  functions  of 
the  brain  may  possibly  be  separated  and  localized.  The  work  is  entitled 
■Observationes  Mcdicce  IncisioniJms  Cadaveruni  Anatomicis  Illustra- 
.t(B,  was  published  separately  in  1762,  and  was  reprinted  in  Sandifort's 
Thesaurus  Dissertationiim  in  1778.  Notwithstanding  these  early  hints 
at  cerebral  localization,  the  scientitic  world  continued  to  believe  with 
Flourens  (1794- 1867)  that  all  the  faculties  occupied  the  same  place, 
that  to  perceive  and  to  will  constituted  essentially  the  same  faculty,  and 
that  this  faculty  resided  in  a  single  organ. 

The  mapping  out  of  the  brain  surface  into  sensory,  motor  and  other 
areas  is  distinctly  a  recent  advance  in  physiology;  the  explanation  of 
the  correlation  of  these  areas,  and  of  the  dependence  of  mind  upon 
brain,  is  still  an  unsolved  problem. 

The  subject  of  cerebral  localization  is  one  oi  unequal  magnitude, 
according  as  it  is  looked  at  from  the  standpoint  of  the  surgeon,  the 
physiologist,  or  the  psychologist.  In  its  consideration  the  practical 
bearings  have  been  so  generally  uppermost  it  has  happened  that  only 
those  parts  of  the  brain  have  received  the  largest  amount  of  study 
which  could  be  reached  by  the  surgeon's  knife.  Certain  superficial 
-sensory  and  motor  areas  have  been  the  most  completely  established, 
though  these  areas  probably  represent  the  coarsest  and  most  primitive 
functions  of  which  the  brain  is  capable.  It  is  obvious  that  other  and 
■deeper  parts  of  the  encephalon  play  an  important,  if  not  really  a  more 
important  role  in  the  tout  ensemble  of  brain  activity,  and  that  the  local- 
ization of  the  functions  of  these  parts  is  quite  as  much  of  a  desideratum 
scientifically  as  is  the  localization  of  the  sensory  and  motor  areas  of 
the  cortex.  The  physiologist  is  called  upon  to  explain  the  function  and 
presence  of  the  following  deposits  of  gray  matter  in  the  cranium,  the 
localization  phenomena  of  some  of  which  are  already  fairly  well 
imderstood : 

Cerebral  cortex;  olfactory  lobes;  corpora  striata  (caudate  and 
lenticular  nuclei)  ;  optic  thalami  (and  pulvinar)  ;  corpora  geniculata 
(external  and  internal);  corpora  mamillaria;  corpora  subthalamica ; 
corpora  quadrigemina  (anterior  and  posterior)  ;  epiphysis;  hypophysis; 
red  nuclei ;  substantia  nigra  ;  cerebellar  cortex  ;  cerebellar  nuclei ; 
pontile  nuclei ;    corpora  olivaria ;    nodal  nuclei ;    cranial  nuclei. 

These  gray  deposits  have  each  their  special  raison  d'etre,  and  all 
doubtless  play  their  part  in  the  sum  total  of  brain  activity.  It  is  a 
matter  of  extreme  difficulty  and  of  intense  interest  to  define  accurately 
their  functions.  The  more  exact  diagnoisis  O'f  focal  lesions  and  the 
more  rational  explanation  of  mentalization  both  call  loudly  for  a  solu- 
tion of  this  problem.  The  question  involves  more  than  that  of  making 
a  mere  surgical  diagnosis;  it  involves  the  whole  subject  of  normal  and 
abnormal  mental  and  cerebral  phenomena.  Physiology  must  here  pro- 
ceed hand  in  hand  with  psychology  and  endeavor  to  localize  the 
encephalic  seat  of  such  manifestations  as  memory,  volition,  intellection, 
imagination,  etc.,  or  at  least  the  seat  of  their  highest  manifestation. 

For  the  practical  purposes  of  diagnosis  and  surgical  interference, 
the  study  of  the  cerebral  localizations  must  include  also  certain  other 
parts  of  the  encephalic  mass,  as,  for  instance,  the  centrum  semiovale. 


7l6  THE   XOX-XEURONIC  DISEASES 

the  corpus  callosum,  the  internal  capsule,  the  crura  cerebri  and  other 
association  and  projection  tracts. 

In  discussing,  therefore,  the  cerebral  localizations  from  the  widest 
standpoint,  one  is  obliged  to  discuss  the  function,  or  functions,  of  the 
entire  encephalon,  its  psychoses  as  well  as  its  neuroses.  Only  by  such 
a  wide  discussion  can  one  hope  to  avoid  confusion  and  prevent  the 
splitting  up  of  the  theme  into  disconnected  and  irrelevant  facts.  As  our' 
knowledge  of  the  functions  of  each  part  of  the  encephalic  mass  becomes 
more  precise,  the  so-called  schools  of  localizationists  become  more  and 
more  amalgamated. 

Among  the  investigators  of  cerebral  localization  there  are  at  pres- 
ent three  schools  of  varying  degrees  of  prominence.  In  a  general 
wa}-,  it  may  be  said  that  the  English-speaking  ph3'siologists  regard  the 
sensory  and  motor  areas  of  the  brain  as  more  or  less  separate  and  dis- 
tinct, and  as  centers  for  the  direct  reception  and  emission  of  sensory 
and  motor  impulses.  The  Germans  incline  to  the  view  that  these  areas- 
are  the  centers  for  the  direct  reception  and  emission  of  nervous  im- 
pulses, but  that  they  coincide  or  more  or  less  intermingle.  The  French 
and  Italian  investigators  study  the  question  more  from  the  psycho- 
logical side,  and  place  less  stress  upon  the  separation  or  commingling- 
of  the  sensory-miOtor  areas  than  they  do  upon  the  doctrine  that  the 
cortex  is  a  general  center  for  the  representation  of  motor  and  sensory 
images.  Psychosis,  according  to  the  latter,  is  a  sensory-motor  phe- 
nomenon, and  mentalization  is  the  product  of  the  combined  activities 
of  the  sensory  and  motor  areas.  They  hold  that  the  direct  sensory- 
motor  elements  are  lower  down  than  the  cortex ;  that  impulses  of 
cerebral  origin  are  as  much  peripheral  as  are  those  starting  from  the 
skin ;  and  that  voluntary  action  is  as  much  of  a  reflex  as  is  an  ordinary 
involuntarv'  spinal  reflex.  This  of  course  is  a  mere  outline  statement 
of  the  three  view's  in  vogue. 

Before  taking  up  cerebral  localization  in  detail,  I  desire  to  empha- 
size the  fact  that  many  of  the  higher  so-called  cortical  centers  subserve 
in  some  prominent,  yet  unaccountable,  w^ay  very  complicated  psycho^ 
physical  processes.  Such  processes,  for  instance,  are  speech,  waiting, 
reading.  And  yet  these  are  doubtless  very  elementan,-  psycho-physical 
processes  in  comparison  with  those  that  probabh'  underlie  what  are 
called  imagination,  reasoning  and  general  intellectiori. 

It  has  always  seemed  to  me  to  be  a  crude  conception  of  psycho- 
logical processes  of  all  sorts  to  suppose  that  they  were  each  individually 
under  the  absolute  and  sole  control  of  certain  small  areas  in  the  cortex. 
The  sharp  differentiation  made  by  some  physiologists  between  the 
cortical  centers,  the  narrow  w^ay  in  which  they  limit  them  and  the  dis- 
tinct functions  which  they  assign  to  them,  as  though  there  were  hardly 
any  commingling  or  interconnection  between  them,  has  long  seemed  to 
me  to  be  puerile,  grossly  materialistic  and  absolutely  unwarranted  by 
any  scientific  proof  worthy  of  the  name. 

There  is  no  doubt  that  the  brain,  like  the  spinal  cord,  is  a  great 
compound  and  complex  organ.  It  has  relatively  independent  functions 
in  its  various  parts.  These  parts  and  functions,  however,  are  never 
absolutely  independent.     Their  independence  is  only   so   far  as   they 


THE   XOX-XEUROXIC  DISEASES 


717 


--subserve  the  particular  purposes  of  motion  and  sensation.  So  far  as 
we  now  know,  there  is  only  one  type  of  motor  impulse,  five  of  sensory 
impulses  which  again  are  somewhat  subdivided.  The  former  are 
■emissive,  the  latter  are  receptive.  Beyond  these  we  know  of  no  dis- 
tinct, well-defined  impulses  passing  in  or  out  of  the  brain. 

I  have  referred  to  all  of  this  elsewhere.  I  repeat  it  here  because 
I  desire  to  emphasize  the  distinction  between  these  ingoing  and  outgoing 
impulses,  and  what  is  called  psychosis.  A  psychosis  is  distinctly  not 
the  same  as  a  motor  or  a  sensory  mipulse.  A  psychosis  is  a  compound, 
■complicated  phenomenon.  Its  elements  are  motor  and  sensorv,  but  it 
itself  is  a  combination  of  elements.  A  psychosis  is,  therefore,  most 
emphatically  a  function.  The  function  is  the  interplay  and  inter- 
rningling  of  the  elementary  motor  and  sensory  elements  in  such  a  wav 
as  to  eventuate  in  the  psychosis.  If  the  basic  elements  are  normal  and 
the  interplay  is  normal,  or  according  to  commonly  accepted  standards, 
the  psychosis  will  be  normal.  If  the  basic  elements,  wholly  or  in  part, 
are  disordered,  or  if  their  inter-connections  and  inter-relationships  are 
abnormal  or  different  from  the  commonly  accepted  standards  (as  de- 
picted in  the  relative  degrees  of  intelligence,  education,  etc.),  the  psy- 
chosis will  actually  be,  or  seem  to  be,  abnormal.  This  is  a  psychological 
truth  boldly  and  briefly  stated  here  because  space  will  not  permit  of 
further  elaboration  of  it. 

The  reader  who  wishes  to  study  this  view  of  the  mind  for  himself 
is  referred  to  the  writings  of  Wundt,  the  leading  exponent  of  modem 
physiological  psychology. 

Speech,  reading  and  writing,  as  I  have  pointed  out  elsewhere,  are 
not  mere  motor  and  sensory  phenomena.  They  are  the  expression  of  a 
high  order  of  psychosis.  It  follows,  therefore,  that  they  are  not  sub- 
served alone  by  fixed  small  centers  in  the  cortex,  btxt  by  most  compli- 
cated intra-cerebral  mechanisms,  of  which  the  so-called  cortical  centers 
are  but  the  prominent  outposts,  as  it  were. 

All  statements,  therefore,  such  as  that  the  anterior  lobes  subserve 
the  higher  mental  powers ;  that  Broca's  center  regulates  motor  speech ; 
that  the  occipital  lobe  is  the  memory  center  for  visual  images,  must 
be  taken  only  relatively.  In  every  complicated  act  that  is  more  than  a 
mere  emission  of  a  motor  impulse,  or  the  reception  of  a  simple  sensory 
impulse,  in  a  word,  in  ever}'  psychic  phenomenon,  however  small  or 
vast  it  may  be,  so  long  as  it  is  psychic  and  indicates  psychic  processes, 
the  whole  brain  must  be  conceived  as  taking  a  greater  or  less  part  in 
the  process.  Psychosis  is  a  brain  function,  not  a  function  of  its  mere 
constituents. 

With  this  understanding  of  the  nature  of  what  are  called  the 
cerebral  localization  centers.  I  will  proceed  to  discuss  them  briefly  in 
detail. 

The  Cerebral  Cortex. — Local  disease  of  the  prefrontal  lobes  does 
not  give  rise  to  any  very  definite  localizing  symptoms.  It  has  been 
determined  experimentally  that  at  the  base  of  the  first  and  second 
frontal  convolutions  is  a  small  area  which  controls  the  lateral  move- 
ments of  the  head,  the  elevation  of  the  eyelids,  and  the  dilatation  of  the 
pupils.     This  has  not  been  well  established  in  man,  however.     Aside 


7i8 


THE  NON-NEURONIC  DISEASES 


from  these  areas,  the  prefrontal  lobes  are  usually  credited  with  the  ex- 
pression of  the  higher  intellectual  life.    It  has  been  observed  that  lesions 
of  these  lobes  cause  a  change  in  the  disposition  and  temperament    a 
lack  of  self-control,  undue  irritability,  loss  of  the  power  of  attention 
loss  of  memory,  general  apathy,  foolishness,  and  a  tendency  to  lauo-h 
and  cry  immoderately  without  adequate  cause.    According  to  Flechsfc 
a  delirium  of  grandeur  accompanies  irritative  lesions,  to  be  followelf 
later  on  by  a  loss  of  judgment  and  general  mental  hebetude 

Phelps  has  recently  analyzed  295  cases  of  brain  injury  "and  con- 
cludes that  the  frontal  lobes,  and  especially  the  left  frontal  lobe,  is  the-' 

FIGURE  186. 


lTjLt\l"^^'Z  "'"'t*''^f"o"  phenomena.  It  has  been  long  recos- 
mzed  hat  the  entire  left  s.de  ot  the  brain  is  superior  to  the  ritht  bSt 
.t  IS  startling  to  learn  that  we  only  think  with  our  left  frontal  obi 
Phelps  observes  that  n,  every  mstance  in  vvhieh  a  laceration  was  con 
fined  to  the  nght  lobe,  the  mental  faculties  were  unaffected  This  mav- 
explan,  some  of  the  puzzling  cases  in  which  brain  iniurv  sometimes 
profoimdly  affects  the  mind  and  sometimes  does  not  ^°'"<5t'mes 

In  calculatmg  the  degree  of  mental  deterioration,     the     observer 
must  g,ve  due  consideration  to  the  patient's  previous   nental  capStv 

prefrontal  Z^'V^wT'"'^'  "t  ^*^!^™^'^  b*'  '«-<"-  """ted'^^tW 
pretrontal  lobes.    If  the  lesion,  such  as,  for  instance,  a  tumor  increase- 

n  size  so  as  to  produce  an  irritative,  followed  by  a  destruc  ive   chano: 
be  tcompttd"l'°'"°'rK°?'  '';'  *— ™t»ned  sympton^     to 


THE  NON-NEURONIC  DISEASES 


719 


According  to  Bruns,  Oppenheim,  Bernhardt  and  others,  tumors 
of  the  frontal  lobes  cause  a  disturbance  of  equiHbrium  identical  with  the 
so-called  cerebellar  ataxia.  Moeli  and  Wernicke  had  already  made 
mention  of  this  frontal  ataxia.  A  tract  from  the  frontal  lobe  descends 
in  the  median  part  of  the  foot  of  the  cerebral  cms  as  far  as  the  nuclei 
of  the  pons.  These  nuclei  are  connected  by  fibres  running  thro-ugh  the 
middle  peduncles  with  the  cerebellar  hemisphere  of  the  opposite  side. 
Bruns,  who  was  the  first  to  call  special  attention  to  the  probable  cause 
of  this  frontal  ataxia,  argues  that  the  highest  volitional  centers  for 
the  great  trunk  musculature  send  impulses  to  the  cerebellum  by  way 
of  this  fronto-ponto-cerebellar  tract  and  thus  exercise  a  certain  voli- 
tional control  over  the  latter's  coordinating  function.  Much  uncer- 
tainty surrounds  our  knowledge  of  this  tract,  however.  Mills  declares 
that,  in  his  experience,  pure,  uncomplicated  disturbance  of  equilibrium 
resembling  cerebellar  ataxia  has  not  often  been  present  in  tumors  of 
the  frontal  lobes.  In  two  cases  of  cerebral  tumor  reported  by  Wiener, 
in  which  the  neoplasm  encroached  upon  the  frontal  lobe,  there  was 
pronounced  ataxia.  It  may  be  that  in  certain  cases  of  internal  hydro- 
cephalus in  which  there  are  a  peculiar  staggering  gait  resembling  that 
of  cerebellar  ataxia  and  an  absence  of  indications  of  pressure  in  and 
around  the  fourth  ventricle,  as  in  a  case  recently  brought  to  my  clinic, 
the  ataxia  is  due  to  pressure  upon  the  frontal  lobes  by  the  fluid  in  the 
lateral  ventricles.  Ataxia,  when  a  symptom  of  cerebral  disease,  ap- 
pears under  three  forms,  each  being  caused  respectively  by  lesions  in 
the  motor  region,  in  the  internal  capsule,  and  in  the  parietal  lobe. 

The  sensorial  areas  of  the  cortex  are  made  at  the  present  day  to 
include  the  gyrus  foniicatus  (Ferrier,  Schafer,  Horsley  and  Flechsig), 
the  hippocampal  convolution,  the  procuneus,  portions  of  the  parietal 
convolutions  (von  Monakow),  and  the  posterior  part  of  the  central 
convolutions  (Flechsig,  Hosel).  In  a  general  way  the  sensory  area 
includes  the  postero-parietal  parts  of  the  hemispheres.  This  seems  to 
be  well  established  by  pathological  observations  in  man,  as  well  as  by 
experiiTuentation  upon  animals.  It  must  be  remembered  that  Ferrier's 
observations  in  regard  to  the  centers  of  sensation  were  made  mostly 
upon  monke3's  and  the  lower  animals  and  that  focal  epilepsies,  which 
finally  terminate  in  a  general  convulsion,  indicate  that  the  human  is  far 
higher  and  more  intricate  in  structure  than  is  the  animal  brain. 

It  is  greatly  to  be  regretted  that  patients  presenting  symptoms  of 
a  lesion  in  the  motor  zone  of  the  cortex  are  not  more  frequently  and 
minutely  examined  with  regard  to  general  sensation.  In  many  of  the 
cases  of  paralysis  reported  in  literature  there  is  no  mention  whatever 
of  sensation;  and  in  others  in  which  the  attempt  has  been  made  to 
discover  the  sensibility  of  the  skin,  the  methods  adopted  have  been  so 
crude  and  unscientific,  and  the  results  obtained  so  meagre  and  indefi- 
nite, that  the  report,  in  this  respect  at  least,  is  almost  valueless.  In 
comparison  with  the  motor  tests  for  the  localization  of  a  cortical  lesion, 
sensory'  tests  will  probably  always  remain  less  efficient.  The  variation 
of  the  personal  equation  alone  is  enough  to  shake  one's  confidence  in 
sensory  symptoms ;  and  to  properly  perform  these  tests  there  must  be 
exercised  an  unusual  amount  of  patience,  shrewdness  and  insight  into 


720  THE  NON-NEUROMIC  DISEASES 

human  nature.  The  instruments  of  precision  must  be  employed  in 
every  conceivaible  manner  and  frequently  at  most  unexpected  moments. 
Unlike  the  testing  for  paralysis,  we  are  here  made  to  rely  almost  solely 
upon  the  patient  and  his  subjective  feelings.  Hence  we  must  study 
closely  the  patient's  idiosyncrasies  and  peculiar  temperament,  and  make 
due  allowance  for  his  past  experiences  and  present  intellectual  status. 
His  entire  physical  condition  must  at  the  same  time  be  taken  into 
consideration,  for  if  there  be  a  paresis  present,  for  example,  a  sensory 
response  may  be  very  materially  m.odified  by  the  inability  of  the  muscles 
to  act  and  manifest  the  appropriate  motor  response.  1  have  known  of 
erroneous  sensory  diagnoses  being  made  just  in  this  way. 

Notwithstanding  all  these  difficulties  and  drawbacks,  it  is  ex- 
tremely desirable  that  every  case  of  paralysis  be  carefully  and  accurately 
examined  for  general  sensation ;  for  our  knowledge  of  the  location  of 
the  sensory  centers  is  at  the  present  day  much  less  definite  than  that 
of  the  motor  centers.  Moreover,  the  experiments  of  the  laboratory 
seem  to  favor  the  view  that  the  sensory  areas  of  the  cortex  are  sep- 
arate and  distinct  from  the  motor  areas,  while  clinico-pathological 
data  intimate  that  they  are  identical,  or  at  least  are  partly  coincident. 

As  long  ago  as  1888,  and  as  recently  as  1894,  Dana  contributed 
two  valuable  and  exhaustive  studies  upon  the  relationship  of  the  motor 
and  sensory  areas.  Basing  his  arguments  and  proofs  upon  laboratory 
experiments  and  clinical  observations,  he  concludes  that  injuries  and 
destruction  of  the  motor  cortex  are  accompanied  by  disturbance  of 
cutaneous  and  musculo-articular  sensations.  He  holds  that  the  motor 
cortex  is  essentially  motor,  not  sensory  in  the  way  that  Bastian  holds 
it  to  be.  The  parietal  lobe  is  the  great  seat  of  sensation,  but  the  motor 
cortex  is  a  ''sensory-memory-motor  organ." 

On  the  other  hand.  Mills  reiterated  in  1902  what  he  stated  in 
1898,  that  he  believed  in  the  separate  localization  in  the  cerebrum  of  the 
representation  of  sensation  and  of  movements. 

In  regard  to  the  location  of  the  centers  for  cutaneous  sensations — 
touch,  pain,  temperature  and  even  the  sensation  commonly  kno'wn  as 
the  "muscular  sense" — many  views  have  been  advanced.  The  general 
consensus  of  opinion  holds  that  the  optic  thalamus  is  the  basal  ganglion 
for  the  reception  of  sensory  impulses  from  the  outer  world.  Luys, 
Ferrier,  von  Monakow,  Fournier  and  Crichton  Brown  so  taught,  though 
Flourens,  Longet,  Tamburini  and  Schiff  attributed  motor  functions  to 
the  ganglion.  Above  the  thalamus  the  sensory  paths  radiate  through 
the  corona  and  terminate  chiefly  in  the  cortex  of  the  parietal  and  tem- 
poro-sphenoidal  lobes.  Below  the  thalamus  the  sensory  paths  are  clear- 
ly distinguishable  from  the  motor.  Do  these  two  paths  so  unite  or 
intermingle  above  the  ganglion  as  to  terminate  in  the  same  cortical 
areas,  or  do  they  still  remain  sharply  and  wholly  apart,  one  set  (motor) 
going  to  the  central  convolutions,  the  other  set  (sensory)  turning  back 
to  end  in  the  postero-parietal  lobes? 

In  his  earlier  experiments  Ferrier  found  that  injury  to  the  hip- 
pocampal  convolution  and  cornu  ammonis  produced  loss  of  tactile  sensi- 
bility on  the  opposite  side  of  the  body.  He  therefore  located  the  center 
for  tactile  sensibility  in  the  region  of  the  hippocampus.    This  was  con- 


THE   XOX-XEUROXIC  DISEASES  72 1 

firmed  by  Yeo  in  his  experiments  upon  monkeys.  Horsley  and  Schafe: 
have  extended  the  views  of  Ferrier,  and  as  a  result  of  their  investiga- 
tions have  concluded  that  the  whole  of  the  limbic  lobe  (including  the 
callosal  and  hippocampal  regions)  preside  over  the  sensations  of  touch 
and  pain,  if  not  exclusively,  at  least  to  a  very  large  extent.  In  some  of 
their  experiments  the  loss  of  sensation  was  accompanied  by  moto*)- 
phenomena,  which  they  attributed  to  unintentional  injury  to  the  motor 
area  during  the  performance  of  the  operation.  As  opposed  to  Munk 
and  Schiff,  who  would  possibly  argue  from  this  the  identity,  in  part  at 
least,  of  the  motor  and  sensory  areas,  they  state  that  in  some  of  their 
experiments  there  was  paresis  of  the  lower  limbs,  with  anaesthesia  of 
the  upper  limbs,  and  in  others  anaesthesia  without  paralysis.  There 
seems  to  be  some  very  intimate  connection,  at  all  events,  between  the 
limbic  lobe  and  the  central  convolutions ;  for  when  we  recall  how  fre- 
quently sensory  aurfe  and  other  parsesthesise  precede  and  accompan}- 
Jacksonian  symptoms  produced  by  a  limited  lesion  in  the  motor  cortex, 
we  are  compelled  to  admit  the  extreme  intimacy,  if  not  the  identity, 
of  the  motor  and  sensory  areas.  Many  of  these  focal  lesions  do  not 
extend  deep  enough  to  involve  the  radiating  fibres  from  the  sensory 
areas  and  their  mutual  influence  must,  therefore,  be  entirely  cellular 
and  transmitted  from  one  to  the  other  by  associating'  neurones.  The 
influence  may  be  merely  of  an  inhibitory  sort,  for  clinically  the  anses- 
thesia  accompanying  such  forms  of  local  paralysis  is  never  complete, 
but  is  rather  of  the  inhibitory  type.  Brown-Sequard  gave  special  atten- 
tion to  the  extensive  inhibitory  functions  of  the  nervous  system,  and  in 
the  light  of  his  investigations  such  an  explanation  is  not  entirely  un- 
warrantable. If  the  sensor}-  and  motor  areas  were  identical,  it  would 
be  hard  to  comprehend  how  a  limited  focal  lesion  could  give  rise  to  a 
complete  paralysis  and  incomplete  anaesthesia  in  related  parts  of  the 
Ixxiy.  Both  sets  of  cortical  cells  would  presumably  be  simultaneously 
injured  and  the  anaesthesia  W'Ould  run  parallel  in  extent  and  severity 
with  the  amount  of  paralysis. 

There  is  a  suggestion  in  the  recent  observations  of  Sherrington 
and  Griinbaum  that  may  explain  the  conflict  of  views  in  regard  to 
sensation  as  a  function  of  the  central  convolutions.  These  experi- 
menters found  in  their  elaborate  examination  of  all  types  of  anthropoid 
apes  only  the  pre-central  (ascending  frontal)  convolution  to  be  motor. 
No  motor  response  was  ever  obtamed  by  stimulation  of  the  post-central 
convolution  (ascending  parietal). 

Flechsig  includes  the  post-central  convolution  m  the  tactile  radia- 
tion. 

All  that  can  be  atfirmed  positively,  then,  is  that  the  sensory  con- 
ducting tract  passes  to  a  large  extent  into  the  central  convolutions, 
though  its  sphere  of  radiation  is  to  be  found  elsewhere,  particularly  in 
the  parietal  lobes  (von  Monakow).  Some  hold  that  only  touch  and 
■  muscular  sense  are  appreciated  by  the  central  areas,  while  other  sensa- 
tions, especially  that  of  pain,  are  to  be  located  in  the  gyrus  fomicatus. 
The  stereognostic  sense  is  located  by  von  Monakow  in  the  centra!  areas, 
by  others  in  the  parietal :  but,  as  I  have  shown  elsewhere,  this  is  such 
a  complex  sense  that  it  can  hardly  be  justly  assigned  to  any  one  special 


J^T.  THE   NON-XEURONIC  DISEASES 

area.  Mills  locates  it  in  the  superior  parietal  convolution.  Tlie  parietal 
lobe  is  held  responsible  for  the  perception  of  the  muscular  sense  by 
Nothnagel,  Luciani,  j\Iills  and  others,  a  view  which  has  been  supported 
from  clinical  observations  by  Vetter,  Basset  and  von  Monakow.  As 
I  have  also  shown  elsewhere,  it  is  not  at  all  improbable  that  even  here 
in  regard  to  the  muscular  sense,  the  motor  zone  has  come  into  active 
play  and  had  much  to  do  with  the  sense  of  position.  It  is  to  be  noted 
that  Charcot  and  Pitres  doubted  the  sensory  importance  of  the  motor 
regions. 

In  regard  to  the  cortical  visual  area  there  is  still  some  dispute, 
though  speaking  generally  it  may  be  said  to  coincide  with  the  occipital 
lobe.  The  cuneus  and  the  parts  around  the  calcarine  fissure  (Hen- 
schen)  are  usually  assigned  as  its  limits.  Oppenheim  teaches  that  the 
gyrus  fusiformis  (lateral  occipi to- temporal),  lingualis  (median  occipito- 
temporal), and  first  occipital  convolution  should  probably  be  included. 
As  everybody  knows,  destruction  of  this  area  causes  bilateral  hemi- 
anopsia of  the  opposite  side.  Total  blindness  follows  extirpation  of 
both  occipital  areas.  Further  localization  of  the  visual  conceptions  of 
space,  light  and  color  is  quite  impossible,  though  there  are  many 
hypotheses  proposed.  The  angular  g}'rus  is  no  longer  regarded  as  a 
center  for  visual  sensations.  The  disturbance  of  sight  which  Ferrier 
and  others  long  ago  attributed  to  injury  of  the  gyrus  is  now  known 
to  have  been  caused  by  involvement  in  the  injury  of  the  visual  con- 
ducting paths  that  run  through  and  near  it.  It  has  been  recorded  that 
lesions  of  the  left  inferior  temporal  lobe,  the  supra-marginal  gyrus, 
cause  alexia — inability  to  read — without  disturbance  of  the  ability  to 
speak. 

The  cortical  area  for  the  sense  of  smell  has  been  localized  in  the 
gyrus  uncinatus,  as  injury  here  has  in  some  mstances  produced  anos- 
mia (Hughlings  Jackson).  In  a  case  of  anosmia  reported  by  Schafer 
and  Frey  there  was  atrophy  of  the  olfactory  tract  and  changes  in  the 
gyrus  imcinatus  and  horn  of  ammon.  The  olfactory  ajjparatus  is  much 
atrophied  in  man  as  compared  with  the  lower  animals.  From  his  com- 
parative studies  Edinger  is  led  to  assign  the  cortical  areas  for  smell 
to  the  lobus  pyriformis  and  the  cornu  ammonis.  Professor  Onodi,  of 
Budapest,  notes  that  in  a  case  of  cacosmia  there  was  found  a  tumor 
in  the  right  gyrus  hippocampi.  Hallucinations  of  smell  have  been  asso- 
ciated with  tumors  of  the  gyrus  uncinatus  and  gyrus  fornicatus,  though 
Edinger  doubts  the  power  of  the  gyrus  fornicatus  to  perceive  sensa- 
tions of  smell.  The  cacosmia  in  this  case  may  well  have  been  a  mere 
"neighborhood  symptom."  Hemorrhages,  emboli  and  tumors  of  the 
temporal  lobe  have  been  accompanied  by  loss  O'f  smell,  and  the  same 
explanation  is  probably  applicable  in  these  cases. 

The  cortical  area  for  the  perception  of  taste  has  not  yet  been  dis- 
covered. It  is  probably  near  and  closely  related  to  the  center  for  the 
sense  of  smell.  Paget  believed  that  the  perception  oi  thirst  and  hunger 
was  somehow  associated  with  the  basal  surface  of  the  temporal  lobe. 

The  center  for  hearing  is  somewhat  better  known,  and  is  generally 
accepted  as  coinciding  more  or  less  with  the  upper  convolution  of  the 
temporal   lobe — that  part  of  the  convolution,  according  to  Fleclisig, 


THE  NON-NEURONIC  DISEASES  723 

which  lies  hidden  in  the  fossa  of  Sylvius.  Ferrier  at  first  located  this 
center  positively  in  the  superior  temporal  convolution  of  monkeys.  The 
experiments  of  Brown  and  Schafer,  however,  showed  conclusively  that 
even  when  both  temporal  lobes  were  removed  there  was  no  loss  of  the 
power  of  hearing.  In  reply  to  Ferrier  and  Yeo,  these  experimenters 
remarked  that  they  had  "frequently  observed  that  monkeys  which  have 
experienced  no  cerebral  lesion  whatever  will  sometimes  fail  to  start  or 
show  any  sign  of  hearing  at  the  report  oif  a  pistol,  whilst  others  will 
react  very  strongly  to  such  a  noise."  Might  not  this  be  easily  accounted 
for  on  the  basis  of  the  association  of  ideas,  some  monkeys  having  from 
their  individual  experience  in  some  way  become  fearful  of  certain  kinds 
of  noise,  while  others,  lacking  such  experience,  remain  indifferent  to 
them?  If  such  were  the  case,  it  would  open  the  way  for  the  considera- 
tion of  the  superior  temporal  gyrus  as  a  mere  psychic  or  memory 
center  for  hearing,  and  thus  harmonize  the  two  opposing  views  of 
Ferrier  and  Yeo  on  the  one  hand,  and  of  Brown  and  Schafer  on  the 
other.  As  a  matter  of  fact,  it  is  now  pretty  generally  accepted  that 
the  superior  temporal  convolution  is  the  seat  of  mind  audition  an4 
that  its  destruction  causes  word-deafness,  and  not  sound-deafness. 
This  sensory  aphasia  literally  consists  of  a  loss  of  the  power  of  recog- 
nizing word  sounds  and  their  constructive  association.  The  victims  of 
this  form  of  aphasia  are  in  the  plight  of  one  who  is  talking  tO'  a  for- 
eigner whose  language  he  is  absolutely  ignorant  of.  When  such  a 
patient  suffers  from  a  bilateral  lesion  in  the  superior  temporal  convolu- 
tions he  is  said  to  have  "cortical  deafness." 

In  this  connection  it  is  well  to  remember  that  this  psychic  word- 
center  is  the  most  important  of  the  group  of  centers  involved  in  the 
production  of  speech.  Its  proximity  to  the  island  of  Reil  may  account, 
therefore,  for  the  fact  that  lesions  of  the  island  usually  cause  dis- 
turbance of  the  power  to  correlate  the  speech  centers,  and  thus  pro- 
duce such  symptoms  as  paraphasia,  lapsus  linguae,  defective  word  and 
sentence  forniation,  etc.  See  further  the  section  on  the  disturbances  of 
language. 

Our  knowledge  of  the  motor  areas  of  the  cerebral  cortex  is  much 
more  definite,  so  far  as  their  location  is  concerned,  than  is  our  knowl- 
edge O'f  the  sensory  areas.  The  examination  of  motor  manifestations, 
both  in  the  laboratory  experimentally,  and  at  the  bedside  clinically,  is 
susceptible  of  a  high  degree  of  accuracy  as  compared  with  the  exam- 
ination of  sensory  phenomena.  As  a  result  of  extensive  experimenta- 
tion vipon  the  lower  animals  and  of  clinico-pathological  observation  in 
man,  it  has  come  to  be  established  that  the  motor  zone  corresponds 
with  the  central  convolutions  on  either  side  of  the  fissure  of  Rolando,, 
the  adjoining  parts  of  the  frontal  and  parietal  lobes,  the  paracentral! 
lobule,  and  the  supramarginal  gyrus.  There  are  no  known  sharply 
defined  boundaries  to  this  zo^ne.  Its  center  or  rather  centers  of  maxi- 
mum energy  seem  tO'  lie  along  the  central  convolution  just  in  front  of 
the  fissure  of  Rolando.  In  comparison  with  both  anterior  and  posterior 
central  convolutions,  the  areas  of  the  frontal  and  parietal  lobes  lying; 
contiguous  to  them  play  a  minor  role.  The  experiments  made  recently 
upon  the  apes  by  Sherrington  and  Griinibaum  localize  the  motor  center 


724  THE   KOX-XEUROXIC  DISEASES 

absolutely  in  front  of  the  fissure  of  Rolando.  There  was  no  response 
of  a  motor  character  whatever  to  stimulation  of  the  post-central  (as- 
cending parietal)  convolution.  The  view  is  fast  gaining  ground  that 
there  are  no  pure  motor  centers  behind  the  Rolandic  fissure.  The  so- 
called  motor  areas  thus  indicated  control  each  the  musctUature  of  the 
opposite  half  of  the  body.  This  control  is  not  direct,  but  is  exercised 
through  certain  lower  deposits  of  gra}-  matter.  They  are  bilateral 
areas,  therefore,  and  in  both  hemispheres  subserve  the  representation  of 
definite,  and  purposive  movements  produced  by  groups  of  muscles 
rather  than  the  individual  muscles  themselves.  They  are  the  teachable 
memory  areas  for  acquired  movements.  ^Nlost  authorities  regard  them 
as  purely  motor  in  function,  while  others  look  upon  them  as  sensory- 
motor. 

Focal  lesions  of  these  areas  provoke  mo)iospas»is  and  unilateral 
convulsions,  followed  by  an  oncoming  paralysis  which  may  vary  in 
type,  according  to  the  location,  character,  and  extent  of  the  lesion.  The 
paralysis  which  succeeds  the  spasm  is  more  or  less  localized  in  extent 
and  degree.  It  is  of  the  monoplegic  type,  involving,  however,  related 
muscles  that  functionate  in  the  expression  of  particular  movements 
rather  than  the  single  muscles.  If  the  lesion  is  unlateral  and  extensive, 
the  paralysis  is  of  the  facio-brachio-crural  type,  a  true  hemiplegia. 
This  paralysis  is  accompanied  by  an  exaltation  of  the  spinal  reflexes. 
It  always  begins  in  the  same  part —  or  rather  the  spasm  that  precedes 
it — in  diflferent  attacks,  as  for  instance,  the  toes,  the  fingers,  the  face. 
The  hemiplegia  is  not  crossed,  the  face  and  body  being  affected  on 
the  same  side.  It  is,  of  course,  on  the  side  opposite  that  of  the  lesion. 
There  is  no  direct  involvement  of  the  nuclei  of  the  cranial  nerves. 
Muscles  that  usually  work  together,  as  for  instance,  those  of  degluti- 
tion and  respiration,  and  which  are  equally  represented  in  both  cere- 
bral hemispheres,  exhibit  but  little  paresis  or  ^\se  are  so  quickly  com- 
pensated for  in  the  unaftected  hemisphere  that  their  weakness  passes 
unnoticed.  The  more  complex  and  individualized  the  muscles  are  in 
their  normal  activity  the  more  will  they  be  paralyzed  ;  hence  the  upper 
extremity  shows  a  higher  degree  of  paralysis  than  the  lower.  There  is 
no  atrophy  of  the  muscles  and  the  electrical  reactions  remain  normal. 
Late  contractures  occur  in  the  parts  paralyzed. 

In  the  lower  third  of  the  central  convolutions,  just  above  the 
fissure  of  Sylvius  and  embracing  the  lower  end  of  the  Rolandic  fissure, 
are  located  the  centers  for  the  face,  the  tongue,  and  the  upper  part  of 
the  oesophagus.  Just  anterior  to  this  center,  at  the  posterior  extrem- 
ity of  the  third  frontal  convolution,  lies  Broca's  well-known  center  of 
speech,  while  behind  it  is  a  small  area  that  controls  the  movements  of 
the  larynx.  The  larngeal  muscles  are  rarely  paralyzed  as  they  work 
together  and  in  lesions  of  one  side  or  the  other  are  quickly  compen- 
sated for.  The  speech  center  is  a  bilateral  center,  but  is  only  active 
apparently  on  the  left  side  in  right-handed  people.  The  right  speech 
center  is  active  in  left-handed  people  and  can,  by  training,  be  made  to 
compensate  in  some  cases  for  loss  of  the  left  center.  These  centers 
are  called  the  memory  centers  for  the  emission  or  motor  part  of  speech, 
hence  their  disease  gives  rise  to  motor  aphasia. 


THE   XON-XEUROXIC  DISEASES  725 

Passing  upward  along  the  fissure  of  Rolando,  we  meet  seriatim 
the  centers  for  the  fingers,  the  hmid,  the  arm,  and  the  shoulder,  the 
maximum  points  of  the  centers  seeming  to  occupy  especially  the  mid- 
dle third  of  the  precentral  convolution. 

In  the  upper  third  of  the  convolutions  are  the  centers  for  the  leg, 
the  foot,  the  toes,  and  the  hallux,  the  last  being  found  close  to  the  mar- 
gin of  the  hemisphere  and  even  extending  well  over  into  the  paracen- 
tral lobule.  On  account  of  the  nearness  of  these  marginal  centers 
of  both  hemispheres  to  one  another,  paraplegic,  better  stated  as  diple- 
gic,  conditions,  are  relatively  frequent,  as  Charcot  pointed  out. 

Just  in  front  of  the  upper  part  of  the  precentral  convolution  the 
great  trunk  musculature  is  said  to  be  represented.  Horsley  and  Shafer 
locate  the  trunk  center  in  the  marginal  convolution.  Munk  believes 
that  it  lies  in  the  frontal  lobes,  while  Jackson  assigns  it  entirely  to  the 
cerebellum. 

It  must  be  remembered  that  all  of  these  centers  shade  oflf  into  one 
another  so  that  no  sharp  outline  can  be  assigned  to  any  one  of  them 
individually.  They  are  the  only  cortical  motor  areas  that  can  be  ac- 
cepted at  the  present  day  with  anything  like  positiveness  in  man.  Ex- 
periments upon  the  monkey  have  indicated  that  these  areas  may  again 
be  subdivided  and  smaller  areas  detected  for  the  representation  of  small 
and  special  forms  of  movement.  Within  the  lower  centers,  for  instance, 
we  find  clearly  represented  the  laryngeal,  masticatory  and  deglutitory 
muscles,  though  there  is  some  discussion  as  to  the  accuracy  of  all  of 
them  in  regard  to  certain  details.  Lateral  movements  of  the  head,  ele- 
vation of  the  eyelids,  and  dilatation  of  the  p!fpils  are  all  represented, 
according  to  the  observations  of  Ferrier  upon  monkeys,  in  the  posterior 
ends  of  the  first  and  second  frontal  convolutions. 

The  visceral  muscles  and  vasomotor  system  do  not  seem  to  have 
any  representation  at  all  in  the  cerebral  cortex,  though  that  hardly 
seems  possible  when  we  remember  how  the  emotions  affect  the  circu- 
lation of  the  face  and  how  even  the  viscera  are  perceived  at  times  in 
the  realm  of  consciousness.  Their  bilaterality  and  close  unity  of  func- 
tion, as  well  as  the  fact  that  all  the  organs  of  vegetative  life  are  more 
especially  under  the  control  of  the  sympathetic  nervous  system,  may 
account  for  the  lack  of  their  higher  representation  in  the  cortex.  Some 
authorities  declare  that  a  regulating  influence  upon  the  heart  and  blood 
vessels,  upon  the  heat  production  and  upon  the  visceral  nervous  appa- 
ratus is  exercised  in  the  opposite  half  of  the  body  b}'  centers  located  in 
and  near  the  central  convolutions.  These,  however,  together  with  the 
centers  for  the  bladder  and  rectum  and  for  the  trophic  regulation  of 
the  musculature  in  general,  though  supposed  to  reside  in  and  about  the 
motor  zone,  are  all  entirely  hypothetical.  Certainly  no  symptoms  in 
unlateral  disease  of  the  cerebral  cortex  have  yet  afforded  us  any  basis 
whereon  to  locate  or  even  to  assume  the  existence  of  such  centers. 

Those  who  maintain  that  the  histological  structure  of  the  central 
convolution  affords  a  clue  to  their  proper  function  reason  beyond  the 
facts.  Gowers  says,  for  instance,  that  "'it  is  instructive  to  note  that  in 
this  part  are  found  the  largest  ganglion  cells  met  with  in  the  cortex, 
cells  comparable  to,  though  exceeding  in  size,  the  certainly  motor  cells 


y2.^  THE  NON-KEURONIC  DISEASES 

of  the  anterior  cornua  of  the  spinal  cord."  On  the  other  hand,  we  find 
in  the  hippocanipal  convokition,  which  is  admitted  to  be  sensory  in  func- 
tion, pyramidal  cells  very  similar  to  those  found  in  the  central  convo- 
lutions. They  lie  just  beyond  what  is  known  as  the  stratum  radiatum. 
Furthermore,  these  large  cells  have  never  as  yet  been  absolutely  proved 
to  be  motor.  They  may  be  muscular,  in  the  sense  that  they  are  in 
immediate  connection  with  the  musculature  of  the  body  and  capable 
of  a  grosser  and  more  vigorous  form  of  activity  than  are  the  more 
delicate  receptive  sensory  cells.  Neurones,  whether  of  the  motor  or 
sensory  type,  are  all  alike  in  their  intimate  structure  so  far  as  we  know, 
and  their  exhibition  of  neurility  is  to  all  intents  and  purposes  the  same 
everywhere.  When  we  remember  that  sensation  itself  is  but  a  mode 
of  motion,  we  can  understand  that  these  giant-cells  may  differ  from  the 
smaller  ones  in  degree  rather  than  in  kind.  The  reflex  character  of 
most  of  the  sensory-motor  phenomena  would  seem  to  indicate  that  both 
sets  of  neurones  possess  the  faculty  of  receiving  and  emitting  nervous 
impulses  and  it  is  hard  to  escape  the  conclusion,  therefore,  that  the 
essential  differences  in  their  functions  are  the  result  of  the  nature  of 
the  terminal  end-organs  with  which  they  are  respectively  connected. 
As  an  essential  part  of  the  neurone  doctrine,  it  is  now  taught  even 
more  emphatically  than  heretofore  that  the  terms  sensory  and  motor 
as  applied  to  the  nervous  elements  have  more  regard  to  their  peri- 
pheral end-organs  than  to  their  innate  structure  or  even  to  their  cen- 
tral connections. 

Physicists  are  resolving  all  phenomena  into  molecular  motion,  the 
differences  in  the  phenomena  into  the  different  forms  of  molecular 
motion.  Light,  heat,  electricity  are  but  the  expression  of  the  differ- 
ent modes  of  movement  among  the  molecules  of  matter.  Nervous 
activity  has  not  infrequently  been  likened  to  electricity,  but  whether 
the  comparison  be  true  or  not,  it  is  more  probable  that  the  former  is 
as  much  a  mode  of  molecular  motion  as  is  the  latter.  Chemical  changes 
accompany  both  and  chemical  changes  are  the  result  of  atomic  trans- 
formations. Both  sensory  and  motor  phenomena,  nervous  as  well  as 
muscular,  are  alike  the  result  of  molecular  movements.  The  simple 
muscular  contractions  are  recognized  as  the  direct  expression  of  mole- 
cular vibrations  within  the  muscular  elements  and  the  reflex  circle, 
beginning  in  a  peripheral  irritation,  running  through  the  center  from 
sensory  to  motor  cell  and  finally  passing  out  again  to  terminate  in  gross 
muscular  contractions,  is  simply  the  transmission  of  the  same  molecu- 
lar disturbance,  differing  in  degree,  but  not  in  kind,  throughout  the 
various  parts  of  the  arc.  This  is  so  universally  accepted  now  by  science 
that  its  reiteration  seems  almost  like  a  truism,  but  for  my  present  pur- 
pose of  showing  the  universality  of  the  one  phenomenon  needs  to  be 
repeated.  If  the  reader  cares  to  pursue  this  hne  of  thought  further,  he 
may  consult  Gowers'  admirable  little  brochure  entitled.  The  Dynamics 
of  Life,  in  which  the -author  most  elaborately  and  convincingly  eluci- 
dates the  fact  that  all  neuro-muscular  phenomena  are  but  the  mani- 
festation of  chemical  phenomena  and  that  these  phenomena  are  but  the 
expression  of  atomic  and  molecular  motion,  the  origin  of  which  motion 
is  to  be  attributed  primarily,  so  far  as  we  are  capable  of  knowing,  to 


THE  NON-NEURONIC  DISEASES  •J2.J 

the  solar  influence  through  Hght  and  heat.  Nay,  more.  Even  the 
higher,  psychic  manifestations  of  nerve  force  can  be  reduced  by  analy- 
sis to  real  or  representative  movement,  even  the  gross  muscular  move- 
ments, as  has  been  well  pointed  out  by  Romanes  in  his  Mental  E-voln- 
tion  in  Animals. 

The  most  positive  knowledge  we  possess  in  regard  to  the  functions 
of  the  cortex  is  that  the  central  convolutions  somehow  preside  over 
the  movements  of  the  body.  And  yet,  as  Gowers  says,  "We  need  noi 
conceive  that  these  parts  subserve  no  other  function  (we  shall  pi€S- 
ently  see  reason  for  believuig  that  they  have  sensory  as  well  as  motor 
functions)."  Injury  to  these  convolutions  produces  spasm  or  paraly- 
sis ;  and  so  far  as  we  know,  these  symptoms  are  not  produced  by  cor- 
tical lesions  outside  of  these  convolutions  or  their  immediate  neigh- 
borhood. That  these  are  not  the  only  centers  which  preside  over  vol- 
untary movements  is  to  be  inferred  from  many  experiments  upon  ani- 
mals. A  rabbit  whose  entire  cerebrum  has  been  removed  can  still 
run ;  and  according  to  Goltz,  there  was  no  complete  paralysis,  but  only 
a  slight  anaesthesia  observed  in  a  dog  whose  whole  brain  except  one 
occipito-parietal  lobe  was  excised. 

It  is  an  old  established  fact  that  removal  of  the  cerebral  hem- 
ispheres, olfactory  ganglia,  optic  lobes,  corpora  striata,  and  optic 
thalami  does  not  eventuate  in  the  loss  of  voluntary  motion  and  gen- 
eral sensibility.  There  is  loss  of  intelligence  and  of  rational  inhibi- 
tion, but  the  animal  still  executes  purposive,  instinctive  movements 
which  are  quite  different  from  the  simple  reflex  acts  depending  upon 
the  spinal  cord.  Hence  arises  the  question,  what  is  the  nature  of  these 
disturbances  of  voluntary  motion  caused  by  the  destruction  of  the  cor- 
tical motor  areas?  A  dog  deprived  of  h'is  two  sigmoid  gyri  does  not 
manifest  motor  paralysis,  if  by  that  term  is  meant  absolute  loss  of 
motility.  There  is  not  a  single  physiologist  who  denies  such  an  ob- 
servation ;  hence  the  ground  for  the  criticisms  of  Goltz,  the  distin- 
guished opponent  of  the  localization  theories.  The  motor  areas  must 
preside  therefore  in  some  special  way  over  the  muscular  apparatus  and 
not  directly,  as  at  first  seemed  to  be  the  case.  In  1876  Hitzig  spoke  of 
the  ef^'ects  of  cortical  lesions  in  the  motor  area  as  "the  expression  of 
an  abnormal  representative  action;"  in  other  words,  as  the  result  of 
a  destruction  of  the  motor  images  belonging  to  certain  voluntary 
movements.  The  muscles  of  the  animal  are  not  paralyzed,  but  the 
animal  no  longer  possesses  the  mental  pictures  or  ideal  representations 
of  the  movements  it  should  make  or  desires  to  make. 

Nothnagel  and  Bastian  favor  the  theory  of  Plitzig,  but  they  differ 
from  him  in  locating  a  center  for  the  "muscular  sense"  outside  of  the 
central  lobules.  The  former  declared  to  the  Sixth  Congress  for  Internal 
Medicine,  held  at  Wiesbaden,  that  he  had  never  known  focal  lesions 
of  the  motor  zone  to  produce  loss  of  the  muscular  sense,  but  that  such 
lesions  were  often  accompanied  by  loss  of  the  tactile  sense.  In  a 
paper  published  in  Medicine  I  suggested  that  the  so-called  "muscular 
sense"  is  but  a  differentiated  expression  of  the  tactile  sense.  Noth- 
nagel places  the  sensory  area  in  the  parietal  lobes,  where  he  also  lo- 
cates, with  Seguin,  the  special  center  for  the  muscular  sense..     Noth- 


728  THE   NON-NEURONIC  DISEASES 

nagel  further  affirms  that  the  parietal  lobes  bear  the  same  relationship 
to  the  central  and  paracentral  lobules  that  the  convolution  or  area  of 
Broca  bears  to  the  cortical  hypoglossal  and  laryngeal  motor  areas.  In- 
jury to  the  parietal  centers  may  produce  ataxia  without  true  paralysis, 
and  injury  to  the  central  areas  may  cause  paralysis  without  the  loss 
of  the  muscular  sense.  This  is  somewhat  of  a  return  to  the  limitation 
views  of  Ferrier  as  originally  propounded  ;  and,  in  fact,  both  Nothnagel 
and  Charcot  separate  the  motor  areas  from  the  centers  for  cutaneous 
and  muscular  sensibility.  For  Charcot,  however,  the  cortical  motor 
centers  are  the  seat  of  motor  representations  or  conceptions  which 
must  necessarilv  precede  the  accomplishment  of  any  conscious  volun- 
tary movement,  while  the  muscular  sense  or  kinsesthesic  sensibility  of 
Bastian  is  subserved  by  the  cortical  centers  for  sensation. 

According  to  Schifif,  the  so-called  motor  areas  are  entirely  sen- 
sory ;  their  activity  is  largely  of  the  nature  of  a  reflex ;  and  the  paraly- 
sis due  to  their  destruction  is  really  the  result  of  the  loss  of  tactile  sen- 
sibility. Munk  does  not  believe  that  these  centers  determine  move- 
ments directly  or  in  any  sort  of  reflex  manner,  but  merely  by  the  awak- 
ening of  the  mental  images  or  representations  of  both  general  sensi- 
bility and  motility.  These  ideational  centers  are  not  in  immediate 
connection  with  the  individual  muscles,  nor  do  they  exert  their  in- 
fluence directly  for  their  individual  activity.  As  Dr.  Theodore  W. 
Fisher  tersely  puts  it,  "The  will  can  only  control  and  the  mind  is  only 
conscious  of  movement  in  the  mass."  The  fact  that  stimulation  of 
certain  areas  of  the  cortex  produces  movement  of  certain  groups  of 
muscles  and  eventuates  in  the  coordinated  movements  of  the  segments 
of  the  limbs  shows  that  movements,  and  not  muscles  are  represented 
in  the  cortex.  Many  of  the  opponents  of  Ferrier  have  lost  sight  of. 
this  fact  because  this  investigator  insisted  so  strenuously  upon  the  ana- 
tomical distinction  and  separation  of  the  sensory  and  motor  areas,  and 
upon  the  sharp  limitations  of  the  latter  to  the  central  lobes. 

Munk's  theory  is  popular  in  Germany  and  makes  the  so-called 
motor  areas  almost  entirely  sensory.  The  activity  of  these  centers 
results  in  "conceptions  of  movements"  rather  than  in  movements  them- 
selves. They  are  the  psychical  source  of  the  impulses  which  farther 
down  the  tract  (possibly  in  the  basal  ganglia  or  anterior  cornua  of 
the  cord)  are  transformed  into  the  true  motor  stimuli  that  set  the  mus- 
cles into  action.  The  cortical  motor  area  is  therefore  named  by  Mimk 
the  "Sense-sphere"  (Filhlsphdre).  Cowers'  objection  to  this  theory 
is  that  the  "sense  of  innervation,"  an  element  of  the  threefold  "con- 
ception of  movement,"  is  a  sense  of  something  which  is  not  itself  sen- 
sory and  which  is  commonly  termed  motor  and  that  destruction  of  this 
region  causes  loss  of  this  "motor"  function  out  of  all  proportion  to  any 
demonstrable  sensory  loss.  The  first  of  these  objections  seems  inade- 
quate to  me ;  for  it  is  a  fact  as  Strieker  and  others  have  shown  that 
movements  are  preceded  by  psychical  representations,  which  representa- 
tions must  obviously  be  of  a  sensory  character.  Franck  inclines  to 
the  theory  of  a  reflex  action  being  the  essential  function  of  the  motor 
areas.  He  believes  that  the  motor,  like  the  sensory,  zones  are  only 
the  points  of  departure  for  voluntary  motor  impulses  while  the  true 


THE   NON-NEURONIC  DISEASES  ']2'^ 

motor  apparatus  or  executive  centers  are  to  be  found  in  the  cellular 
elements  of  the  medulla  oblongata  and  spinal  cord.  All  of  the  cortical 
areas,  according  to  this  author,  are  merely  centers  of  voluntary  asso- 
ciation. We  know  that  the  sensory  ,and  motor  elements  of  the  cortex 
are  united  by  associating  tracts,  just  as  they  are  lower  down  in  the 
cord,  to  complete  the  reflex  arcs.  The  reflex  phenomena,  both  spinal 
and  cerebral,  necessarily  presuppose  such  a  functional  union  of  the 
sensory  and  motor  radicles.  This  it  seems  to  me  is  quite  adequate  to 
explain  the  occasional  association  of  the  two  sets  of  symptoms  when, 
the  lesion  happens  to  be  limited  to  one  or  the  other  area. 

Formerly  all  reflex  functions  were  supposed  to  belong  exclusively 
to  the  spinal  cord ;  but  to-day  we  consider  the  cerebral  centers  as  much 
the  centers  for  reflex  action  as  are  the  spinal.  Many  of  the  Jacksonian 
epilepsies  are  undoubtedly  of  simple  reflex  origin.  Mills  reported  a 
case  in  1880,  clearly  Jacksonian  in  type,  in  which  there  had  been  seiz- 
ures for  eleven  years  as  the  result  of  a  fibroma  in  the  hand.  When 
the  tumor  was  excised,  the  epileptic  seizures  ultimately  disappeared. 
'Tn  the  normal  brain,"  Mills  writes,  "no  reflex  actions  can  be  performed 
without  exciting  to  action  secondary  volitional  movements,  which  no 
longer  require  the  stimulating  influence  of  a  reflex  action."  The  ab- 
sence of  gross  cortical  lesions  in  some  forms  of  Jacksonian  epilepsy, 
and  Heidenhain's  experiments  in  hypnotism,  with  other  observations 
and  facts,  all  prove  conclusively  the  refl.ex  function  of  the  cortical  areas 
of  the  brain. 

Franck  speaks  of  them  as  psychomotor  centers,  because  they  con- 
trol by  their  psychical  influence  the  true,  lower  motor  apparatus.  He 
says  that  "in  examining  the  movements  produced  by  the  excitation  of 
points  under  the  control  of  the  cerebral  cortex,  they  may  be  regarded 
as  analogous  to  reflex  movements ;  but  the  essential  difference  between 
the  movements  so  started  and  the  ordinary  reflexes  consists  in  the  point 
of  departure  of  the  original  impulse.  In  one  case  it  is  cerebral,  in  the 
other  cutaneous ;  but  in  every  case  it  is  peripheral  in  relation  to  the 
center  of  motion  (medullary  centers)."  Strictly  speaking,  then,  the 
pyramidal  tracts  transmit  afferent  and  not  efferent  impulses  to  the 
motor  cells  of  the  cord  and  medulla.  Marique  adopts,  in  part,  this 
reflex  theory  as  explanatory  of  the  functions  of  the  cortical  motor 
areas;  for  he  found  that  simple  sq>aration  of  the  motor  from  the 
sensory  areas,  as  a  result  of  cutting  the  associating  tracts,  produced 
the  same  form  of  paralysis  as  when  the  cortical  motor  areas  themselves 
were  removed.  He  concluded,  therefore,  that  the  motor  areas  could 
not  act  of  themselves,  but  that  functionally  they  were  dependent  upon 
the  impulses  transmitted  to  them  from  the  sensory  areas  of  the  parieto- 
occipital region.  This  question  is  far  from  being  settled,  however,  since 
such  varying  results  have  been  obtained  in  the  experiments  of  Franck 
and  Pitres,  Marique,  Vareth,  Exner  and  Paneth. 

According  to  Soury,  Lisso  has  collected  since  1882  some  eighty- 
eight  cases  in  which  there  was  disturbance  of  sensation  when  the  lesion 
was  confined  to  the  motor  area.  Hence  Tripier  and  Gilbert  Ballet  have 
named  the  cortical  area  the  "sensitive-motor  zone."  Exner  adnaits  that 
the  different  areas  for  tactile  sensibility  of  the  various  parts  of  the 


y^O  THE  NON-NEURONIC  DISEASES 

'body  are  closely  intermingled  with  the  motor  areas.  In  his  study  of 
aphasia,  Dejerine  says :  "These  disturbances  of  cutaneous  sensibility 
accompany  the  beginning  of  the  paralysis  itself  in  the  majority  of  cases  ; 
sometimes  they  even  precede  the  latter.  These  phenomena  are  not  rare 
in  the  course  of  a  hemiplegia  of  cortical  origin  and  they  deserve  close 
study."  The  lesion  in  Dejerine's  case  was  confined  exclusively  to  the 
motor  cortex,  leaving  the  sensory  paths  intact.  Dupuy  notes  that 
Horsley  reported  to  the  Congress  of  Brighton,  in  1886,  that  the  removal 
of  a  pant  of  the  motor  cortex  in  three  patients  for  epileptoid  seizures 
symiptomatic  of  cortical  lesions  resulted  in  the  partial  or  complete  loss 
of  sensibilit}'.  Seguin  and  Weir  reported  the  case  of  a  man,  aged 
thirty-nine,  who  complained  in  the  autumn  of  1882  of  severe  head  pain 
and  convulsive  attacks  limited  to  the  right  side  of  the  neck  and  face. 
From  1885  these  attacks  occurred  very  frequently  and  were  associated 
with  a  sensation  of  cold.  The  spasms  involved  the  rig'ht  arm  and  hand 
as  well  as  the  face.  Finally  paresis  supervened  in  these  parts  and  was 
accompanied  by  aphasia  and  agraphia.  The  diagnosis  was  tumor  in 
the  facial  center  of  the  left  motor  zone.  Operation  proved  it  to  be  a 
sarcoma,  about  an  inch  in  thickness,  nesting  beneath  the  foot  of  the 
second  frontal  and  the  anterior  border  of  the  ascending  frontal  convo- 
lutions. A  report  of  the  case  in  the  Journal  of  Mental  and  Nervous 
Disease,  December,  1888,  one  year  after  the  operation,  states  that  there 
was  unquestionably  anaesthesia  of  the  cheek,  hand  and  forearm  to 
contact  tests  as  well  as  with  the  sesthesiometer.  There  was  also  anaes- 
thesia of  the  lower  part  of  the  face,  lips  and  inside  of  the  cheek.  From 
the  study  of  the  sensory  tracts  and  of  a  series  of  American  cases  of 
cortical  lesion,  Starr  came  to  the  conclusion  that  the  motor  and  sensors- 
areas  coincided,  though  the  latter  extended  beyond  the  former  and  in- 
cluded the  postero-parietal  lobe  as  well  as  the  Rolandic  region.  Four 
of  the  cases  in  Starr's  list  belonged  to  Mills,  and  in  reviewing  his  notes 
the  latter  came  to  the  conclusion  that  they  at  least  did  not  support  the 
inference  drawn  by  Starr.  From  a  careful  review  of  one  hundred 
and  thirty-seven  cases,  Dana  decided  that  the  sensory  (tactile  sensa- 
tion) and  motor  areas  were  coextensive.  In  the  discussion  of  Dana's 
paper,  Starr  and  Seguin  argued  with  the  author,  while  Mills  favored 
the  teaching  of  Ferrier — namely,  that  the  center  for  tactile  impressions 
is  to  be  found  in  the  gyrus  fornicatus  and  gyrus  hippocampi.  Sher- 
rington and  Griinbaum's  experiments  tend  to  negative  the  idea  thai 
the  gyrus  fornicatus  is  concerned  with  common  sensation. 

Strieker  maintains  that  motion  and  sensation  are  so  intimately  re- 
lated that  they  are  almost  identical.  His  views  may  be  portrayed  most 
clearly  by  means  of  an  illustration.  When  one  represents  to  himself,  for 
instance,  the  movements  of  a  cloud,  the  muscles  of  the  eyes  undergo 
the  same  sort  of  a  sensation  as  though,  they  were  actually  gazing  at  a 
moving  cloud.  By  checking  this  muscular  sensation  within  the  eyes, 
the  mental  image  of  the  cloud  immediately  ceases  its  movement.  The 
cloud  seems  absolutely  stationary. 

Among  the  Italians,  Lussana  and  Lemoigne  maintain  that  there  are 
sensory  and  motor  areas  in  the  cerebral  hemispheres,  but  that  they  do 
not  act  upon  one  another  after  the  manner  of  a  simple  reflex.     Tam- 


THE  NOX-XEURONIC  DISEASES  73 T 

burini,  Luciani  and  Seppilli  have  elaborated  since  1876  the  theory  tha: 
the  "motor  zone"  consists,  on  the  one  hand,  of  the  center  for  cutane- 
ous and  muscular  sensibility  and,  on  the  other,  of  the  centers  for  motor 
ideations.  This,  it  will  be  recognized,  is  a  very  elaborate,  mixed  and 
comprehensive  hypothesis.  It  well  illustrates,  says  Soury,  the  eclectic 
tendencies  of  the  Italian  school.  As  a  general  rule  the  Italians  are 
as  much  opposed  to  the  views  of  Hitzig  and  Nothnagel  as  they  are  to 
those  of  Schiff  and  Goltz.  They  lean  somewhat  toward  the  theories  of 
Terrier  and  his  English  followers.  In  other  words,  they  believe  that 
the  paralysis  caused  by  injury  of  the  cortical  motor  areas,  pathological 
or  experimental,  is  neither  ataxic  nor  reflex.  It  is  decidedly  and  en- 
tirel}'  a  paralysis  in  the  truest  sense  of  the  word.  Such  at  least  seems 
to  be  the  opinion  of  Albertoni  and  Michieli,  Lussana  and  Lemoigne, 
Tamburini,  Luciani,  Seppilli,  Maragliano,  Bianchi,  Palmerini,  Ton- 
nini  and  others.  In  the  language  of  ^laragliano,  all  motor  phenomena 
should  be  regarded  "as  dependent  upon  true  voluntary  motor  centers, 
which  are  capable,  without  the  intermediation  of  any  other  motor  cen- 
ters, of  starting  into  activity  the  muscular  apparatus  of  the  body." 
£qually  concise  and  clear  in  their  statements  are  Luciani  and  Tam- 
burini. These  authors,  unlike  Terrier,  locate  even  the  centers  of  vol- 
untary motion  in  the  basal  ganglia,  especially  the  corpora  striata. 
Injury  to  these  ganglia  as  well  as  to  the  corresponding  centers  of  the 
■cortex  does  not  result  in  ataxia,  or  in  the  phenomena  of  incoordination ; 
nor  is  any  alteration  of  general  sensation  to  be  detected  in  animals 
whose  motor  zones  have  been  operated  upon.  The  striate  body,  it 
will  be  remembered,  is,  according  to  Terrier,  the  general  center  for 
movements  which  were  once  voluntary  but  which  have  afterward  be- 
come automatic.  Thus  a  dog  can  still  run  and  swim  if  the  striate  body 
is  left  intact,  though  the  corresponding  cortical  areas  may  have  been 
removed.  Luciani  and  Tamburini  endow  the  basal  ganglia  with  the 
same  pyschic  functions  possessed  by  the  cortical  areas  and  thus  differ 
considerably  from  Terrier.  They  speak  of  them  as  psychomoter  cen- 
ters, probably  meaning  thereby  that  the  basal  ganglia  as  well  as  the 
cortical  areas  are  in  direct  connection  with  the  sensory  centers.  "The 
basal  ganglia."  they  say,  "and  especially  the  corpora  striata,  possess 
the  same  physiological  value  as  the  centers  for  voluntary  motion  do ; 
or,  in  other  words,  these  ceilters  can  be  put  into  action  directly  by 
ps3fcho-sensitive  sensorial  processes."  When  these  authors  promul- 
gated the  above-mentioned  ideas,  it  was  supposed  that  the  function  of 
the  striate  bodies  was  motor ;  now,  however,  it  is  known  that  the  hemi- 
plegias which  result  from  hemorrhage  in  this  region  are  caused  by 
the  injury  done  to  the  internal  capsule.  In  fact,  the  striate  bodies  have 
been  transformed  completely  into  cysts  without  a  paralysis  occurring 
so  long  as  the  internal  capsule  remained  untouched.  Hence  these  earlier 
views  of  Luciani  and  Tamburini  are  now  regarded  as  quite  untenable. 
Nevertheless,  it  must  be  admitted  that  the  recent  study  of  the  striate 
bodies  (caudate  nuclei)  especially  by  Baginsky  and  Lehmann  seems  to 
demonstrate  that  there  was  a  modicum  of  truth  in  the  earlier  views  of 
these  Italian  authors. 

The  so-called  paralysis  which  results  from  a  destructive  lesion  of 


'J2i'2  THE   NON-NEURONIC  DISEASES 

the  excitable  zone  of  the  cerebral  cortex  is  believed  by  some  of  the 
Italian  investigators  to  be  due  entirely  to  a  loss  of  sensation.  Silvio 
\'enturi,  of  Padua,  adopted  this  ataxic  theory  as  far  back  as  1878.  It 
was  Schiff,  the  distinguished  predecessor  of  Luciani  in  the  chair  of 
physiology  at  Florence,  who  became  the  chief  exponent  of  this  sen- 
sory explanation  of  the  paralysis.  In  187 1,  the  year  after  the  experi- 
ments of  Fritsch  and  Hitzig,  the  editor  of  L'lmparziale  medico,  in- 
spired by  Schiff,  wrote  that  all  the  immediate  effects  of  injury  to  the 
so-called  motor  centers  of  Hitzig  were  really  the  result  of  a  disturbance 
of  sensibility  and  were  limited  entirely  to  that  sphere.  In  several  Flor- 
entine publications,  issued  in  1873  and  1876,  Schiff  recalls  these  facts. 
According  to  this  physiologist,  a  dog  with  a  cerebral  lesion  is  not 
affected  with  any  loss  of  energy  in  the  muscles  of  the  opposite  half 
of  the  body,  but  merely  with  an  absence  of  the  feeling  of  surety  and 
power  of  adjustment  in  its  various  movements  because  of  the  loss  of 
tactile  sensibility.  The  general  movements  of  leaping  and  running  are 
all  w^ell  performed,  but  there  are  marked  evidences  of  an  uncertainty^ 
in  regard  to  the  position  of  the  limbs.  This  angesthesia  is  entirely  cuta- 
neous, according  to  Schiff.  while  the  sensibility  to  pain  and  pressure  re- 
mains unaffected.  x\lterations  of  the  sense  of  pressure  and  of  tempera- 
ture are  caused  by  the  increased  depth  of  the  cerebral  mutilations^ 
While  these  views,  together  with  the  experiments  of  Schiff,  are  not 
accepted  by  the  majority  of  ph3'-siologists,  they  have  had  their  influence 
in  greatly  modifying  the  original  theories  of  many  in  regard  to  the 
motor  character  of  the  so-called  motor  areas.  Hitzig  himself,  who 
was  so  vigorous  an  upholder  of  the  purely  motor  theory,  has  altered 
his  conceptions  to  such  an  extent  as  to  refer  to  these  motor  phenomena 
under  the  name  of  disorders  of  the  muscular  conscience.  Schiff's. 
theory  is  that  of  a  pure  reflex.  An  impulse  from  the  periphery  is  sent, 
inward  to  the  brain  and  there  within  some  hitherto  undiscovered  sub- 
cortical centers  it  is  transmuted  into  an  eft'erent  impulse  which  is  sent 
out  again  to  the  muscular  apparatus.  This  cerebral  reflex,  he  insists, 
is  similar  to  the  spinal  reflex  and  the  phenomena  due  to  its  disturb- 
ance are  similar  to  the  reflex  phenomena  due  to  injury  of  the  posterior 
columns  of  the  cord.  It  should  be  observed  that  Schiff  locates  the  re- 
flex centers,  not  in  the  cortex  itself,  but  somewhere  beneath  the  cor- 
tex. Von  Monakow  holds  that  all  bilaterally  acting  muscles,  such  as 
those  of  respiration,  deglutition,  and  mastication  are  innervated  from 
some  unknown  subccf-tical  centers  that  vary  slightly,  if  at  all,  from 
the  cortex.  There  have  been  many  objections  and  objectors  to  these 
views  of  Schiff  and  his  following  in  regard  to  them  is  quite  small.  It 
must  be  admitted,  however,  that,  like  his  opponent,  Hitzig,  he  has  done 
valuable  service  to  the  science  of  cerebral  localization ;  for  if  Hitzig 
discovered  the  results  of  injury  to  the  motor  areas  of  the  cortex,  Schiff 
revealed  those  due  to  injury  of  the  centers  for  tactile  sensation.  To 
judge  from  the  doctrines  of  Munk,  Luciani  and  Seppilli,  the  future 
will  have  to  acknowledge  Schiff,  as  well  as  Flitzig,  as  one  of  its  fore- 
runners. When  Schiff  asserts  that  "one  thing  is  positive,  there  are 
no  cortical  centers,"  we  are  somehow  forcibly  reminded  of  GoJtz^ 
Though   the    former   enumerated   many   objectors,   chiefly    among   the 


THE  NON-NEURONIC  DISEASES 


'7'n 


iollowers  of  Ferrier,  such  as  Lussana,  Tamburini,  Bechterew  and  Hors- 
Jey,  his  teachings  have  acted  as  a  wholesome  check  upon  the  too  rapid 
assumption  that  all  movements  of  the  body  originate  from  certain  lim- 
ited areas  of  the  cerebral  cortex.  They  have  induced  experimenters 
to  study  somewhat  more  minutely  the  character  of  all  muscular  move- 
ments, the  relation  of  the  centers  for  this  movement  to  the  centers  for 
sensation,  and  the  influence,  if  there  be  any,  of  the  higher  mental  fac- 
ulties, the  purely  psychic  functions  of  the  brain. 

Tamburini  has  attempted  a  reconciliation  of  the  two  opposing 
-views  just  described.  He  admits  it  is  probable  that  the  points  of  the 
cortex  where  the  inpouring  sensory  impulses  are  transformed  into  out- 
_going  motor  impulses  correspond  identically  with  the  cortical  areas  upon 
which  so  much  study  has  been  expended.  In  his  own  words,  "Each  of 
these  centers  may  be  at  the  same  time  the  focus  for  the  reception  and 
perception  of  the  sensory  excitations  sent  inward  from  a  given  part 
of  the  body  and  the  pomt  of  departure  for  the  voluntary  centrifugal 
impulse  going  to  the  muscles  of  the  same  part."  This,  he  believes,  ex- 
plains the  absence  of  sensibility  in  the  direct  production  of  localized 
movements ;  for  in  the  one  instance  the  electric  current  takes  the  place 
•of  the  nervous  current  or  impulse  and  in  the  other  the  removal  of  the 
cortical  centers  must  necessarily  abolish  the  perception  of  the  peripheral 
impressions.  In  conjunction  with  Luciani,  Tamburini  has  extended 
the  same  theory  in  regard  to  the  excito-motor  zone  of  the  cortex  to  the 
centers  for  sight  and  hearing.  The  movements  of  the  ear  and  eye- 
ball, initiated  by  a  sensor}'  impression  at  the  periphery,  are  not  of  the 
nature  of  a  pure  reflex,  as  Ferrier  believes,  but  simply  the  result  of 
the  intermingling  of  the  corresponding  sensory  and  motor  elements  of 
the  cortex.  In  other  words,  corresponding  sensory  and  motor  cells  lie 
in  close  juxtaposition  within  the  various  cortical  areas.  These  views  of 
Tamburini  seem  to  be'  supported  by  an  anatomical  as  well  as  by  a  phys- 
iological basis ;  for,  as  I  have  already  pointed  out,  the  region  of  the 
hippocampus  major,  which  Ferrier  and  his  followers  assert  is  sensory 
in  function,  contains  a  row  of  large  pyramidal  cells  between  the  medul- 
lary center  and  the  so-called  stratum  radiatum.  These  cells  are  iden- 
tical, so  far  as  their  microscopical  appearances  are  concerned,  with  the 
supposed  motor  cells  of  the  central  convolutions  and  anterior  horns  of 
the  cord. 

In  this  connection  it  is  interestuig  and  suggestive  to  note  Fiechsig 
thinks  that  for  every  sensory  path  (corticopetal)  there  is  a  correspond- 
ing motor  (corticofugal)  path.  For  instance,  beside  the  auditory 
myelogenetic  area  in  the  first  temporal  convolution,  there  is  a  cortico- 
fugal area  or  radiation  which  he  believes  is  motor,  though  this  has  not 
yet  been  demonstrated.  And  so  on  for  all  the  sensory  motor  couplets 
which,  taken  en  masse  for  the  entire  brain,  make  up  his  primordial 
zones  or  regions  of  early  development. 

In  1880  Luciana,  who,  like  Seppilli,  found  that  the  effects  of  a 
circumscribed  lesion  within  the  motor  zone  of  the  cortex  were  not  only 
paralysis  or  paresis,  but  also  a  more  or  less  pronounced  alteration  of 
the  muscular  and  cutaneous  sensibility,  wrote  that  "the  motor  centers 
and  the  sensory  centers,  which  together  perform  a  very  complex  func- 


734  '^"^£   XOX-XEUROXIC  DISEASES 

tion,  are  intermingled  or  lie  in  the  closest  proximity  ( //;  gran  vicinanzay 
within  the  cerebral  cortex."  He  verified  the  phenomena  described  by 
Munk,  but  he  did  not  look  upon  the  paralysis  as  psychical  in  character ; 
that  is.  as  the  result  of  the  loss  of  mere  sensation  of  mental  images  or 
psychic  representations.  It  was  purely  organic  and  depended  directly 
upon  the  injury  to  the  motor  cells,  just  as  the  disturbed  sensibility  de- 
pended upon  the  injury  to  the  neighboring  sensory  elements.  The  mo- 
tor centers,  therefore,  like  the  centers  for  sight  and  hearing,  were  of  a 
complex  nature  and  in  reality  were  sensory-motor.  Luciani  says,  "the 
motor  centers  are  not  localized  within  the  cortical  area,  called  up  to 
the  present  time  'the  motor  zone,'  a  name  which  we  must  hereafter 
abandon,  since  this  zone  is  not  exclusively  motor.  All  the  various  re- 
gions, of  the  cortex  are  more  or  less  strewn  w'ith  special  motor  centers. 
In  order  to  be  positive  of  having  destroyed  all  the  motor  centers,  one 
mjst  remove  the  entire  cerebral  cortex."  This  is  a  remarkable  state- 
ment of  a  singularly  comprehensive  theory,  and  leads  us  back  once 
more  to  the  vigorous  contentions  of  the  school  of  Goltz  and  somewhat 
to  the  teaching  of  Flechsig. 

Danillo  has  demonstrated  that  when  the  occipital  lobe,  which  is 
supposed  to  be  entirely  sensory  in  function,  is  stimulated,  the  move- 
ments of  the  eyes  are  not  simply  reflex,  as  Ferrier  believed,  because 
they  are  still  observed  when  after  the  ablation  of  the  entire  cortex  of  the 
occipital  lobe  the  underlying  white  substance  is  electrically  excited.  In 
this  white  substance,  therefore,  there  must  be  motor  fibres  springing 
directly  from  the  cortex  of  the  occipital  lobe,  unless  we  imagine  that 
these  same  fibres  go  to  the  central  lobules  and  through  them,  rather 
than  directly,  transmit  the  motor  impulse  to  the  muscles  of  the  eye. 
Even  such  an  hypothesis,  hovi^ever,  would  represent  the  process  within 
the  occipital  lobe  cortex  as  reflective,  but  the  outgoing  impulse  in  such 
a  case  w^ould  be  transmitted  into  an  ordinarx'  motor  one  before  it  finally 
reached  the  eye  muscles. 

Bechterew  finds  that  when  the  so-called  motor  areas  of  the  cen- 
tral lobules  are  separated  from  the  occipital  centers,  stimulation  of  the 
latter  still  gives  rise  to  the  same  muscular  response.  He  argues,  fur- 
thermore, that  the  movements  of  these  muscles  cannot  possibly  be  of 
the  nature  of  a  simple  reflex,  because  they  are  always  uniform  and 
localized  within  the  same  group.  Stimulation  of  the  occipital  cortex 
excites  motor  points  therefore  that  do  not  belong  to  the  so-called  motor 
zone  whose  fibers  pass  only  through  the  pyramidal  fasciculi  of  the 
cord.  These  mixed  centers  being  thus  situated  outside  of  the  cor- 
tical areas  to  which  the  pyramidal  fasciculi  run  require  for  their  ex- 
citation a  much  stronger  and  longer  current ;  their  destruction  does  not 
involve  manifest  disturbances  of  motion  ;  and  the  movements  which 
they  give  rise  to  are  not  very  clearly  differentiated  from  those  caused 
by  excitation  of  the  true  motor  zone.  t>echterew  reasons  that  the  sen- 
sory areas  do  contain  motor  centers,  or  at  least  motor  elements,  and 
he  accounts  for  the  fact  of  their  stimulation  requiring  a  stronger  cur- 
rent and  one  longer  in  duration  on  the  ground  that  they  do  not  connect 
with  their  corresponding  muscles  through  the  intermediation  of  the 
anterior  roots  of  the  spinal  cord,  but  through  certain  masses  of  gray 


THE  XOX-XEUROXIC  DISEASES  735 

matter  situated  deeply  within  the  cerebral  hemispheres,  probably  the 
optic  thalami.  According  to  Bechterew,  then,  there  are  two  sorts  of 
motor  centers  within  the  cerebral  cortex.  One  variety  is  easily  ex- 
citable and  is  found  in  the  central  convolutions  ;  the  other  is  not  so 
easily  excited  and  is  scattered  in  among  the  sensory  centers.  This  au- 
thor bases  his  views  chiefly  upon  his  experiments  on  new-born  animals, 
in  which  the  movements  of  the  ear  and  the  conjugate  movements  of 
the  eyes  can  only  be  produced  by  direct  stimulation  of  the  correspond- 
ing areas  of  the  cortex  one  week  and  one  month  respectively  after  the 
movements  of  the  limbs  have  been  elicited  by  excitation  of  the  central 
convolutions.  It  is  not  to  be  doubted,  therefore,  that  the  sensory  areas 
of  the  cortex  contain  some  motor  elements  and  exercise  some  special 
influence  over  the  associated  muscular  apparatus.  From  this  rapid 
review  of  the  modern  theories  current  among  the  English  and  Con- 
tinental physiologists,  we  note  clearly  that  there  is  a  grov/ing  tendency 
to  believe  that  the  rhotor  centers  of  the  central  convolutions  have  sen- 
sory elements  more  or  less  intermingled  with  them. 

Thus  far  I  have  discussed  only  the  localizations,  so  far  as  they  ard 
known,  in  the  cerebral  cortex  ;  but  these  do  not  by  any  means  include 
all  of  the  localizations  in  the  brain.  The  functions  of  the  basal  ganglia, 
the  arrangement  of  the  projection  tracts  especially  as  they  course 
through  the  internal  capsule  and  the  functions  of  the  cerebellum  are  all 
sufliciently  known  to  afl:ord  some  clue  as  to  the  location  of  lesions  in 
these  parts. 

As  the  white  matter  of  the  hemispheres  consists  of  association, 
commissural  and  projection  tracts,  a  lesion  within  them  cannot  be 
sharply  diagnosticated  and  distinguished  from  a  lesion  of  the  cortical 
areas  with  which  they  are  connected.  From  the  standpoint  of  surgery, 
it  is  extremely  desirable  to  be  able  to  distinguish  a  cortical  from  a  sub- 
cortical lesion  and  even  if  possible  the  depth  of  the  subcortical.  Not 
many  lesions  are  entirely  and  completely  cortical,  and  many  of  those 
which  are  often  supposed  to  be  cortical  are  discovered  upon  post  mor- 
tem to  be  subcortical.  Tumois  of  the  centrum  ovale  usually  give  rise 
to  more  extensive  symptoms  than  do  those  of  equal  size  in  the  cortex. 
In  other  words,  the  nearer  the  lesion  is  to  the  cortex  the  more  likely 
it  is  to  produce  spasm  and  paralysis  or  paraesthesia  and  ansesthesia  in, 
for  instance,  the  arm,  the  leg,  or  a  part  of  the  face,  while  on  the  other 
hand  the  farther  it  is  away  from  the  cortex,  as,  for  instance,  in  the 
internal  capsule,  the  more  likely  it  is  to  provoke  a  hemiplegia  or  a  hem- 
iansesthesia.  The  spreading  out  of  the  tracts  above  the  capsule  explains 
clearly  enough  the  reason  why  cortical  lesions  tend  to  produce  mono- 
plegias and  subcortical  more  extensive  paralyses.  Though  not  abso- 
lutely reliable,  this  distinction  is  an  important  and  valuable  one.  Seguin 
made  a  careful  study  of  the  dififerential  signs  between  the  cortical  and 
subcortical  tumors,  and  in  a  general  way  concluded  that  cortical  lesions 
produced  "localized  clonic  spasm,  epileptic  attacks  beginning  with  local 
spasm,  followed  by  paralysis  ;  early  appearance  of  local  cranial  pain 
and  tenderness ;  increased  local  cranial  temperature ;"'  w^hereas  sub- 
cortical lesions  gave  rise  to  "local-  or  hemi-paresis  followed  by  spasm ; 
predominance  of  tonic  spasm :  absence,  small  degree  or  very  late  ap- 


736  THE  NOX-XEURONIC  DISEASES 

pearance  of  local  headache  and  of  tenderness  to  percussion  ;  normal 
cranial  temperature." 

Among  the  subcortical  lesions  those  of  the  infernal  capsule  are  of 
special  significance.  On  account  of  the  course  of  the  middle  cerebral 
artery,  hemorrhage  into  the  internal  capsule  or  its  immediate  neigh- 
borhood, the  corpora  striata  and  optic  thalami,  occurs  more  frequently 
than  it  does  into  the  centrum  semiovale  or  on  to  the  cortex.  Usually 
the  extravasation  of  blood  causes  such  an  extensive  destruction  of 
tissue  that  a  localization  diagnosis  is  quite  out  of  the  question ;  and 
even  were  the  focal  lesion  in  the  internal  capsule  to  be  so  small  as  t» 
confine  its  deleterious  influence  to  only  certain  of  the  tracts  passing 
through  it,  a  diagnosis  infra  vifam  between  capsular  and  cortical  dis- 
turbance would  be  often  impossible  and  always  extremely  difficult.  To 
attempt  a  localization  diagnosis  of  a  diminutive  lesion  within  the  cap- 
sule, one  must  know  clearly  the  relative  positions  of  the  various  tracts 
that  run  through  it.  The  anterior  two-thirds  of  the  posterior  limb  of 
the  capsule  are  occupied  by  the  projection  tracts  from  the  motor  areas 
of  the  cortex.  These  fibres  hold  approximately  the  same  relative  posi- 
tion to  each  other  that  the  areas  of  the  cortex  do  among  themselves ; 
that  is,  beginning  at  the  knee  of  the  capsule  and  passing  backward, 
we  meet  the  face,  arm  and  leg  tracts,  which,  however,  are  not  sharply 
defined,  but  blend  with  each  other  at  the  line  of  separation.  Horsley, 
Beevor,  and  others  have  located  the  bundles  of  fibres  for  the  glossal, 
masticatory,  and  laryngeal  muscles  in  the  knee  of  the  capsule.  Von 
Monakow  says  that  the  speech  path  positively  passes  through  the  cap- 
sular knee.  When  this  part  of  the  capsule  only  is  involved  in  a  lesion, 
there  occurs  paralysis  of  the  inferior  branch  of  the  facial  nerve  and  of 
the  hypoglossal  of  the  opposite  side.  If  the  disease  is  upon  the  left 
side  disturbance  of  the  speech  will  also  occur.  In  the  posterior  third 
of  the  posterior  limb  of  the  capsule  course  the  sensory  projection  tracts 
that  terminate  in  the  cortex,  those  from  the  visual  areas  of  the  occip- 
ital lobe  being  the  farthest  behind.  In  the  anterior  limb  of  the  capsule 
is  to  be  found  the  fronto-pontile  tract  of  Brissaud,  about  which,  how- 
ever, there  is  still  much  diversity  of  opinion.  Injury  to  this  anterior 
limb  causes  no  definite  localizing  symptoms.  With  this  picture  of 
the  internal  capsule  in  the  mind,  the  diagnostician  might  attempt  a  local- 
ization of  a  small  lesion,  but,  as  I  have  indicated  above,  he  could 
not  feel  sure  of  the  correctness  of  his  diagnosis.  Usually  a  lesion  of 
the  capsule  is  so  large  and  destructive  that  the  accompanying  paralysis 
assumes  the  form  of  a  total  hemiplegia,  the  well-known  facio-hypo- 
glossal-brachio-crural  type,  of  the  opposite  half  of  the  body.  With 
this  hemiplegia  is  associated  more  or  less  hemian^esthesia. 

The  following  symptoms  are  supposed  to  indicate  tumor  of  the 
corpus  callosiim:  General  symptoms  of  brain  tumor  such  as  head- 
ache, etc. ;  gradual  hemiplegia  followed  by  paraplegia :  great  mental 
dulness ;  sleepiness ;  stupidity ;  indifference  to  the  external  world  and 
a  low,  inanimate  condition  generally ;  absence  of  the  cranial  nerves ; 
terminal  coma  and  death.  There  is  much  doubt  about  all  this,  however, 
as  the  symptomatology^  is  so  general  and  includes  so  much  that  is  in- 
dicative of  tumor  of  the  ventricles.    A  definite  localization  of  the  lesion 


THE   XOX-XEUROXIC  DISEASES  737 

is  therefore  extremely  difficult  if  not  quite  impossible.  The  bilaterality 
-of  the  paralysis  and  its  irregular  type,  when  taken  in  conjunction  with 
the  mental  deterioration  and  general  signs  of  intra-cerebral  tumor,  are 
highly  suggestive,  but  hardly  much  more.  In  Schuffer's  collected 
twenty-five  cases  of  tumor  of  the  corpus  callosum,  ten  exhibited  optic 
neuritis,  while  in  seven  it  was  absent.  Headache  was  wanting  in 
fifteen.  In  all  of  the  cases  there  was  a  change  in  the  mentality,  m- 
cluding  weakness  of  the  intellect  and  memory,  somnolence,  etc.  Con- 
vulsions occurred  in  eleven.  Disturbances  of  sensibility  were  exceed- 
ingly rare.  ^Mental  changes  are  more  constant  with  tumors  of  the  cor- 
pus callosum  than  with  tumors  in  other  parts  of  the  brain.  When 
such  mental  changes  are  unaccompanied  by  any.  definite  localizing 
.SN-mptoms.  a  tumor  of  the  corpus  callosum  ought  always  to  be 
thought  of. 

Complete  destruction  of  and  focal  lesions  within  the  corpora 
striata  do  not  give  rise  to  any  definite  localizing  symptoms.  The  old 
idea  that  the  caudate  nucleus  has  something  to  do  with  the  automatic 
movements  of  running,  walking,  etc.,  and  that  the  lenticular  nucleus 
(globulus  pallidus)  is  associated  with  the  sensory  paths  is  not  well 
established.  Lesions  of  these  bodies  only  reveal  themselves  when  they 
■cause  paralysis  by  pressing  upon  the  internal  capsule.  There  are  no 
S}-mptoms  with  small,  inherent  lesions. 

The  optic  thalami  are  clearly  in  close  relationship  with  the  gen- 
•eral  and  special  sensory  areas  of  the  cortex.  The  expression  of  the  emo- 
.tions  is  somehow  connected  with  these  ganglia,  for  when  they  are  in- 
volved in  cases  of  cerebral  paralysis,  the  involuntary  manifestation  of 
delight,  joy,  sorrow,  disgust,  etc.,  seems  to  be  impossible.  The  psychic 
reflexes  such  as  laughing  and  crying,  are  disturbed.  Lesions  of  the 
posterior  part  of  the  thalami,  namely,  the  pulvinar,  cause  partial  blind- 
ness, though  this  is  not  absolutely  certain.  A  tumor  of  the  pulvinar  and 
.adjacent  parts  will  produce  a  hemianopsia  which  may  be  distinguished 
from  a  hemianopsia  of  occipito-cortical  origin  by  the  hemiopic  pupillary 
reaction,  since  these  primary  visual  centers  control  the  movements  of 
the  pupils  through  the  third  nerve.  Disturbances  of  hearing,  taste, 
-smell,  and  the  tactile  and  general  muscular  senses  have  all  been  attrib- 
uted to  disease  of  the  optic  thalami,  but  none  of  them  have  been  posi- 
tively established.  ]\Iodifications  of  coordination  and  even  general 
muscular  atrophy  on  the  opposite  side  of  the  body  have  also  been  seen. 
It  is  obvious  that  as  the  optic  thalami  are  closely  connected  with  the 
corresponding  cortical  centers,  a  differential  diagnosis  between  a  thala- 
mic and  a  cortical  lesion  is  quite  impossible.  In  a  case  of  a  lesion  con- 
fined solely  to  this  ganglion,  reported  by  Hunter,  there  was  as  usual 
a  loss  of  the  senses  of  smell,  of  sight,  of  hearing  and  of  touch  :  the 
v/oman  sank  gradually  and  remained  a  stranger  to  all  external  im- 
pressions. The  extensive  character  of  these  symptoms  would  of  course 
suggest  a  basal  rather  than  a  cortical  lesion,  but  even  in  such  a  case 
it  would  be  difficult  to  say  just  how  much  of  this  symptomatology-  was 
due  to  pressure  upon  the  internal  capsule  rather  than  to  injury  to 
the  thalami.  In  spite  of  our  fairly  accurate  knowledge  of  the  anatom- 
ical connections  of  the  basal  ganglia,  we  know  verv  little  about  the 


738  THE   XON-NEURONIC  DISEASES 

functions  of  this  part  of  the  brain.  Though  Bechterew  regards  these 
gangha  as  reflex  organs  controlhng  the  muscular  apparatus  by  means 
of  both  centrifugal  and  centripetal  fibers,  and  though  he,  with  Xoth- 
nagel  and  Brissaud,  looks  upon  the  optic  thalamus  as  a  center  for  the 
involuntary  automatic  movements,  the  subconscious,  non-volitional 
psycho-reflexes  of  the  body,  his  views  are  still  largely  hypothetical.  In- 
voluntary movements  have  been  observed  in  disease  of  the  thalamus, 
and  Nothnagel  has  shown  that  the  same  cause  will  give  rise  to  a 
crossed  paralysis  "observed  only  in  laughing  while  the  nerve  still  obeys 
the  will"  (Oppenheim).  Still  more  questionable  than  all  this  are  the 
views  of  Bechterew,  Schiff,  Lussana,  Sinkler,  and  others  that  the 
cardiac,  gastric,  intestinal,  sexual,  vasomotor,  secretory  and  trophic 
centers  are  located  in  the  optic  thalamus.  In  a  word  then,  the  basal 
ganglia  do  not  at  the  present  day  present  any  definite  localizing  symp- 
toms, and  granting  that  they  did,  it  would  scarcely  be  of  much  practical 
value  to  us  beyond  the  making  of  a  diagnosis  excluding  the  cortex,  for 
these  ganglia  are  not  amenable  to  surgical  interference. 

The  anterior  corpora  quadrigeuiUia,  together  with  the  external 
geniculate  bodies  and  pidvinar,  constitute  the  primary  centers  for 
sight.  The  geniculate  bodies  seem  to  be  the  chief  terminus  of  the 
optic  fibers,  and  in  this  respect  are  closely  associated  with  the  pulvinar. 
Bechterew  alleges  as  a  result  of  his  experiments  that  lesions  of  the 
anterior  quadrigeminal  bodies  produce  blindness,  but  this  has  not  been 
observed  in  man.  Their  relationship  to  the  pupillary  reflex  and  ciliary 
muscles  (Henschen,  von  Monakow)  is  still  problematical.  Stilling  be- 
lieved that  some  of  the  fibres  of  the  optic  tract  could  be  traced  to  the 
corpora  siihthalaniica.  but  in  regard  to  this  there  is  no  certainty.  No 
localizing  symptoms  are  known  in  connection  with  Luys'  body,  though 
much  is  said  about  its  role  in  the  maintenance  of  equilibrium  and  of 
coordination.  The  same  is  said,  however,  of  the  corpora  quadri- 
gemina,  the  geniculate  bodies,  and  pretty  nearly  all  the  basal  ganglia, 
all  of  which  brings  to  mind  the  words  of  Foster,  who,  when  comment- 
ing upon  the  interpolation  of  ganglionic  masses  in  the  course  of  a  con- 
tinuous tract,  such,  for  instance,  as  the  optic  tract,  says :  ''All  day 
long  and  every  day,  multitudinous  afferent  impulses  from  eye  and  ear 
and  skin  and  muscle  and  other  tissues  and  organs  are  streaming  into 
our  nervous  system.  .  .  .  By  the  checks  and  counterchecks  of 
cerebral  and  spinal  activities  all  these  impulses  are  drilled  and  mar- 
shaled and  kept  in  orderly  array  till  a  movement  is  called  for;  and  thus 
we  are  able  to  execute  at  will  the  most  complex  bodily  manoeuvres, 
knowing  only  zvhy  and  unconscious  or  but  dimly  conscious  hozu  we 
carry  them  out." 

The  posterior  corpora  quadrigemina  and  internal  genicidate  bodies 
are  usually  given  the  function  of  controlling  the  reflex  movements 
associated  with  hearing.  Von  Monakow  is  not  fully  satisfied  that  the 
internal  geniculate  bodies  have  anything  to  do  with  audition.  Fibres 
from  the  cerebellum  enter  both  the  posterior  quadrigeminal  tubercles 
and  the  internal  geniculates,  so  that  one  of  the  signs  of  lesion  in  or 
near  them  is  disturbed  equilibrium.     Beyond  this  we  know  of  no  symp- 


THE  XOX-XEUROXIC  DISEASES  739 

toms  that  are  produced  by  focal  lesions  limited  solely  to  the  corpora 
quadrigemina  and  geniculate  bodies. 

The  red  nucleus  of  the  tegmentum  belongs  to  the  cerebellar  sys- 
tem, and  therefore  subserves  in  part  the  maintenance  of  equilibrium. 
The  nucleus  dentatns,  the  olivary  body,  the  red  mtcleus,  and  the  gray 
matter  of  the  pons  all  bear  a  general  relationship  to  the  cerebellar  cor- 
tex the  same  as  the  corpus  striatum  and  the  optic  thalamus  do  to  the 
cerebral  cortex.  They  all  connect  ultimately  with  the  anterior  horns 
of  the  cord.  No  special  localizing  symptom  can  therefore  be  assigned 
to  the  red  nucleus. 

Lesions  of  the  corpora  mamillaria  are  not  known  by  any  localiz- 
ing signs. 

Tumors  of  the  hypopliysis  or  pituitary  body,  especially  of  the  ante- 
rior part  of  it,  are  so  often  associated  with  the  general  symptomatology 
of  acromegaly  that  they  have  almost  come  to  be  regarded  as  the  cause 
of  this  disease.  Histological  structure  and  embryological  development 
both  demonstrate  that  the  anterior  part  of  the  pituitary  body  is  a  glan- 
dular organ  rather  than  a  part  of  the  cerebrum,  a  fact  wdiich  might 
explain  in  part  the  relationship  between  it  and  acromegaly.  In  the 
Remsta  sperimentale  di  freniatria,  1892,  is  a  report  of  the  results  of  the 
destruction  of  the  pituitary  gland  in  thirty  experiments  upon  dogs  and 
cats.  Complete  destruction  proved  rapidly  fatal ;  partial  destruction, 
less  rapidly.  The  animal  was  profoundly  prostrated  and  exhibited  a 
change  of  character.  There  was  muscular  weakness  with  clonico-tonic 
convulsions.  The  breathing  became  difficult.  Anorexia  alternated  with 
bulimia.  Alkaline  polyuria  was  present,  accompanied  by  polydipsia, 
depressed  temperature,  and  emaciation  out  of  all  proportion  to  the 
anorexia.  The  inference  was  drawn  that  the  destruction  of  the  gland 
eventuated  in  the  formation  and  accumulation  of  some  special  toxic 
substance  within  the  organism.  The  localizing  symptoms  of  slow  dis- 
ease in  this  gland  are  therefore  neighborhood  symptoms,  acromegaly 
and  some  other  signs  of  general  emaciation.  Among  the  neighbor- 
hood symptoms  that  should  be  closely  studied  in  suspected  tumor  are 
such  as  are  referable  to  involvement  of  the  optic  chiasm,  the  circle  of 
Vv'illis,  and  the  structures  in  and  about  the  third  ventricle. 

Lesions  of  the  epiphysis  or  pineal  gland  can  only  be  suspected  from 
neighborhood  symptoms  which  point  to  implication  of  the  optic  thalami 
and  the  parts  about  the  midbrain.  Such  symptoms,  however,  are  usu- 
ally too  general  to  be  of  any  very  great  value  in  making  a  localization 
diagnosis. 

Focal  disease  of  the  crura  cerebri  is  rare,  but  when  present  may 
be  recognized  by  a  hemiplegia  and  possibly  a  hemianesthesia.  There 
is  no  way,  however,  of  distinguishing  such  a  lesion  from  one  involving- 
the  corresponding  motor  and  sensory  areas  of  the  cortex,  except  by  re- 
membering that  the  sensory-motor  area  is  much  more  confined  in  the 
crura  than  in  the  cortex,  and  hence  will  exhibit  a  more  widespread  set; 
of  symptoms  with  the  same-sized  lesion.  In  tumor  of  the  crura,  fur- 
thermore, the  third  nerve  will  in  all  probability  be  implicated,  giving- 
,  rise  to  a  "crossed  paralysis,"  hemiplegia  alternans.  In  this  form  o£ 
hemiplegia  the  degeneration  occurs  in  the  central  neurone  for  the  body 


740  THE  NON-NEURONIC  DISEASES 

antl  the  peripheral  neurone  for  the  eye ;  therefore  the  body  muscles  ex- 
hibit a  spastic  form  of  paralysis  while  those  for  the  eye  are  affected 
with  a  flaccid  paralysis  and  degenerative  atrophy. 

The  localization  of  lesions  in  the  pons  and  the  meduUa  is  largely 
a  matter  of  remembering  the  location  and  arrangement  of  the  cranial 
nerve  nuclei.  Symptoms  showing  an  involvement  of  the  pyramidal 
tracts  are  the  principal  ones  in  pontile  lesions.  Tumors  of  the  pons 
often  cause  conjugate  deviation  of  the  eyes,  which,  unlike  the  same 
symptom  when  produced  by  cerebral  disease,  is  in  a  direction  away  from 
the  side  of  the  lesion.  Especially  true  is  this  of  tumors  lying  near  the 
cephalic  border  of  the  pons.  Lesions  lying  above  a  horizontal  line 
drawn  roughly  through  the  points  of  emergence  of  the  trigeminal 
nerves  cause  a  hemiplegia  and  facial  paralysis  on  the  opposite  side  of 
the  body,  also  a  probable  involvement  of  the  third  nerve.  Lesions  be- 
low this  line  produce  a  hemiplegia  of  the  opposite  side  of  the  body  and 
paralysis  of  the  same  side  of  the  face.  This  facial  paralysis  is  central 
and  must  be  distinguished  from  that  caused  by  disease  of  the  facial 
root  fibres  or  nuclei.  The  electrical  reactions  will  not  be  those  of  a 
peripheral  paralysis ;  the  paralysis  itself  will  be  more  or  less  incom- 
plete, though  more  pronounced,  than  a  paralysis  due  to  a  lesion  of 
the  facial  tract  higher  up  in  the  pyramidal  paths  or  in  the  cortex. 
Tumors  upon  either  side  of  the  pons  which  encroach  upon  the  peduncles 
give  rise  to  forced  movements  of  the  body,  the  movements  being  either 
toward  or  away  from  the  seat  of  the  lesion.  V^asomotor  phenomena, 
such  as  pallor,  flushing,  temperature  changes,  mucous  hemorrhages, 
and  epistaxis,  have  all  been  attributed  to  disease  of  the  pons.  Disturb- 
ances of  hearing  and  of  taste  have  been  observed  by  Mills  in  disease  of 
the  lateral  aspect  of  the  pons.  Vertigo,  ataxia,  and  trismus  may  even 
occur  as  irritative  symptoms  of  pontile  lesions. 

Most  authors  declare  that  no  known  symptoms  result  from  lesions 
m  the  lateral  lobes  of  the  cerebellum.  All  localizations  in  this  part  of 
the  brain  are  referred  to  the  middle  lobe  or  vermis.  Disease  of  this 
lobe  is  supposed  to  be  indicated  by  disturbances  of  equilibrium,  forced 
movements,  and  a  peculiar  gait  known  as  cerebellar  ataxia.  Such  is 
the  teaching  of  Nothnagel.  It  should  be  remembered,  however,  that 
in  the  middle  lobe  decussate  all  the  tracts  that  course  from  all  parts 
of  the  cerebellar  cortex,  and  that  it  may  be  these  tracts  that  are 
especially  affected  in  disease  of  the  vermis.  Kuh  says  he  has  seen  a 
case  in  which  an  angeio-sarcoma  had  almost  totally  destroyed  the  mid- 
dle lobe,  and  yet  there  never  was  any  indication  of  incoordination. 
Mills  does  not  regard  the  cerebellum  in  any  part  as  a  latent  region. 
In  tumors  of  the  lateral  lobes  the  general  symptoms  of  an  encephalic 
growth  receive  a  special  cerebellar  stamp.  The  vomiting,  vertigo,  and 
optic  neuritis,  which  is  more  frequent  in  cases  of  cerebellar  tumor  than 
of  tumors  elsewhere  in  the  enceplialon,  are  more  or  less  increased  and 
are  accompanied  by  signs  of  compression  upon  the  neighboring  parts 
of  the  medulla  and  corpora  quadrigemina.  Most  of  the  symptoms 
attributed  to  cerebellar  disease  are  really  pressure  symptoms.  The  ver- 
tigo, vomiting,  and  headache  can  only  be  considered  as  valuable  local- 
izing signs  by  exclusion  of  other  parts  of  the  brain.     Inco5rdination, 


THE  NON-NEURONIC  DISEASES  74I 

vertigo,  and  dysarthria,  or  scanning  speech,  are  the  only  symptoms 
that  may  be  said  to  more  or  less  definitely  indicate  a  cerebellar  lesion. 
With  these  nystagmus  and  occipital  headache  are  highly  suspicious. 
Jackson  and  Russel  have  credited  the  cerebellum  with  a  special  influ- 
ence upon  the  great  trunkal  muscles,  but  this  is  probably  due  in  part 
to  its  general  coordinating  function.  On  account  of  the  wide  connec- 
tion of  this  part  of  the  brain  with  almost  all  the  other  parts  of  the  en- 
cephalon  above  and  the  spinal  cord  below,  the  general  function  of  it 
is  believed  to  be  that  of  securing  the  higher  automatic  and  psycho- 
reflex  movements.  Even  its  great  function  of  maintaining  the  equi- 
librium is  in  all  probability  due  to  its  relationship  to  the  eighth  or 
space-sense  nerve.  The  wonder,  therefore,  is  that  the  localizing  symp- 
toms in  connection  with  the  cerebellum  are  as  definite  as  they  are. 

According  to  Bechterew,  the  olivary  bodies  subserve  the  function 
of  coordination,  the  impulses  reaching  the  cerebellum  by  way  of  the 
decussating  cerebello-olivary  tract.  No'  known  localization  symptoms 
have  as  yet  been  attributed  directly  to  the  olives.  According  to  the 
same  authority,  the  superior  olives  act  as  a  reflex  center  for  correlating 
the  movements  of  the  head  and  eyes  with  auditory  impressions. 

A  consideration  of  the  localizing"  symptoms  in  connection  with  the 
pontile,  nodal  and  cranial  nuclei  would  involve  a  discussion  of  the 
cranial  nerves. 

Thus  far  I  have  attempted  to  give  a  brief  resume  of  the  modern 
views  upon  the  sensory  motor  functions  of  the  brain,  and  in  doing  so 
I  have  incidentally  pointed  out  the  localization  symptoms  of  focal  dis- 
ease within  the  encephalic  mass.  The  localization  of  the  mind  and  the 
relationship  of  these  sensory  motor  functions  to  mientalization  is  a  vastly 
more  difficult  problem.  Nevertheless  I  will  briefly  attempt  toi  indicate 
the  probable  direction  which  its  future  solution  will  take. 

Luys  long  ago  remarked  that  certain  convolutions  were  distended 
and  hypertrophied  when  certain  mental  symptoms  were  present.  In  • 
cases  of  delirium  with  delusions  and  hallucinations  he  found  a  pro- 
nounced gibbosity  of  the  paracentral  lobule  to  which  a  strictly  motor 
function  is  usuafly  assigned.  Clinical  observation  has  so^  far  shown 
that  only  the  motor  zone  possesses  epileptogenous  characteristics, 
though  with  epilepsy  there  are  associated  many  sensory  phenomena.  It 
is  unfortunate  that  in  Luys'  observations  no  mention  was  made  as  to 
whether  the  delusions  and  hallucinations  partook  oi  the  motor  rather 
than  of  the  sensory  type ;  that  is,  whether  they  were  mental  representa- 
tions of  abnormal  kinesis  or  sesthesis.  They  seemed  to  show,  at  all 
events,  that  the  cortical  areas,  both  motor  and  sensory,  are  ideational 
and  psychic,  psychomotor  and  psycho-sensory  rather  than  simply  or- 
ganic. Mickle  showed  that  hallucinations  were  due  mostly  to  lesions 
in  the  sensory  centers  of  the  brain. 

The  cells  of  the  sensory  areas  are  preeminently  receptive,  and 
neither  physiological  experiinent  nor  clinico-pathological  observation 
has  yet  proved  that  they  are  in  any  way  emissive,  except  so  far  as  they 
may  send  inhibitory  impulses  into  the  motor  and  into  other  sensory 
centers  whereby  there  may  be  such  a  thing  as  a  tactile  paralysis  or  a 
sensory  aphasia.    There  can  be  little  doubt  that  these  sensory  cells  are 


742  THE   XOX-XEUROXIC  DISEASES 

connected,  mediately  or  immediately,  with  the  motor  cells  of  the  cortex. 
These  two  sets  of  cells,  thus  intimately  associated,  form  the  summit,  or 
bend,  as  it  were,  of  the  arc  about  which  travel  certain  sensory  motor 
impulses,  and  in  all  likelihood  constitute  the  true  physical  basis  of 
mind.  Von  Alonakow  declared  at  the  Thirteenth  International  Medical 
Congress,  held  in  1900.  that  he  believed  that  the  diverse  elements  which 
had  to  do  with  the  psychical  functions  were  scattered  all  over  the  entire 
cerebral  cortex.  The  gross  character  of  the  general  sensibility  and 
movements  of  the  body,  as  compared  with  the  special  senses,  necessi- 
tates a  larger  and  grosser  development  of  the  centers  that  subserve  the 
former  functions  than  those  that  subserve  the  latter.  This  may  be  the 
reason,  too,  why  they  are  more  readily  determined  than  the  latter.  In 
connection  with  sight  and  hearing,  however,  there  is  pretty  conclusive 
proof  that  the  sensory  and  motor  cells  are  in  close  juxtaposition  or  at 
least  functional  association.  It  is  a  warrantable  inference  therefore 
that  the  same  ideational  centers  cap,  as  it  were,  the  arcs  about  which 
play  the  afferent  and  efferent  impulses  from  the  eye  and  ear.  Hence  I 
take  it  that  the  cerebral  cortex  is,  after  all,  only  a  grand  reflex  center, 
the  summit  of  the  highest  reflex  arc.  It  is  far  more  delicately  organ- 
ized, more  richly  endowed  with  elements,  and  more  keenly  specialized 
than  the  reflex  centers  of  the  cord,  but  in  all  other  respects  it  is  quite 
comparable  to  the  latter,  both  functionalh"  and  structurally. 

Midwa}-  between  the  sensory  and  motor  elements  and  in  countless 
interconnections  with  them  are,  of  course,  countless  neurones  and  path- 
ways, commissural  and  associational  tracts.  Alind  rests  upon  the  whole 
basis,  afferent,  interpolated,  and  efferent  tracts  and  centers.  It  is  a 
product  of  their  activity  and  not  a  thing  with  a  local  habitat  in  this 
particular  spot  or  ganglionic  mass.  This  does  not  deny  the  possible 
existence  of  a  metaphysical  mind,  but  physiological  and  physiological 
psychology  is  incapable  of  taking  up  that  question. 

The  morphological  and  embryological  development  of  the  brain 
throws  a  flood  of  light  upon  the  relations  existing  between  the  motor 
and  sensory  elements.  Among  the  invertebrates  there  is,  strictly  speak- 
ing, no  such  brain  or  spinal  cord  as  we  find  among  the  higher  order  of 
animals.  Nevertheless,  the  spinal  cord  of  the  latter  is  clearly  fore- 
shadowed in  the  series  of  sensory-motor  ganglia  with  their  respective 
projecting  nerves  found  in  the  individual  segments  of  the  invertebrate. 
\\'e  know  that  in  the  articulates  and  insects  each  segment  is  furnished, 
as  it  were,  with  a  little  brain  of  its  own,  which  is  nothing  more  nor  less 
than  the  summit  of  the  reflex  arc  for  that  particular  segment.  We 
furthermore  know  that  the  ganglia  of  the  more  forward  segments  of 
the  creature  are  but  a  hyperdevelopment,  caused  by  an  increase  of  local 
function,  of  that  part  of  the  primitive  cord  or  elementary  chain  of 
ganglia.  The  explanation  of  the  cranial  nerves  is  only  possible  upon  a 
study  of  them  from  the  evolutional  and  embryological  standpoint ;  for 
whereas  the  visceral  components  of  some  of  them,  as,  for  instance, 
the  vagus,  are  still  traceable  to  their  primitive  segmental  origin,  others 
have  disappeared  or  become  incorporated  with  adjoining  sensory  and 
motor  nerv^es  as  to  quite  obscure  their  primitive  simple  arrangement. 
In  the  lower  cord  the  visceral  components  of  the  segmental  nerve  sup- 


THE   XOX-XEUROXIC  DISEASES  743 

ply  have  completely  disappeared  or  been  replaced  by  the  sympathetic, 
leaving  only  the  cutaneous  and  muscular  nerve  supply  represented  ni 
the  posterior  and  anterior  roots.  All  of  which  proves  the  primitive 
segmental  structure  of  the  entire  cerebro-spinal  axis.  In  some  of  the 
higher  representatives  of  the  worms  and  insects  the  ganglia  of  the 
most  anterior  part  of  the  body  become  massed  together  and  undergo  a 
somewhat  fuller  development  to  subserve  the  purpose  and  function  of 
special  senses.  In  this  way  they  assume  in  a  measure  the  general  char- 
acteristics of  the  vertebrate  brain,  and  in  their  further  phylogenetic  de- 
velopment become  so  complex  and  changed  in  form  and  location  as  to 
involve  their  corresponding  nerves  iri  the  same  confused  and  complicat- 
ed condition.  Hence  the  absence  of  that  simplicity  among  the  cranial 
nerves  that  we  see  in  the  arrangement  of  the  spinal  nerves. 

Note  the  exquisite  arrangement — exquisite  for  simplicity — of  the 
nen^ous  system  of  the  white  ant  (TeniiesJ,  of  the  fly  fMiiscaj,  and  of 
the  scorpion  spider  fThelyphonus  caudatusj.  In  all  of  these  creatures 
the  various  segmental  ganglia  are  connected  with  each  other  like  the 
cells  of  an  electric  battery.  Some  of  them  are  so  far  advanced  in  de- 
velopment that  they  simulate,  without  representing,  the  brain  and  spinal 
cord  of  the  highest  order  of  animals.  In  the  vertebrates  and  even  in 
tiieir  highest  representatives,  man  and  the  apes,  the  primitive  inverte- 
brate structure  of  the  whole  cerebro-spinal  axis  is  not  wholly  lost.  As 
Owen  says,  a  vertebrate  is  a  clothed  sum  of  segments,  and  therefore 
is  nothing  but  a  higher  invertebrate.  In  the  lowest  vertebrate,  the 
amphioxus,  there  is  only  a  spinal  cord  without,  comparatively  speaking, 
any  brain ;  and  in  all  of  its  habits  this  humble  creature  closely  resem- 
bles the  invertebrates.  Whether  it  be  finally  accepted  or  not  that  the 
human  skull  is  composed  of  a  number  of  metamorphosed  vertebrae,  the 
emibryological  development  of  the  brain  and  spinal  cord  out  of  the  one 
continuous  germ  layer  and  the  remarkable  similarity  of  the  brain  and 
cord  in  their  more  gross  structure  and  functions,  are  all  extremely 
indicative  of  the  primitive  characteristics  of  the  encephalon  of  man. 
If  there  be  any  truth  whatever  m  the  principle  of  evolution,  it  seems 
to  me  that  it  is  not  irrational  to  look  upon  the  brain  of  the  highest 
vertebrates  as  a  more  highly  developed  portion  of  the  spinal  marrow  or 
ganglia  of  the  cord  lying  most  frontad. 

In  speaking  of  what  he  calls  the  neurone-complex  in  its  relation  to 
brain  function,  von  "Monakow  says  that  it  is  the  smn  of  individual 
neurones,  which  articulate  one  from  the  other,  forming  progressively 
coordinate  systems  (projection  systems  of  ]\Ieynert),  of  which  system.s 
the  neurones  become  greater  and  greater  in  extent  as  they  approach  the 
cortex  (cells  of  projection  and  association)  the  minimum  of  which  is 
necessary  to  produce  in  the  adult  a  simple  nervous  act  such  as  a  lumin- 
ous impression.  Romanes,  in  his  Mental  Evolution  in  Animals,  adopts 
a  somewhat  similar  view  when  be  undertakes  an  explanation  of  con- 
sciousness and  its  dependence  upon  the  integrity  of  the  cerebral  cortex ; 
for  he  likens  cortical  activity  to  the  reflex  function  of  the  lower  parts 
of  the  central  nervous  system,  and  then  says  that  consciousness  is  the 
result  of  the  increased  resistance  which  the  original  sensory  impulses 
meet  with  in  their  passage  through  the  more  highly  developed  complex 


744  THE   NON-NEURONIC  DISEASES 

and  intricate  structure  of  the  cortex.  As  von  Monakow  notes,  the 
sensory  tracts,  upon  which  consciousness  and  intellection  primarily  de- 
pend, are  composed  of  a  great  number  of  these  "neurone-complexes," 
all  of  a  similar  nature,  the  more  central  of  which  are  myelinized  first, 
while  the  more  peripheral  ones  are  myelinized  later. 

If  all  this  be  so,  we  should  expect  some  similarity  between  the 
arrangement  of  the  sensory-motor  elements  of  the  brain  and  those  of 
the  vertebral  segments  of  the  cord.  The  motor  cells  would  not  be 
identical  with,  but  might  lie  in  close  proximity  and  intimate  relationship 
with  the  corresponding  sensory  cells.  The  extreme  simplicity  of  the 
arrangement  of  the  cells  in  the  cord  is,  of  course,  quite  obliterated  in 
the  brain  by  the  overcrowding  of  so  vast  a  number  of  nervous  elements 
in  so  confined  a  space  as  the  cranium.  The  rolling  about  of  the  en- 
cephalic ganglia  in  their  embryological  and  evolutional  development,  so 
as  to  accommodate  themselves  to  the  constrained  limits  of  the  skull,, 
results  in  a  more  or  less  complete  disappearance  of  that  relative  and 
simple  arrangement  of  the  sensory  and  motor  elements  seen  in  the 
vertebral  segments  of  the  cord.  We  can  clearly  recognize,  however, 
that  the  ganglia  and  cerebral  cortex  are  like  the  centers  of  the  sensory 
motor  reflex  arcs  found  in  the  cornua  of  the  cord.  It  is  observable,  for 
instance,  in  the  relative  arrangement  and  mutual  development  and  de- 
pendence of  the  motor  and  sensory  areas  of  the  brain.  General  sensa- 
tion is  the  least  specialized  of  man's  sensory  functions,  and  being  co- 
extensive with  the  entire  surface  of  the  body,  proves  man's  connection 
with  the  lower  animals.  The  contemporaneous  development,  the  simi- 
larity in  extent  and  the  relative  anteroposterior  location  of  the  cortical 
sensory  and  motor  areas,  all  reveal  their  connection  with  similarly  re- 
lated parts  of  the  body  and  their  homology  with  the  sensory-motor  arcs 
of  the  cord.  Their  unusual  development  in  size  and  functio^nal  activity 
gives  them  a  preponderance  over  the  corresponding  segmental  elements 
of  the  cord,  and  in  their  function,  especially,  makes  them  to  appear  as 
though  they  were  voluntary  while  the  latter  are  involuntary.  But  vol- 
untary and  involuntary  are  relative  terms,  merely  expressing  different 
degrees  of  the  same  form  of  nervous  activity.  The  psychic  functions  of 
the  cerebral  cortex  are  involuntary  quite  as  much,  if  not  in  so  glaring  a 
manner,  as  are  the  involuntary  functions  of  the  various  segments  of 
the  cord.  They  are  both  alike  a  form  of  reflex  action,  but  instead  of  the 
cerebral  reflexes  being  direct  and  unconscious,  as  the  spinal  reflexes  are, 
the  more  sensitively  and  highly  organized  character  of  the  cortex  causes 
them  to  assume  the  nature  of  consciousness  and  self-will, while  the  con- 
nection of  the  cortex  with  the  segments  of  the  cord,  as  these  in  turn  are 
again  connected  with  one  another,  causes  the  cortical  reflexes  to  be 
transmitted  and  perceived  through  the  medium  of  the  spinal  centers 
rather  than  directly  from  the  periphery  of  the  body.  In  regard  to  the 
special  senses  of  sight  and  hearing,  the  reflex  sensory-motor  arc  does 
net  pass  through  the  cord  or  its  ganglia,  but  is  limited  solely  to  the 
encephalic  gangHa,  while  their  sensory  elements  are  always  posterior 
to  and  more  or  less  in  close  proximity  with  the  motor  elements  just 
as  they  are  in  the  spinal  segments. 

The  bilaterality  of  the  cord,  both  in  structure  and  in  function,  is 


THE  NON-NEURONIC  DISEASES  745 

duplicated  in  that  of  the  encephalon.  At  the  session  of  the  Societe  de 
biologic  dc  Paris,  May  25,  1889,  M.  Dupuy  reported  a  case  that  showed 
the  identity  of  the  two  hemispheres  of  the  brain  in  regard  to  function. 
The  patient  possessed  the  power  of  moving  the  two  eyes  in  different 
directions  simultaneoush'.  Even  the  perceptive  centers  seemed  to  be 
distinct,  in  spite  of  the  opinion  of  Horsley  to  the  contrary,  for  the 
young  woman  saw  objects  with  one  eye,  and  when  she  tried  to  use  both 
eyes  together  to  view  the  same  object  she  was  overcome  with  dizziness. 
Magnan  has  had  four  cases  of  this  sort,  one  of  which  he  reported  in 
full.  The  patient  heard  one  class  of  statements  in  one  ear  and  another 
in  the  opposite  ear.  Agreeable  ideas  only  were  readily  received  on  one 
side  of  the  head,  disagreeable  ones  on  the  other.  The  independence 
of  the  hemispheres  has  for  a  long  time  been  a  subject  of  discussion  and 
partial  acceptance  among  neurologists.  Dr.  C.  L.  Bruce  reported  in 
Brain,  1895,  a  case  of  double  consciousness  in  regard  to  which  he  con- 
cluded that  there  was  right  hemispheric  melancholia  or  dementia,  with 
left  hemispheric  mania.  Kiernan  has  also  reported  twO'  cases  which  led 
him  to  believe  in  the  independent  action  of  the  hemispheres.  The  com- 
ing possibility  of  a  complete  independence  of  action  on  the  part  of  the 
hemispheres  in  regard  to  their  higher,  or  psychic,  function  would 
seem  to  be  foreshadowed  in  the  fact  already  well  recognized  that  the 
more  complex  and  independent  movements  of  the  body,  such  as  those 
of  the  hand,  have  less  of  a  bilateral  representation  in  the  cortex  than 
do  those  movements  which  are  less  complex,  such  as  the  movements 
of  the  respiratory  and  deglutitory  muscles.  Speech  and  its  mechanism 
have  attained  such  an  exalted  degree  of  development  and  specialization 
that  they  are  already  subserved  by  one  hemisphere  independently  of  the 
other.  Phelps'  recent  conclusions  from  a  large  clinico-pathological 
analysis,  that  the  left  brain  is  the  preeminent  seat  of  the  mental  faculties, 
is  indicative  of  the  independence,  in  part  at  least,  of  the  hemispheres. 
Brown-Sequard  insisted  long  ago  upon  the  identity  of  function  in  the 
two  hemispheres,  and  physiologists  are  now  beginning  to  recognize  the 
truth  of  this  fact  and  to  admit  the  possibility  of  their  independence  of 
action.  The  whole  question  is  most  interestingly  discussed  by  Dr. 
Ireland  in  his  work  The  Blot  on  the  Brain. 

I  conclude,  therefore,  that  man's  mental  activity  is  largely  auto- 
matic and  purely  reflex ;  that  the  cortical  centers  for  ideation  are  con- 
stituted, localized  and  interrelated  much  like  the  reflex  centers  of  the 
cord,  but  that  the  larger  and  more  complex  development  of  the  former 
confers  upon  them  the  possibility  of  a  higher  and  more  complex  form 
of  activity ;  that  the  sensory  and  motor  elements  of  the  cortex  are  not 
identical,  but  are  separate,  are  closely  intermingled,  and  are  most 
intimately  associated  with  one  another  in  function  ;  and,  finally,  that 
mentalization  is  somehow  subserved  by  the  entire  cortex  and  its  more  or 
less  independence  of  action  in  the  two  hemispheres. 

If  this  progressive  dififerentiation  of  function,  based  upon  the 
principle  of  simple  reflex  action,  continues  within  the  encephalon  as  it 
has  up  to  the  present  time  in  the  evolutional  development  of  the  whole 
nervous  system  in  animals,  it  may  ultimately  happen  that  the  mind  will 
acquire  the  power  of  thinking  upon  two  or  more  subjects  at  one  and 


746  THE  XOX-NEUROXIC  DISEASES 

the  same  moment.  Its  capabilities  in  this  direction  will  be  immensely 
enhanced,  and  the  old  dictum  of  the  psychologists  that  the  association 
of  two  or  more  ideas  is  always  consecutive,  never  coincident,  will  be 
overthrown.  In  his  essay  upon  the  Alolecular  Dynamics  of  the  En- 
cephalon,  published  in  the  American  Journal  of  Insanity  for  October, 
1889,  Dr.  Williams  hints  at  this  future  possibility.  "Who  knows,''  he 
asks,  "but  that  the  more  fully  evolved  mind  of  the  future  shall  learn, 
after  the  present  mind  has  come  to  look  with  stunned  discouragement 
upon  the  vast  field  of  knowledge  presented  to  its  view  by  an  advanced 
civilization, /gradually  to  so  adjust  its  fibres  and  its  vessels  by  isolating 
them  into  separate  fields  momentarily  (since  the  isolation  is  the  acme 
aimed  at  by  the  higher  mind  in  its  concentrated  workings  to-day),  that 
consciousness  may,  in  fact,  come  to  be  not  a  single  energy,  but  a  double, 
triple,  quadruple  or  multiple  energy  ?  Imagine,  for  example,  the  school 
boy  of  the  thirtieth  century  studying  his  mathematics  visually  with 
concentration,  while  orally  listening  to  a  lecture  on  a  different  topic. 
In  all  seriousness,  there  seem  to  be  some  reasons  for  believing  that  such 
a  seemingl}-  paradoxical  mentality  may  be  evolved."  The  tendency  of 
mental  and  brain  development  is  certainly  in  this  direction.  It  is 
already  so  striking  a  characteristic  of  the  human  mind  as  to  place  man 
in  a  position  above  the  lower  animals.  The  separation  of  the  various 
representative  areas  of  the  cortex,  so  that  even  now  an  animal  can 
feel  a  prick  of  a  pin  in  the  foot,  move  the  paw  and  listen  intently  to 
some  unwonted  sound,  all  at  the  same  instant,  would  seem  to  give 
promise  of  such  a  future  possibility  in  brain  development. 

A  mere  glance  at  the  localization  of  the  various  centers  of  the 
cerebro-spinal  apparatus  suggests  the  similarity  of  the  brain  and  cord 
in  regard  to  their  primitive  structure  and  inclines  one  to  believe  in 
the  more  ancient  and  higher  development,  both  anatomically  and  physi- 
ologically, of  the  more  forward  part  of  this  apparatus.  The  principle 
of  inhibition,  ever  since  its  discovery  in  connection  with  the  cardiac 
nerves,  has  been  applied  to  the  higher  cerebral  functions,  but  with 
variable  success  until  quite  recently.  When  closely  studied  it  appears 
that  inhibition  is  the  highest  function  of  nervous  matter.  To  inhibit  an 
action  and  thus  to  control  it,  presupposes  on  the  part  of  a  nervous  cen- 
ter a  finer  degree  of  organization  than  does  the  power  merely  to  receive 
and  transmit  reflex  impulses.  Inhibition  is  the  basal  phenomenon  of 
the  higher  mind,  and  is  of  such  a  startling  character  that  it  gives  us 
the  notion  of  an  absolute  independence  resulting  in  free  will.  An 
afferent  impulse  is  reflected  into  the  motorial  sphere,  but  is  checked  or 
inhibited  by  some  other  afferent  impulse  or  impulses  before  it  eventu- 
ates into  actual  movement ;  and  at  once  we  jump  to  the  conclusion  that 
our  free  and  independent  will  has  been  the  cause  of  the  motor  phenom- 
ena. The  inhibitory  function  of  the  mind  is  admitted  by  all  the  physi- 
ologists and  psychologists.  The  former  assert  that  were  it  not  for 
this  magnificent  function  of  all  the  cerebral  centers,  or  at  least  of  some 
of  the  highest  among  them,  our  bodies  would  be  kept  in  a  constant 
state  of  convulsion  through  the  manifold  impulses  which  our  nervous 
systems  are  ever  receiving  and  reflecting  outward  again  to  the  muscles. 
JNIills  speaks  of  the  higher  psychical  centers  in  the  forebrain  as  con- 


THE  NON-NEURONIC  DISEASES  ■  747 

stituting  the  "inhibiting  lobe."'  When  we  recollect  that  all  mentalization 
is  based  upon  sensory  and  motor  phenomena,  and  that  the  cortical 
areas  for  the  psychical  representation  of  these  phenomena  are  quite 
fairly  outlined,  we  are  not  surprised  that  there  should  be  so  much 
in3^stery  surrounding  the  functions  of  the  unknown  areas  of  the  brain. 
We  noted  that  injuries  of  the  prefrontal  lobes  always  gave  rise  to 
mental  deterioration  with  abnormal  psychical  phenomicna,  while  the 
best  physiologists  admit  that  one  function  of  this  terra  incognita  of  the 
■cerebral  cortex  is  at  least  that  of  inhibition.  Putting  all  facts  and  in- 
ferences together,  then,  we  may  conclude  that  the  power  of  inhibition  is 
the  last  of  the  acquired  functions  and  is  in  all  probability  the  special 
characteristic  of  the  most  highly  organized  nervous  matter;  that  this 
power  resides  in  the  gray  matter  of  the  prefrontal  lobes  to  a  very  large 
degree ;  and  that  therefore  these  lobes  are  preeminently  the  psychical 
-centers,  though  the  mind  in  toto  is  the  result  of  the  combined  activities 
of  all  the  sensory  motor  elements  of  the  cortex.  We  may  even  infer  that 
this  anterior,  highly  specialized  portion  of  the  brain  differs  from  the 
rest  of  the  nervous  apparatus  in  degree  rather  than  in  kind. 

Not  only  do  the  higher  cerebral  centers  exercise  an  inhibitory  con- 
trol over  the  spinal  cord  and  lower  centers,  but  certain  cerebral  centers 
-clearly  exercise  the  same  function  in  relation  to  other  cerebral  centers. 
I  suggested  this  fact  a  long  time  ago.  This  intracerebral  inhibition  was 
again  pointed  out  by  Pick,  of  Prague,  before  the  Thirteenth  Interna- 
tional Medical  Congress  in  1900,  and  illustrated  by  the  inhibitory  con- 
trol which  the  auditory  speech  centers  exercise  over  the  motor  speech 
-center.  As  is  well  known,  persons  suddenly  attacked  with  word- 
deafness  exhibit  in  addition  to  paraphasia,  a  special  symptom,  log- 
orrhoea.  The  importance  of  this  in  this  connection  is  that  it  furnishes 
the  first  positive  proof  that  in  the  sphere  of  the  higher  psychical  phe- 
nomena, the  mechanism  of  inhibition  enters  just  the  same  as  it  does 
in  the  domain  of  the  lower  nervous  system. 

The  known  sensory  and  motor  cerebral  centers  which  have  been 
described  include,  it  will  be  remembered,  the  central  convolutions,  part 
of  the  first  and  second  temporal,  part  of  the  occipital,  the  hippocampus, 
the  uncus,  and  part  of  the  limbic  lobes.  These  areas  are  in  connection 
with  what  Flechsig  calls  the  projection  system  of  fibres.  In  function 
they  are  identified  with  voluntary  movement,  general  and  tactile  sense, 
hearing,  sight,  smell  and  taste.  They  represent  approximately  about 
one-third  of  the  whole  brain  surface.  The  remaining  two-thirds  do  not 
seem  to  connect  with  parts  of  the  nervous  apparatus  lying  below  the 
brain,  but  with  one  another  and  with  the  parts  already  referred  to. 
Flechsig  calls  these  latter  areas  the  "higher  centers,"'  or  "association 
centers,"  and  believes  that  they  have  to  do  especially  with  the  com- 
plex mental  acts,  a  view,  however,  in  which  he  is  not  well  supported  by 
other  authorities.  As  Sachs  argues,  projection  and  association  fibres 
probably  arise  from  every  cortical  area.  Even  Flechsig  himself  has 
recently  admitted  that  the  projection  and  association  areas  are  not  so 
distinctly  defined  as  he  originally  believed  them  to  be.  The  generally 
accepted'  idea  that  the  frontal  lobes  preside  over  the  higher  psychic 
phenomena  need  not  preclude  the  idea  that  the  entire  cortex  is  more 


748  THE  NON-N  EURO  NIC  DISEASES 

or  less  involved  in  the  act  of  thinking.  As  Hitzig  remarks,  Flechsig's 
opinions  upon  the  purely  intellectual  function  of  the  association  areas, 
are  at  the  present  moment  extremely  hypothetical.  Even  the  theory 
which  localizes  the  so-called  memory-pictures  in  certain  cell  groups 
is  not  absolutely  proved.  About  all  that  can  be  affirmed  positively,  as 
the  result  of  the  brilliant  myelinization  method  of  investigation  em- 
ployed by  Flechsig,  is  that  in  the  cortex  certain  areas  are  primordial,, 
in  which  areas  the  projection  bundles  are  so  much  thicker  than  they- 
are  in  other  cortical  territories  :  and  that  the  development  of  the  sensory 
centers  precedes  in  all  likelihood  that  of  the  cortical  areas  which  serve 
as  a  basis  for  the  intellect.  To  go  further  than  this  and  declare  that 
the  intellect  is  the  result  of  special,  limited  cortical  foci,  with  a  par- 
ticular anatomical  structure,  as  Flechsig  is  inclined  to  do,  is  hardly 
allowable.  The  work  of  Flechsig  is  admitted  by  all,  however,  to  markr 
an  important  advance  in  our  knowledge  of  the  structure  and  function 
of  the  brain. 

In  the  evolution  of  the  nervous  system  the  centers  of  the  medulla 
oblongata  which  preside  ever  the  vital  processes  may  be  the  oldest  in 
time.  They  are  first  because  they  are  necessary  to  life  itself.  They 
take  precedence  phylogenetically.  Ontogenetically,  however,  there  are 
centers  which  precede  even  these  in  importance,  and  if,  as  the  biologists 
tell  us,  the  more  highly  organized  matter  is  probably  the  more  ancient 
(though  this  is  not  an  established  fact  by  any  means),  these  higher 
psychical  centers  may  be,  after  all,  the  oldest  in  time,  while  those  of 
the  medulla  may  be  later  differentiations  of  primitive  nervous  matter 
for  the  special  regulation  of  the  vital  processes.  It  is  not  improbable, 
therefore,  that  the  highly  specialized  inhibitory  centers  of  the  brain 
are  the  most  ancient  portions  of  the  nervous  apparatus,  so  far  as  their 
mere  evolution  is  concerned,  though  from  the  embryological  and  physi- 
ological standpoint  the  cord  is  to  be  regarded  as  the  priinitive  factor. 

In  its  influence  upon  the  next  lower  centers  the  forebrain  may  be 
compared  to  the  entire  brain  itself  in  its  influence  upon  the  centers  of 
the  medulla  and  spinal  cord.  In  both  cases  the  influence  is  chiefly 
inhibitory.  Thus  the  inhibitory  function  is  graduated  from  that  of 
the  highest  psychical  centers  down  to  that  of  the  lowest  organic  cen- 
ters of  the  cord  where  it  is  practically  so  overpowered  by  the  supreme 
inhibitory  influence  of  the  highest  centers,  that  it  appears  to  be  almost 
entirely  absent,  reducing  the  cord,  as  it  were,  to  a  mere  organ  of  gross 
and  unobstructed  reflex  action.  From  its  evolution,  therefore,  the  con- 
clusion may  be  drawn  that  the  entire  cerebro-spinal  axis  is  a  series  of 
connected  sensory  motor  ganglia,  reflex  couplets,  or  arcs,  dififering  in 
its  several  parts  more  in  degree  than  in  kind.  The  more  frontal  ganglia 
subserve  the  purpose  of  psychosis,  which  in  its  highest  manifestation 
is  the  expression  of  an  inhibition  and  which  differs  from  the  spinal  cord 
neurosis  chiefly  in  respect  to  consciousness.  Consciousness  and  its- 
physiological  explanation  are  in  need  of  much  elucidation ;  its  localiza- 
tion is  still  an  undetermined  question.  Brain  and  spinal  cord  are  never- 
theless shown  to  be  mere  arbitrary  divisions  of  a  uniform,  continuous, 
composite  organ  whose  functions  are  more  or  less  the  same  throughout 


THE   XOX-XEUROXIC  DISEASES  749 

all  of  its  parts,  these  functions  being  simply  adaptive  modifications  of 
the  primitive  senscry-niotor  reflex. 

SY^IPTOMS  OF  DISEASE  OF  THE  BRAIX. 

The  nervous  system,  as  I  have  previously  pointed  out,  is  a  uni- 
form, similarly  arranged  network  of  neurones  throughout  all  of  its 
parts.  Every  evidence  points  to  the  fact  that  these  neurones  possess, 
per  se,  the  same  general  functions  wherever  they  may  be  located.  In- 
tracranial neurones  are  no  different,  structurally  or  functionallv,  from 
intraspinal  neurones.  Association  and  commissural  tracts  are  prac- 
tically the  same  as  projection  tracts  and  their  extension  into  peripheral 
nerves.  The  only  dissimilarity  between  different  parts  of  this  vast  and 
beautiful  network  of  irritable  cells  called  neurones  is  to  be  found  in 
certain  adventitious  elements,  such  as  the  sustentacular  structures  and 
the  end-organs. 

The  ner\'ous  system  is  a  single  organ  with  a  single  uniform  func- 
tion. Xeural  irritability  and  self-nutrition  are  its  only  essential  func- 
tions when  it  is  contemplated  apart  from  all  of  its  mere  connections 
with  other  organs  and  its  juxtaposition  to  certain  connective-tissue  and 
vascular  elements.  If  it  were  thus  entirely  independent  and  separate 
from  everything  else,  its  symptomatology  would  be  a  matter  of  mar- 
velous simplicity. 

The  simple  function  of  neurility,  or  nervous  irritability,  inherent  in 
the  neurones,  is,  however,  made  to  appear  very  complex  and  varied  by 
the  fact  that  different  groups  of  neurones  are  connected  with  different 
structures  in  different  parts  of  the  body.  So  far  as  the  neurones  them- 
selves are  concerned,  sensation  is  the  same  in  the  optic  as  it  is  in  the 
spinal  neurones ;  motion  is  the  same  in  the  facial  nerve  neurones  as  it 
is  in  the  cardiac  nerve  neurones ;  secretion  is  the  same  in  the  salivary 
.gland  neurones  as  it  is  in  the  renal  cell  neurones.  To  the  particular 
end-organs  of  sense,  motion  and  secretion,  the  neurones  merely  fur- 
nish a  peculiar  form  of  irritability ;  or,  to  state  it  better,  they  are  irri- 
tated in  their  own  peculiar  way  by  certain  sensory  organs,  which  irrita- 
tion they  transfer,  as  a  form  of  excitability,  over  to  certain  motor  and 
secretory  organs.  The  functions  of  the  nervous  apparatus  may  thus 
T>e  regarded  as  priinarx  and  secondary.  Neurility  and  self-nutrition  are 
its  primary  functions ;  motion,  sensation,  trophism  are  its  secondary 
functions. 

In  the  diagnosis  of  a  nervous  disease  the  pathological  diagnosis 
involves,  and  is  largely  dependent  upon,  the  disturbances  of  the  primary 
functions.  Primary  and  secondary  degenerations,  inflammations,  etc., 
all  have  to  do  with  the  manifestation  of  neurility  and  self-nutrition  in 
the  nervous  elements.  We  have  no  special  names  for  these  primary- 
symptomatic  manifestations  of  disease  in  the  neurones,  because  at  the 
time  that  neurological  nomenclature  was  created  the  neuronic  structure 
of  the  nervous  apparatus  was  unknown.  We  use  the  terms  paralysis, 
irritation,  spasm  sometimes  in  the  sense  of  deficient  or  exaggerated 
neurone  irritability.  It  is  obvious,  though,  that  the  terms  are  used  in 
a  metaphorical   sense.     AVe  are   applying,   in   using  them,  our   ideas 


750  THE   XOX-XEUROXIC  DISEASES 

formed  from  muscular  manifestations  to  the  neurone  manifestations. 
We  say  a  nerve  is  paralyzed,  whereas  the  word  paralysis  specifically 
means  loss  of  motion  or  sensation.  This  loss  of  motion  or  sensation 
may  indeed  be  due  to  the  death  of  the  neurones,  but  it  may  also  be 
due  to  damage  in  the  muscular  tissue  or  sensory  end-oir'gan.  It  is  ob- 
vious that  we  are  in  need  of  a  nomenclature  to  distinguish  neurone  ces- 
sation of  function  apart  from  mere  muscular  or  sensory  cessation  of 
function.  ,  Until  we  have  such  a  nomenclature,  we  must  still  go  on 
applying  terms  symptomatic  of  non-neural  disturbances  to  the  symp- 
tomatic exhibitions  of  pure  neural  disturbances.  Because  of  this  hiatus 
in  neurological  nomenclature,  it  is  all  the  more  imperative  that  we 
should  most  carefully  distinguish  the  neural  from  the  non-neural  mani- 
iestations  of  disease.  We  must  be  careful  not  to  attribute  every 
paralysis  to  nervous  trouble.  We  must  not  imagine  that  every  visual 
disturbance  is  indicative  of  disease  in  the  eyeball.  We  must  not  fancy 
that  every  parsesthesia  is  a  sign  of  neuronic  disorder.  Like  a  great  wall 
around  the  nervous  system  is  the  aggregate  of  all  these  peripheral  end- 
organs  that  are  in  relation  to  it.  Behind  this  wall  is  hiding  the  nervous 
network  which  is  uniform  in  structure  and  function  throughout  all  of 
its  parts.  There  are  diseases  which  belong  to  and  damage  the  end- 
organs  or  outer  wall.  There  are  diseases  that  damage  the  nervous  ap- 
paratus hiding  behind  it.  The  two  must  be  carefully  differentiated,  else 
most  disastrous  blunders  will  be  made. 

Xine-tenths  of  neurological  diagnostic  criteria  involve  the  mani- 
festations in  the  outer  wall  around  the  nervous  apparatus,  the  end- 
organs.  As  these  end-organs  are  so  varied,  we  have  a  varied  symp- 
tomatology'. In  this  way  we  localize  lesions  within  the  nervous  system. 
I  repeat  with  emphasis  that  these  localization  symptoms  which  are 
based  upon  the  secondary  functions  of  the  nervous  apparatus  must  not 
be  imagined  as  giving  us  "any  special  information  as  to  the  primary  or 
neuronic  disturbances.  Inferentially  they  help  us  to  determine  whether 
the  disease  is  neural  or  non-neural,  but  only  inferentially.  The  latter 
must  be  made  out  from  the  etiology  and  certain  special  phenomena  like 
the  electrical  reaction  of  degeneration. 

The  localization  symptoms  being  the  most  obtrusive,  and  those 
upon  which  we  must  largely  depend  in  the  making  of  our  diagnosis, 
it  is  profitable  that  we  should  discuss  them  along  general  lines  before 
taking  them  up  in  detail  under  the  head  of  special  diseases. 

The  ideal  localization  of  neurological  manifestations  would,  of 
course,  be'  the  neuronic.  We  have  attained  this  desirable  goal  in  re- 
gard to  a  few  diseases.  We  recognize  the  neuronic  localization  of  the 
lesion,  for  instance,  in  locomotor  ataxia,  progressive  muscular  atrophy, 
certain  degenerative  neuritides.  In  time  we  may  determine  the  neuronic 
localization  of  many  more,  if  not  all,  of  the  special  diseases  to  which 
the  nervous  apparatus  is  liable.  W^e  may  be  able  in  time  to  localize  the 
neurones  that  are  at  fault  in  hysterical  and  other  psychic  troubles.  At 
present  our  knowledge  of  nervous  physiology  is  so  small  and  coarse 
that  in  many  of  our  localizations  we  cannot  get  farther  than  such  crude 
anatomical  subdivisions  as  the  brain,  spinal  cord  and  nerves.  We  have 
refined  a  little  upon  these  crude  localizations  without  vet  attaining  to 


THE  NON-NEURONIC  DISEASES  75  I 

the  neuronic  refinement  of  them.  Thus,  in  the  brain  we  have  discov- 
ered certain  areas  of  the  cortex  as  having  certain  peripheral  relation- 
ships that  give  them  apparently  distinct,  secondary  functions.  The 
outlines  of  these  areas,  however,  are  still  most  obscure  and  their  inter- 
relationships with  one  another  are  still  mysterious.  In  regard  to  other 
parts  of  the  cortex  and  the  great  central  ganglia  at  the  base  of  the 
brain,  we  know  practically  nothing,  though  functionally  they  are  at  the 
basis  of  mentalization  and  other  cerebral  phenomena. 

In  a  coarse  way,  then,  we  can  distinguish  what  we  are  pleased  to 
call  brain  symptoms.  A  few  of  these  brain  symptoms  have  been  dis- 
cussed in  the  previous  section  upon  the  Physiology  of  the  Brain  and 
Cerebral  Localization.  Here  I  purpose  to  recapitulate  a  few  of  the 
more  important  manifestations  which  indicate  in  a  rough  way  disease  or 
that  part  of  the  nervous  apparatus  that  happens  to  constitute  the  cere- 
brum. The  symptoms  of  disease  of  the  medulla  and  cerebellum  will  be 
considered  later. 

In  the  making  of  a  diagnosis  it  is  important,  first,  to  decide  that 
the  trouble  is  a  brain  disease,  and  secondly,  to  localize  the  lesion  in  some 
part  of  the  brain.  The  former  can  be  decided  from  general  symptoms ; 
the  latter  must  be  made  from  focal  symptoms. 

General  Symptoms  of  Disease  of  the  Brain. — Of  these  head- 
ache is  probably  one  of  the  most  common.  Nearly  every  disease  of  the 
brain,  whether  neuronic  or  non-neuronic,  organic  or  functional,  is  more 
or  less  accompanied  by  headache.  It  must  not  be  inferred  from  this, 
however,  that  all  headaches  point  to  brain  disease.  There  are  many 
nerves  in  and  about  the  head  that  may  be  variously  affected  without  the 
brain  being  the  direct  source  of  the  pain.  Nevertheless,  it  is  a  most 
important  truth  that  when  the  brain  is  affected,  headache  is  sometime 
or  other  present. 

It  would  lead  me  too  far  to  discuss  cerebral  headaches  here;  es- 
pecially as  I  have  taken  up  the  subject  of  cephalalgia  in  a  special 
chapter. 

By  itself,  headache  is  of  very  little  value  as  a  symptom.  In  con- 
junction with  other  symptoms  it  is  of  the  greatest  value.  In  organic 
cerebral  disease  the  headache  is  somewhat  definitely  localized,  is  asso- 
ciated with  tenderness  upon  percussion,  is  more  or  less  constant,  though 
it  may  be  with  periods  of  exacerbation,  and  is  of  a  dull,  boring  char- 
acter, or  sharp,  knife-like  and  penetrating.  It  is  increased  by  such 
sensory  irritation  as  loud  noises,  bright  light,  sudden  jars  caused  by 
coughing,  sneezing,  etc.  Circulatory  disturbances  may  modify  it.  In 
the  psychoneuroses,  such  as  hysteria  and  neurasthenia,  it  is  apt  to  be 
more  diffuse,  variable  as  to  intensity  and  location,  and  to  a  certain 
extent  under  the  influence  of  the  mind. 

Vomiting  of  a  particular  type  is  characteristic  of  brain  disease. 
It  is  spoken  of  as  cerebral  or  nervous  vomiting.  The  suddenness  of 
it  has  caused  it  to  be  named  "projectile"  vomiting.  It  is  frequently 
associated  with  headache,  and  comes  and  disappears  with  the  nervous 
exacerbations.  It  is  usually  not  dependent  upon  the  ingestion  ol  food, 
but  may  take  place  at  most  unexpected  times.  It  is  devoid  of  strain. 
In  all  these  respects  it  is  unlike  the  vomiting  of  gastric  disorder.     The 


752  THE   XOX-XEURONIC  DISEASES 

vomiting-  of  alcoholism  is  a  gastric  symptom.  The  vomiting  of  fever, 
ur.nemia,  migraine,  hysteria  and  some  cases  of  neurasthenia  is  due  to 
cerebral  disturbance.  The  most  characteristic  form  of  projectile  emesis 
is  seen  in  tumor  of  the  cerebellum  and  medulla.  In  coiiibination  with 
other  symptoms  it  is  all  but  pathognomonic  of  disease  here.  It  occurs 
in  meningitis,  abscess,  hemorrhage  and  other  lesions  that  increase  the 
intracranial  pressure.  Irritation  of  the  gastric  vagus  center  in  the 
medulla  is  the  probable  explanation  of  it. 

Xaiisea  may  or  may  not  accompany  the  vomiting.  Sometimes  it  is 
very  distressing.  Occasionally  it  occurs  without  the  hyperemesis. 
Vomiting,  with  or  without  nausea,  associated  with  cephalalgia  and  not 
accountable  for  on  the  ground  of  gastric  trouble,  should  arouse  the 
strongest  sort  of  a  suspicion  of  intracranial  disease.  An  immediate 
examination  of  the  eyes  is  then  called  for  to  determine  the  absence  or 
presence  of  choked  disc. 

Vertigo  is  not  an  important  brain  symptom.  It  is  not  the  same 
as  incoordination  or  mere  loss  of  equilibrium,  which  is  so  marked  a 
feature  in  cerebellar  disease.  As  I  have  discussed  the  nature  of  vertigo 
in  considerable  detail  in  a  section"  by  itself,  I  will  omit  further  consid- 
eration of  it  here. 

Temperature. — Elevation  of  the  temperature  accompanies  many 
affections  of  the  brain,  but  it  is  due  to  the  general  disease  process  and 
not  to  the  special  fact  that  the  latter  is  located  in  the  brain.  Infectious 
inflammatory  states  produce  fever  when  they  attack  the  brain,  just  the 
same  as  when  they  attack  any  other  organ.  It  is  not  alw^ays  easy  to 
determine  how  much  of  the  temperature  is  due  to  the  general  infection 
and  how  much  to  the  local  intlammation  constituting  part  of  that 
general  infection.  A  tubercular  meningitis  may  exhibit  an  elevated 
temperature,  not  on  account  of  the  inflamed  meninges  so  much  as  on 
account  of  the  general  constitutional  tuberculosis. 

Sometimes  there  is  a  rise  of  temperature  in  disease  of  the  brain 
when  the  pathological  process  is  not  markedly  inflammatory.  It  is  then 
the  expression  of  a  disturbed  nervous  function.  Very  high  tempera- 
tures occur  thus.  Lesions  of  the  pons  and  medulla,  especially,  provoke 
such  pure  neurotic  temperatures.  They  may  even  run  as  high  as  io8 
degrees  F.  and  be  very  misleading.  In  hysteria,  neurasthenia  and  other 
neuroses,  neurotic  elevation  of  temperature  certainly  does  occur  at 
times.  There  are  supposed  to  be  heat  regulating  centers  in  the  brain, 
and  they  probably  are  intimately  associated  with  the  vasomotor  centers. 
It  is  a  difficult  matter  at  times  to  differentiate  a  mere  nervous  elevation 
of  temperature  from  one  due  to  an  infectious  or  inflammatory  process. 
It  may  be  said,  however,  that  pure  nervous  temperatures  are  apt  to 
be  sudden,  changeable  and  temporary.  The  pulse  does  not  exhibit  any 
corresponding  relationship  to  them.  When  they  are  very  high  they 
are  usually  bad  signs. 

Sometimes  there  is  a  serious  intracranial  disease  without  any 
alteration  of  the  temperature. 

In  the  initial  stage  of  cerebral  hemorrhage  the  temperature  drops 
below  the  normal. 

Pulse. — It  is  a  curious  fact  that  the  pulse  may  be  much  less  fre- 


THE  NON-NEURONIC  DISEASES 


753 


<-jnent  in  febrile  disease  of  the  brain  than  it  would  be  with  the  same 
febrile  affection  in  any  other  organ.  In  some  diseases  of  the  brain  it 
may  be  subnormal.  This  is  seen  in  tumor  and  abscess.  Simple  inflam- 
matory and  infectious  processes  usually  have  a  rapid  pulse,  thoug-h 
there  is  less  frequently  here  than  in  disease  elsewhere  a  correspondence 
between  the  pulse  and  the  temperature.  A  rapid  pulse  may  indicate 
■damage  to  the  vagus  center  in  the  medulla.  The  slow  pulse  of  menin- 
gitis in  children,  of  apoplexy  and  of  general  intracranial  pressure  is 
believed  to  be  due  to  over-action  of  the  inhibitory  .center  upon  the  heart. 

Respiration. — The  respiratory  phenomena  of  brain  disease  are 
numerous  and  important.  The  respirations  are  usually  diminished 
when  the  brain  functions  are  lowered.  I  recently  saw  a  dangerous  ex- 
ample of  this  in  a  case  of  chronic  lead  encephalopathy.  In  coma  and 
stupor  it  is  often  lessened.  In  meningitis  and  apoplectic  strokes  it 
assumes  the  Cheyne-Stokes  type  and  becomes  a  bad  omen.  This  type 
of  breathing  occurs  in  other  diseases,  such  as  pneumonia,  scarlet  fever, 
■diphtheria,  opium  poiso^ning,  but  it  is  a  less  grave  symptoiTi  in  them 
than  it  is  in  brain  disease. 

In  the  Cheync-Stokes  breathing  there  is  a  remarkable  cycle  of 
increasing  and  decreasing  depth.  There  are  first  a  few  superficial 
breaths.  These  gradually  increase  in  rapidity  and  depth  and  become 
noisy.  Then  a  fall  takes  place  until  there  is  actual  cessation.  After 
a  pause,  however,  the  slight  respiratory  movements  begin  again,  grad- 
ually increase  in  intensity,  until  there  is  a  deep  dyspnoeal  breathing 
once  more  and  the  respirations  again  lessen.  The  pupils  usually  con- 
tract and  the  heart  action  diminishes  during  the  pause,  which  may 
last  from  five  to  forty  seconds.  The  duration  of  the  cycle  may  be 
fifteen  to  seventy-five  seconds.  Never  do  the  respirations  of  each 
•cycle  exceed  thirty  in  number. 

Sometimes  the  respirations  begin  with  great  suddenness.  Some- 
times they  begin  and  terminate  suddenly.  This  has  been  seen  in 
meningitis  and  is  known  as  Biot's  type  of  breathing. 

Irregular  breathing  and  cessation  of  breathing  occur  in  disease  of 
the  medulla.  Under  such  circumstances  the  heart  has  been  seen  to 
■continue  in  action  and  death  was  prevented  by  artificial  respiration. 

Renal  syuiptoms  may  be  indicative  of  disease  of  the  brain,  but 
more  often  they  are  concomitant  manifestations.  Albuminuria  and 
glycosuria,  more  frequently  polyuria,  accompany  lesions  in  the  medul- 
la. Cardiac  disease  and  renal  trouble  are  not  infrequently  associated 
with  cerebral  vascular  disorders.  Mental  disorders  are  the  cause  of 
urinary  and  fzecal  incontinence  when  there  is  no  paralysis  of  the  vesical 
and  rectal  sphincters.  The  polyuria  of  the  neuroses  and  psychoneuroses, 
such  as  hysteria  and  certain  spasmodic  troubles,  need  only  to  be  men- 
tioned. 

Psychic  Symptoms.  Psychosis. — The  symptoms  which  I  have 
considered  up  to  this  point  are  so  general  in  character  that  they  only 
point  to  intracranial  disease  when  they  are  associated  with  other  more 
suggestive  signs.  Many  of  them  occur  in  other  diseases.  They  are 
therefore  not  in  the  least  distinctively  encephalic. 

The  symptoms  which  we  are  now  about  to  take  up  point  to  the 


754  THE  XOX-XEUROXIC  DISEASES 

brain,  but  while  often  dependent  directly  upon  brain  disease,  they  are 
not  necessarily  so  in  all  cases. 

A  psychosis  means  a  mental  aberration,  an  unusual  exhibition  of 
mental  manifestation.  Were  we  acquainted  with  the  true  nature  of  the 
mind,  there  would  be  less  confusion  in  connection  with  these  symp- 
toms and  their  localizing  w^orth  would  be  greater  than  it  is. 

The  seat  of  the  mind  is  assumed  to  be  the  brain ;  some  say  the 
anterior  part  of  the  frontal  lobe.  It  has  even  been  affirmed  that  in 
right-handed  people  it  is  in  the  anterior  left  frontal  lobe.  As  a  matter 
of  fact,  we  know  nothing  of  its  localization.  It  probably  has  its  chief 
focus  of  manifestation  in  the  brain  cortex,  because  there  the  highest 
neurone  cell-bodies  are  located,  but  that  its  existence  is  not  due  solely  to 
the  cortex  in  its  healthy  state  is  shown  by  the  fact  that  it  can  be  made 
to  exhibit  most  extraordinary  and  even  insane  manifestations  by  dis- 
ease in  parts  of  the  body  remote  from  the  brain.  In  other  words,  mind 
is  more  or  less  coextensive  with  the  nervous  mechanism. 

How  are  we  to  explain  this  apparent  contradiction  that  the  mind 
is  located  in  the  brain  and  yet  is  so  subject  to  remote  neural  disorders? 
It  seems  to  me  that  no  psychology  offers  so  clear  an  explanation  as 
does  the  voluntaristic  psychology  so  ablv  taught  by  AVundt,  of  Ger- 
many. 

The  mind  As  not  a  thing  or  entity  with  a  local  seat.  It  is  but  the 
name  which  we  apply  to  the  internal  interplay  of  the  afferent  impulses 
one  upon  the  other.  It  is  a  pure  function,  a  secondary  product.  Even 
the  use  of  the  term  product  is  misleading,  for  mind  is  not  even  pro- 
duced from  something;  it  is  the  something  itself,  and  that  something 
is  the  inner  operation  of  the  thousand  and  one  impulses  passing  up  to 
the  brain  along  the  afferent  path\vays  and  playing  against  and  in  and 
out  among  themselves.  They  are  the  same  impulses,  perhaps  slightly 
modified  in  the  cord,  that  started  from  the  periphery,  but  now  in  their 
aggregate  complex  intermingling  constitute  what  we  call  the  mind. 
Mental  activity  is  but  the  inside  view  of  the  neurone  activities  whose 
outside  view  is  given  us  by  physiology. 

Physiology  is  the  objective  contemplation  of  elementary  nei^'ous 
functions ;    psychology  is  their  subjective  contemplation. 

Physiology  and  psychology  are  thus  facing  each  other  and  are 
explaining  from  directly  opposite  points  of  view  the  same  set  of  neural 
manifestations.  They  both  analyze  and  combine  the  phenomena  which 
present  themselves  in  the  workings  of  the  nervous  system  on  the 
outward  and  the  inward  sides  respectively.  Outwardly  the  physio- 
logical elements  are  the  neurones  and  their  manifestations  under  vari- 
ous stimuli.  Inwardly  the  psychological  elements  are  the  sensations 
and  feelings.  When  the  outer  elements  are  collected  together  and 
work  normally,  we  have  a  normal,  physiological  nervous  apparatus ; 
when  the  inner  elements  are  taken  in  the  aggregate  and  work  together 
normally,  we  have  the  normal  manifestation  of  mind.  The  psychic 
elements  include  the  five  senses  and  the  feelings  associated  with  them. 
Out  of  the  innumerable  combinations  and  recombinations  of  these 
psychic  elements  the  various  faculties  of  the  mind,  such  as  the  mem- 


THE   NON-XEURONIC  DISEASES  755 

cry,  the  imagination,  the  will,  the  judgment,  are  evolved.  To  show 
how  would  be,  of  course,  be3'ond  the  province  of  this  work. 

This  physiological  psyclr]ology  and  explanation  of  mind  is  called 
vohmtaristic  because  it  teaches  that  all  of  the  faculties,  like  the  volition, 
are  mere  proicesses.  It  has  long  been  recognized  that  volition  is  but  a 
convenient  term  to  express  the  overflow  of  certain  afferent  impulses  into 
efferent  impulses.  The  will  is  not  something  apart  by  itself ;  it  is  a 
high  order  of  functional  manifestation  between  certain  psychic  ele- 
ments ;  which  psychic  elements  in  turn  are  but  the  inner  representation 
of  the  primary  physiological  sensations.  What  is  true  of  the  will  is 
true  of  the  mind  and  all  of  its  so-called  faculties,  and  hence  the  name 
vohmtaristic  for  this  psychology. 

I  felt  it  necessary  to  introduce  here  this  brief  statement  of  the 
voluntaristic  explanation  of  mind,  because  it  underlies  the  explanations 
of  the  psychoses  presented  in  this  work. 

The  mind  being  thus  seen  to  be  dependent  upon  the  physical  senses, 
just  as  a  chord  struck  upon  the  piano  is  dependent  upon  the  individual 
notes,  but  not  being  the  same  as  *he  physical  senses,  but  rather  the 
result  of  their  aggregate  activities,  just  as  the  musical  chord  is  not  the 
same  as  the  individual  notes,  but  is  something  different  resulting  from 
their  aggregate  sound,  it  can  readily  be  understood  how  it  can  be 
disarranged  by  disturbance  both  in  the  individual  senses  and  in  their 
mere  interrelation  to  each  other.  Just  as  an  inha,rmonious  chord  can 
be  produced  out  of  a  harmonious  chord  upon  the  pianoforte  by  one 
note  of  the  chord  being  broken  on  the  one  hand  or  by  the  introduction, 
abstraction  or  other  disarrangement  among  the  notes  themselves ;  so  a 
psychosis  can  be  set  up  by  a  physical  disease  in  any  one  or  more  of  the 
anatomico-physiological  elements  upon  which  mind  depends,  or  by  a 
functional  disarrangement  among  the  elements  which  otherwise  may  be 
perfectly  normal.  In  this  way  we  can  account  for  mental  symptoms 
that  sometimes  seem  to  be  due  to  actual  physical  disease  and  that  at 
other  times  do  not  seem  to  have  any  apparent  physical  basis  at  all. 
For  example,  maniacal  manifestations  are  sometimes  clearly  due  to 
gross  meningo-encephalitic  changes ;  at  other  times,  as  in  certain  forms 
of  insanity,  they  seem  to  occur  without  any  discoverable  physical  basis. 
Hysterical  exhibitions  are  clearly  enough  due  to  physical  diseases  in 
some  instances ;  in  other  instances  no  changes  of  a  physical  sort  have 
ever  been  detected.  In  the  former  case  the  psychosis  was  a  physical 
phenomenon;   in  the  latter  it  was  purely  a  functional  exhibition. 

The  reader  will  now  understand  why  the  psychic  symptoms  which 
I  am  about  to  tabulate  are  not  absolutely  indicative  of  organic  brain 
disease,  though  they  are  always  indicative  of  the  functional  disturbance 
of  the  mind.  He  w411  also  note  how  important  it  is  not  to  jump  to  an 
immediate  conclusion  that  the  brain  is  diseased  or  the  mind  hopelessly 
affected  as  soon  as  any  of  the  following  mental  symptoms  show  them- 
selves. The  cause  of  these  symptoms  must  always  be  sought  for  first 
in  some  physical  disease.  If  this  is  removed,  they  may  vanish.  Im 
some  cases,  however,  these  mental  symptoms  will  appear  without  the 
existence  of  any  physical  disease.  They  are  probably  the  result  then 
of  disarranged  action  among  the  primary  psychic  elements,  such  as  is 


756  THE  NOX-XEUROXIC  DISEASES 

sometimes  seen  in  the  primary  psychoses  like  the  primary  hysterias  and 
fundamental  insanities.  None  but  ps}chic  treatment  can  hope  to  reach 
these  cases,  and  even  that  cannot  be  expected  to  do  much  in  severe 
examples. 

Wundt  has  shown  that  there  are  two  sets  of  psychic  elements,  the 
psychic  sensations  and  the  feelings,  out  of  which  the  entire  mind  is 
elaborated.  The  sensations  are  the  psychic  counterparts  of  the  physio- 
logical five  senses.  They  combine  and  interplay  to  form  the  memory, 
imagination,  reason,  judgment  and  intellectual  faculties.  The  feelings 
are  the  indefinable  appreciation  of  the  psychical  sensations ;  they  are 
accompaniments  of  the  latter.  Tkey  are  the  result  of  the  functional 
appreciation  of  the  psychic  elements  by  the  combined  product  of  those 
elements,  or  the  beginning  mind  or  ego.  The}-  are  the  counterparts, 
therefore,  in  a  way,  of  the  objectively  combined  physiological  elements 
that  enter  into  the  constitution  of  a  normal  nervous  mechanism.  They 
combine  to  form  emotions,  which  emotions  determine  the  motives,  and 
so  on  up  to  the  elaboration  of.  the  will.  At  the  bottom  of  mind  are  the 
psychic  sensations  and  psychic  feelings ;  at  the  top,  and  gradually 
elaborated  out  of  these  along  two  lines,  as  it  were,  are  the  judgment  and 
the  volition. 

When  the  mind  is  affected  with  disease  the  top,  of  course,  falls 
and  the  amount  of  the  loss  is  proportional  to  the  extent  of  the  disease. 
The  judgment  and  the  will  are  the  first  to  topple.  The  next  lower 
processes  are  thus  left  without  the  inhibition  normally  exercised  upon 
them  by  the  higher  faculties.  In  this  way  we  see  in  disease  the  imag- 
ination on  the  one  hand  running  riot  in  all  sorts  of  delusions,  and  the 
emotions  on  the  other  hand  bursting  out  into  uncontrollable  exaltations 
and  depressions.  If  still  more  of  the  mind  is  overthrown,  the  imagina- 
tion and  the  emotions  disappear,  amnesia  is  present  and  the  victim 
sits  in  a  condition  of  stupor.  The  next  stage  still  lower  is  one  of 
complete  dementia,  with  the  patient  in  a  mere  vegetative  state.  Tlie 
last  stage  is  the  total  abolition  of  all  mind  or  mental  death.  This  last 
condition  is  probably  never  seen  so  long  as  the  lower  or  vegetative 
functions  are  active,  for  even  the  lowest  idiot  has  a  trace  of  a  con- 
scious mind  still  left.  Total  abolition  of  mind  is  only  present  in  death. 
As  a  temporary  condition,  total  abolition  is  seen  in  coma  of  a  profound 
type. 

I  will  now  trace  downward  this  gradual  disappearance  of  the  mind 
as  it  is  seen  in  the  more  common  psychic  manifestations  of  brain 
disease. 

Abnormal  Intellectual  States. — These,  of  course,  are  innumerable 
and  varied,  but  as  they  are  the  outgrowth  of  psychic  sensations,  they 
mvolve  -illusions,  hallucinations  and  delusions.  The  basal  elements  be- 
ing disturbed,  the  composite  ideas  and  all  their  inter-connections  in  the 
most  exalted  forms  of  mental  acts  are  also  disturbed.  Hence  conscious- 
ness, attention,  cognition  and  recognition,  m.emory,  imagination  and 
reasoning  are  all  more  or  less  upset. 

An  illusion  is  a  misinterpretation  of  an  external  impression.  By 
reason  of  disorder  in  the  transmitting  apparatus,  afferent  special  and 
common  sensory  nerves  and  their  endings,  an  impulse  is  perceived  dif- 


THE   XOX-XEUROXIC  DISEASES  757 

ferently  from  what  it  should  be.  The  essential  feature  of  an  illusion  is 
that  there  is  an  actual  external  stimulation  of  the  nerves,  but  it  is  not 
recognized  in  its  true  light.  Illusions  mav  occur  through  any  of  the 
avenues  of  sense,  but  they  are  most  common  in  the  visual  and  auditory 
fields.  The  victim  of  illusions  beholds  a  brother,  say,  and  mistakes  him 
for  a  total  stranger ;  he  hears  a  whistle  and  declares  a  cat  mewed  ;  he 
lifts  a  feather  and  it  seems  like  a  piece  of  lead. 

I\Iild,  temporary  illusions  are  common  enough  in  ordinary  life 
among  perfectly  normal  people.  Our  senses  are  not  perfect  and  they 
are  constantly  giving  us  inaccurate  information;  but  we  immediately 
correct  the  errors  and  so  go  on  as  normal  beings  about  our  occupations. 
The  insane  individual  is  not  able  to  correct  his  illusions  and  so  he 
acts  accordingly  in  a  way  that  is  most  extraordinary  and  unusual. 

The  immediate  cause  of  many  illusions  can  readily  be  discovered 
in  the  afferent  peripheral  apparatus.  It  may  be  wax  in  the  ear  that  is 
disturbing  the  ingoing  auditory  impulses.  A  stone  in  the  bladder 
may  be  interpreted  by  the  patient's  senscrium  as  a  small  animal  that 
has  gotten  in  there.  Most  of  the  so-called  hallucinations  in  childhood 
are  really  illusions.     Pavor  nocturnus  may  sometimes  be  due  to  them. 

In  the  majority  of  cases  the  immediate  cause  of  illusions  is  a  dis- 
order in  the  perceptive  center.  This  is  showm  by  the  fact  that  the 
illusions  often  harmonize  with  the  delusions  present  and  thus  partake 
somewhat  of  the  nature  of  hallucinations.  It  is  obvious  that  an  illu- 
sion does  not  necessarily  represent  a  very  profound  degree  of  mental 
alienation.  It  becomes  a  sign  of  insanity  only  when  it  remains  un- 
corrected. 

A  deeper  degree  of  mental  disturbance  is  revealed  in  a  hallu- 
cination. Here  non-existent  objects  and  impressions  are  perceived; 
or,  in  other  words,  the  sensorium  projects  into  the  outer  world,  through 
the  avenues  of  sense,  its  own  formed  sensations,  which  sensations  are 
the  result  of  a  disorder  in  the  sense-apparatus  or  nerve-center. 

Unlike  illusions,  hallucinations  are  more  than  mere  misinterpreta- 
tions of  veritable  stimuli.  They  are  the  perception  of  stimuli  that  are 
immediate  to  the  sensorium,  but  are  accepted  as  being  veritably  objec- 
tive and  outside  of  the  sense-apparatus. 

Hallucinations  are  also  common  in  normal  life,  but  not  so  com- 
mon as  illusions.  They  are  immediately  corrected  in  the  same  way  as 
the  latter.  The  continuous  feeling  of  the  absent  member  in  an  ampu- 
tated arm  or  leg  is  an  excellent  illustration  of  an  hallucination.  Every 
one  has  heard  a  noise  sometime  or  other  when  there  was  actual  silence, 
or  seen  the  shadow  af  a  figure  when  no  person  was  near.  Illusions  and 
hallucinations  play  a  large  role  in  spiritualistic  phenomena  and  the 
seances  elaborately  built  up  upon  them.  Hallucinations  are  due  to  a 
disorder  of  the  sensory  nerve  centers  and  are  therefore  more  serious  and 
fundamental  than  are  illusions,  which  are  usually  due  to  disease  in  the 
peripheral  sensorv^  apparatus. 

Hallucinations  often  partake  of  the  nature  of  the  patient's  de- 
lusions and  thus  represent  a  most  advanced  state  of  alienation.  His 
delusions  being  of  a  persecutory  character,  say,  he  assumes  a  frightened 
manner,  begs  to  be  protected  and  shows  in  every  way  that  he  imagines 


75^  THE   NON-NEURONIC  DISEASES 

he  sees  those  who  are  going  to  harm  him.  Soiiie  of  the  attitudes  of 
hystero-epilepsy  are  undoubtedly  due  to  these  delusion  hallucinations. 
They  occur  in  some  sane  people  under  high  excitement  and  when  they 
are  between  sleep  and  waking.  Baillarger  calls  these  psychic  hallu- 
cinations, or  pseudo-hallucinations. 

Hallucinations  may  be  due  to  irritations  in  the  cortex,  but  they  are 
not  regarded  as  signs  of  insanity  so  long  as  the  subject  of  them  is 
able  to  correct  them  and  recognize  their  nature.  Hallucinations  under- 
lie many  of  the  assaults  and  murders  committed  by  the  insane. 

Delusions  are  false  beliefs.  Illusions  and  hallucinations  represent 
primary  disorder  in  the  psychic  elements  and  therefore  in  the  psychic 
ideas  which  are  the  outgrowth  oi  these  elements.  When  the  inter-con- 
nections especially  between  these  psychical  ideas  or  compounds  are 
disordered,  delusions  make  their  appearance.  Delusions  are  therefore 
generally  indicative  of  a  most  profound  sort  of  mental  aberration,  be- 
cause they  are  not  immediately  dependent  upon  disorder  in  anatomico'- 
physiological  elements,  but  in  the  functional  interplay  and  inter-cou- 
nection  between  the  psychical  elements  and  compoimds  which  are  de- 
pendent upon  them.  Delusions  are  radical  and  decidedly  mental.  They 
may  be  dependent  upon  a  physical  disease  in  a  physical  basis,  but  they 
are  also,  and  usually,  dependent  upon  a  complicated  and  complex  func- 
tional disturbance  in  a  very  high  order  oi  mechanism. 

Delusions  may  occur  in  health  as  well  as  disease.  It  is  difficult  to 
draw  a  sharp  line  between  the  delusions  of  sanity  and  insanity.  Estab- 
lished beliefs  and  convictions  must  be  taken  into  account.  The  whole 
history  of  mankind  is  full  Oif  false  beliefs.  If  these  are  not  corrected 
by  later  knowledge,  those  who  continue  to  live  under  them  are  not 
considered  insane.  If  they  are  corrected,  then  those  who<  still  retain 
them  are  regarded  as  mentally  unbalanced.  Believers  in  astrology, 
witchcraft  and  mythological  gods  are  deemed  mentally  diseased  if  they 
live  in  the  heart  of  modern  civilization.  They  would  not  have  been 
deemed  so  had  they  lived  in  earlier  times  or  did  they  now  live  among 
barbarians.  Therefore  the  ability  of  the  victim  to  correct  his  delusions 
must  be  considered  when  the  latter  are  being  considered  as  signs  of 
mental  alienation.  Because  we  cannot  always  determine  that  ability, 
from  our  want  of  knowledge  in  regard  to  the  patient's  early  influences, 
education  and  present  environment,  it  is  sometimes  a  difficult  question 
to  decide  as  to  whether  his  delusions  are  insane  or  merely  eccentric. 
The  laity  have  a  ready  rule  for  determining  what  they  consider  de- 
lusions ;  for  they  hold  everybody  crazy  that  do  not  hold  the  beliefs 
that  they  do.  To  the  scientific  physician,  however,  falls  the  arduous 
task  to  compare  the  delusions  with  all  that  makes  up  the  patient's  past 
history  and  his  present  environment,  and  from  that  comparison  deduce 
his  conclusions  as  to  their  sane  or  insane  origin.  It  is  the  province  of 
psychiatry  to  lay  down  the  guiding  principles  whereby  the  physician 
is  to  arrive  at  a  final  opinion. 

Delusions  may  be  sensorial  or  ideal.  The  former  are  founded  upon 
illusions  and  hallucinations.  If  these  are  persistent  and  uncorrected, 
and  the  patient  acts  in  accordance  with  them,  he  is  said  to  be  deluded. 
His  entire  mentalization  is  under  the  control  of  the  illusion  or  hallu- 


THE   NON-NEURONIC  DISEASES  759 

cination.  Ideal  delusions  are  spontaneous  false  concepts,  unrelated  to 
any  sensory  disturbances.  A  patient  who  believes  that  he  is  a  million- 
aire, that  he  has  a  thousand  children,  that  he  is  one  of  the  twelve 
apostles,  is  the  victim  of  an  ideal  delusion.  These  delusions  are  prom- 
inent in  the  religious  sphere  because  religion,  or  man's  dependence 
upon  a  superior,  protecting  Intelligence,  is  an  ancient  and  primitive 
concept.  They  may  occur  in  any  sphere,  however,  especially  the  sexual, 
alimentary  and  in  the  higher  regions  of  thought. 

Many  of  the  obsessions  of  the  ps^xhoneuroses,  the  imperative  con- 
ceptions, the  fixed  ideas,  the  phobias  mentioned  under  the  head  of  neu- 
rasthenia, are  of  the  nature  of  ideal  delusions.  The  difficulty  in  eradi- 
cating them  sometimes  is  recognized  by  every  clinician  and  shows  the 
profound  depth  of  their  origin.  At  other  times,  fortunately,  they  are 
so  slight  as  to  be  scarcely  more  than  the  similar  delusions  held  by  per- 
sons in  perfect  health. 

Delusions  occur  in  toxic  conditions-  (lead,  cannabis  indica,  alcohol, 
etc.),  in  low  adynamic  states,  in  starvation  and  in  the  delirium  of  acute 
general  diseases. 

Abnormal  Emotional  States. — As  I  have  pointed  out,  the  emo'- 
tional  states  are  the  outgrowth  of  those  psychic  elements  called  the 
feelings.  The  feelings  are  the  accompaniments  of  the  psychic  sensa- 
tions. Whereas  the  latter  lead  up  to  the  intellect,  the  feelings  by  com- 
bination and  recoinbination  ultimately  lead  up  to  the  will.  There  are 
mental  disturbances  that  show  themselves  proiminently  in  the  emo- 
tional sphere,  just  as  there  are  others  that  exhibit  themselves  promi- 
nently in  the  intellectual  sphere.  In  most  diseases  both  spheres  are 
more  or  less  implicated  together. 

Tlie  abnormal  emotional  states  assume  the  character  of  exaltations 
and  depressions.  These  range  all  the  way  from  health  up  to  actual 
maniacal  excitation  of  the  most  violent  sort,  or  down  to  a  most  extra- 
ordinary depth  of  melancholic  stupor  or  pure  indifl^erence. 

In  normal  individuals  we  often  observe  a  high  degree  of  emotion- 
ality. Emotions  underlie  the  motives,  as  the  word  itself  indicates — 
e-motives.  These  e-motives  combine  and  overflow  into  the  motor  sphere 
and  we  have  the  manifestation  of  volition.  If  they  are  weak  and  inade- 
quate, there  is  no  volition  and  the  subject  remains  inactive. 

Exaltation  and  depression  are  usually  dependent  upon  the  relative 
activity  of  the  mental  processes.  In  exaltation,  as  its  name  indicates, 
there  is  excess  of  ideation,  of  muscular  power  (apparently?),  of  circula- 
tion, of  visceral  activity  and  of  the  appetites.  These  reactions  are 
stimulating  and  pleasurable.  Hence  exaltation  is  usually  accompanied 
by  an  ecstatic,  satisfied  and  happy  frame  of  mind.  This,  however,  may 
easily  run  over  into  incoherence,  verbal  delirium,  muscular  excitability 
and  physical  violence.  The  condition  is  seen  in  mania,  mania  sine 
delirio,  dementia  paralytica,  etc. 

This  exaltation  may  be  due  to  nervous  weakness  (loss  of  inhibi- 
tion), as  well  as  to  excess  of  nervous  force.  It  may  alternate  with 
states  of  depression. 

Exaltation  is  sometimes  termed  psyclampsia  because,  like  muscular 
spasm,  it  is  a  sort  of  mental  over-action  or  psychic  spasm. 


760  THE   NON-NEURON IC  DISEASES 

Depression  is  usually  accompanied  by  corresponding  physical  con- 
ditions. There  is  general  debility,  lowered  muscular  power,  sluggish 
visceral  functions,  reduced  appetites,  retarded  metamorphosis.  It  is  the 
opposite  of  stimulation  and  therefore  not  pleasurable.  For  this  reason 
it  is  often  iermed  psychalgia,  or  psychic  pain.  There  is  a  want  of  voli- 
tion here,  a  want  of  speech,  a  want  of  interest.  Usually  there  is  intense 
melancholy.  This  may  pass  over  into  complete  stupor  and  indifference. 
An  appearance  of  indifference  must  not  mislead  the  physician,  however, 
into  thinking  that  it  is  real  always.  In  many  cases  there  is  psychic 
hvperjesthesia,  but  it  is  so  keen  and  so  painful  psychically  that  all  other 
psychic  manifes^tations  are  completely  paralyzed  and  an  attitude  of 
utter,  profound  indifference  is  assumed.  Depression  is  seen  in  melan- 
cholia, in  hysteria,  in  neurasthenia  and  in  the  prodromal  stage  of  mania 
and  dementia  paralytica. 

The  consciousness  is  often  disturbed  and  its  disturbance  is  among 
some  of  the  most  important  of  the  brain  symptoms.  Upon  the  basis 
of  the  voluntaristic  psychology,  consciousness  is  the  name  for  the  gen- 
eral synthesis  of  psychical  processes,  in  which  general  synthesis  the 
single  compounds  are  marked  off  as  more  intimate  combinations.  When 
this  inter-connection  of  compounds  (ideas  and  emotions)  is  interrupted, 
there  is  deep  sleep,  a  faint,  or  coma. 

Disturbances  of  consciousness  involve  abnormal  changes  in  the 
combination  of  psychical  compounds,  even  though  the  compounds  them- 
selves show  no  internal  changes  zvhatever.  This  is  a  most  important 
distinction,  for  upon  it  we  can  explain  many  of  the  phenomena  of  dis- 
ease which  involve  the  conscious  state  as  apart  from  the  mere  intellec- 
tual and  emotional  states  referred  to  above.  There  are  probably  in- 
numerable forms  of  disturbed  consciousness,  but  we  recognize  in  prac- 
tical semeiology  only  a  few,  and  these  I  will  now  refer  to  briefly. 

Delirium  is  a  characteristic  disturbance  of  consciousness  in  which 
there  is  mental  confusion  and  excitement  with  hallucinations,  motor 
restlessness  and  illogical  and  incoherent  thinking  expressed  in  words 
and  acts  that  betray  the  condition  present.  The  mental  processes  are 
here  perverted.  The  delirium  may  be  active  or  quiet,  low  and  mutter- 
ing or  wild  and  exhausting.  It  is  not  so  common  a  manifestation  of 
organic  brain  disease  as  it  is  of  cerebral  intoxication,  infection  and 
fever.  In  the  delirium  grave,  or  Bell's  mania,  the  symptom  is  most 
typically  observed.  There  are  alternations  of  active,  loquacious  periods, 
with  violent  struggling  and  attempts  to  leap  out  of  the  window,  etc. 
I  have  often  noticed  that  the  hallucinations  revolved  around  some  line 
of  thought  which  deeply  concerned  the  patient  before  the  disease  ap- 
peared. Hallucinations  of  speech  and  act,  indicating  a  basis  of  fear, 
may  thus  have  some  slight  foundation.  Often,  however,  there  is  no 
accounting  for  the  direction  of  the  hallucinations.  They  seem  to^  spring 
up  utterly  without  rhyme  or  reason. 

Loss  of  Consciousness. — Here  there  is  a  complete  suppression  of 
the  mind.  The  psychic  elements  themselves  have  been  abolished,  or 
their  interplay  has  been  completely  annulled.  This  condition  is  close 
to  sleep.  In  fact,  it  is  a  compulsory  sleep  with  certain  attendant  phe- 
nomena.    It  is  a  very  common  symptom  of  brain  disease.     It  occurs 


THE  NON-NEURONIC  DISEASES  761 

under  many  varied  conditions.  It  may  be  partial  or  complete.  The 
mere  vegetative  functions  of  the  body,  the  heart  action  and  respiration, 
need  not  necessarily  be  affected  in  coma,  though  often  they  are. 
Hebetude,  stupor,  somnolence,  sopor  and  coma  are  all  degrees' of  the 
loss  of  consciousness.  Stimulation  can  arouse  the  patient  less  and  less 
as  he  passes  from  the  first  into  the  last.  In  coma  the  sensations,  the 
reflexes  and  all  avenues  to  the  mind  seem  to  be  absolutely  closed.  The 
whole  brain  is  usually  affected  in  these  conditions. 

Tumor,  abscess,  tuberculous  meningitis  and  other  forms  of  intra- 
cranial pressure  and  intoxication  frequently  are  accompanied  by  mental 
stupor  and  dullness.  The  patient  is  listless  and  indifferent,  but  can 
be  aroused  into  a  momentary  exhibition  of  intelligence.  He  seems  to 
be  resting  under  a  cloud,  which  again  closes  over  his  mind  as  soon  as 
he  is  left  to  himself.  In  somnolence  the  stupor  assumes  a  deeper  shade 
and  resembles  profound  slumber.  In  these  states  the  urine  and  faeces 
are  often  involuntarily  passed,  though  the  sphincters  are  normal.  Food 
placed  in  the  mouth  may  at  first  be  chewed  and  then  is  left  there  with- 
out further  mastication.  The  patient  seems  to  have  suddenly  gone  to 
sleep  in  the  very  midst  of  the  act.  In  coma  there  is  no  response  what- 
ever and  there  is  no  attempt  at  chewing  and  swallowing  unless  the 
coma  is  very  light. 

The  loss  of  consciousness  may  come  on  gradually  or  abruptly.  It 
is  not  the  same  as  syncope  exactly,  and  yet  in  both  phenomena  the 
immediate  cause  is  the  anjemia  of  the  cortex.  Symptomatically  the 
great  feature  of  coma  is  the  loss  of  all  sensibility.  It  is  seen  in  epileptic 
seizures,  in  surgical  cerebral  compression  or  concussion,  in  ursemic 
poisoning,  in  acute  alcoholism,  in  toxic  narcosis  from  opiates,  morphia, 
chloral,  etc.,  and  in  congestive  or  malignant  malarial  fever.  Its  most 
typical  manifestation  is  probably  observed  in  cerebral  apoplexy,  whether 
hemorrhagic  or  embolic. 

The  differential  diagnosis  of  the  different  forms  of  co^ma  will  be 
found  under  the  heads  of  the  disease  in  which  it  occurs.  However,  it 
is  so  important  a  symptom  that  a  brief  recapitulation  will  not  be  out 
of  order  here. 

In  epileptic  coma  one  must  look  for  signs  of  a  previous  attack, 
such  as  the  lacerated  tongue,  the  ecchymoses  on  the  face,  neck  and 
chest,  the  frothy  saliva,  the  involuntary  micturition  or  seminal  dis- 
charge. The  coma  is  of  brief  duration  and  is  followed  by  a  small  rise 
of  temperature. 

The  unconsciousness  of  cerebral  concussion  or  compression  is  asso- 
ciated with  injury  about  the  head  or  body,  oozing  from  the  ears  or 
nose  of  blood,  meningeal  hemorrhage  with  gradual  stupor  without 
pronounced  hemiplegia. 

In  ura:mic  coma  there  is  anasarca  and  'slow  pulse.  If  the  urine  is 
drawn  by  catheter  and  tested,  it  is  albuminous  and  contains  casts.  The 
ophthalmoscope  reveals  a  neuro-retinitis. 

In  alcoholic  coma  the  patient  can  be  aroused.  It  is  more  of  a 
condition  of  stupor.  The  breath  is  alcoholic  and  the  temperature  may 
be  normal  or  subnormal.  Alcohol  can  sometimes  be  found  in  the 
urine. 


762  THE  NON-NliURONlC  DISEASES 

In  )iialignant  malarial  coma  there  are  no  physical  or  paralytic 
symptoms,  though  the  rectal  temperature  is  high.  The  spleen  is  en- 
larged.   The  blood  examination  for  the  plasmodiimi  is  final. 

Opium  narcosis  is  characterized  by  contracted  pupils,  subnormal 
temperature  and  slow  respiration. 

Apoplectic  coma  is  profoundly  paralytic.  There  is  hemiplegia 
with  conjugate  deviation  of  the  head  and  eyes,  the  patient  looking  to- 
wards the  lesion.  The  pupils  are  dilated.  The  temperature,  at  first  sub- 
normal, soon  rises. 

The  Cheyne-Stokes  respiration,  pupillary  changes,  alterations  in 
volume  and  rate  of  the  pulse  beat  are  all  accompaniments,  though  not 
important  ones,  of  the  comatose  state. 

Double  consciousness  is  a  condition  of  the  mind  seen  in  certain 
hysterical  states,  such  as  the  hypnotic  and  somnambulic,  and  in  certain 
forms  of  epilepsy  and  insanity.  The  patient  seems  to  have  both  a 
normal  and  a  morbid  mind  and  she  alternates  from  one  toi  the  other. 
Some  remarkable  cases  of  this  trouble  have  been  seen.  It  is  purely  a 
mental  disorder  and  seems  to  be  due  to  a  partial  abeyance  at  times  of 
the  mind.  It  occurs  in  a  slight  form  in  hysterics  and  sometimes  it  is 
the  caiise  of  the  strange  wanderings  and  doings  of  epileptics. 

Amnesia.  Mental  Failure.- — L.oss  of  memory  is  a  common  sign  of 
brain  disease.  It  occurs  in  the  mildest  neuroses.  It  may  be  soi  marked 
that  the  condition  becomes  one  of  actual  dementia.  Retention  is  the 
first  requisite  of  all  mental  activity.  None  of  the  higher  faculties  can 
exist  if  memory  is  gone.  Chronic  and  disseminated  diseases  of  the 
cortex  usually  have  among  their  earliest  and  prominent  symptoms 
amnesia.  There  are  special  types  of  amnesia,  which,  however,  are  not 
of  sufficient  importance  to  need  detailed  description  here. 

There  are  certain  psycho-sensory  and  psycho-motor  states  that 
might  very  appropriately  be  discussed  here  under  the  head  of  the 
psychic  manifestations  of  brain  disease.  They  are,  for  instance,  word- 
deafness,  word-blindness  or  alexia,  and  the  disorders  of  speech  included 
under  the  name  of  aphasia.  As  I  have  pointed  out  under  the  head  of 
Cerebral  Localizations,  there  are  areas  in  the  cortex  that  in  some 
mysterious  way  subserve  the  performance  of  these  complicated  acts, 
such  as  speech  and  writing.  For  clinical  purposes  we  can  use  these 
acts  as  localizing  signs,  and  for  that  reason  I  will  discuss  them  along 
with  the  other  more  distinctive  focal  signs  of  brain  disease  in  the  fol- 
lowing sections. 

I  desire  here,  however,  to  emphasize  the  fact  that  speech,  reading, 
word-hearing  and  writing  are  psycho-physical  exhibitions,  and  to  pro- 
test against  the  too  common  assumption  that  they  are  the  result  of 
certain  physical  activities  in  certain  limited  groups  of  cells  called 
''cortical  centers."  A  speech-center,  a  writing-center  nmy  indeed  rep- 
resent the  point  of  convergence  or  physical  inter-connection  for  all 
those  anatomico'-physiological  processes  that  underlie  the  correspond- 
ing psycho-physical  manifestations.  Ablation  of  these  centers  neces- 
sarily breaks  up  the  psychic  phenomena  dependent  upon  them  and  ex- 
pressed physically  through  them,  but  that  these  centers  are  special, 
independent  little  organs,  as  it  were,  for  the  performance  of  the  func- 


THE   NON-NEURONIC  DISEASES  763 

tion  of  speech,  of  reading,  of  writing,  etc.,  none  but  the  crudest  tyro 
in  psychological  investigation  would  for  a  moment  believe.  Regarding 
this  point,  which  I  have  long  insisted  upon,  I  can  do  no  better  than 
quote  a  paragraph  from  Wundt:  "When  the  destruction  of  certain 
•cortical  regions  produces  definite  disturbances,  in  voluntary  move- 
ments and  sensations,  or  when  such  a  destruction  interferes  with  the 
formation  of  certain  classes  of  ideas,  it  is  perfectly'  justifiable  to  con- 
clude that  these  regions  furnish  certain  indispensable  links  in  the  chain 
of  physical  processes  which  run  parallel  to  the  psychical  processes  in 
question.  The  assumptions  often  made  on  the  basis  of  these  phenom- 
ena, that  there  is  in  the  brain  a  special  organ  for  the  faculties  of  speech 
and  writing,  or  that  visual,  tonal  and  verbal  ideas  are  stored  in  special 
cortical  cells,  are  not  only  the  results  of  the  grossest  physiological  mis- 
conceptions, but  they  are  irreconcilable  with  the  psychological  analysis 
of  these  functions.  Psychologically  regarded,  these  asumptions  are 
nothing  but  modern  revivals  of  that  most  unfortunate  form  O'f  faculty- 
psychology  known  as  plirenology." 

DISTURBANCES  OF  LANGUAGE. 

Most  authors  treat  of  these  symptoms  under  the  general  name  of 
speech  disturbances.  I  prefer  the  use  of  the  word  language,  because 
it  has  a  broader  meaning  than  the  word  speech  has  come  to  possess  in 
popular  parlance.  I  believe  that  much  confusion  has  been  thrown 
around  this  entire  subject  by  the  difficulty  one  has  in  thinking  of  speech 
in  the  broad  sense  that  we  think  of  language.  Speech  has  come  to  be 
rather  synonymous  with  emissive  language  and  more  particularly 
articulated  emissive  language.  It  is  not  easy  to  think  of  written  speech 
or  mere  pantomimic  speech,  and  it  is  next  to  impossible  to  regard  un- 
worded  speech,  whether  receptive,'  inherent  or  emissive  in  relation  to 
the  brain,  in  the  same  clear,  well-defined  light  that  we  regard  verbal  or 
articulated  speech.  The  word  language,  it  seems  to  me,  is  so  broad  and 
yet  so  accurate  that  it  can  well  replace  the  confusing  word  speech. 

Language  is  the  power  of  commiunicating  ideas  to  another.  It 
makes  no  difference  in  what  manner  or  by  what  agencies  the  co^mmuni- 
cation  is  made,  whether  with  vocal  sounds,  with  recorded  symbols, 
with  gesture  movements,  it  is  all  language.  A  mere  touch  of  the  hand 
may  convey  an  idea  to  a  receptive  subject;  a  simiple  wink  may  mean 
yes  or  no  as  much  as  the  spoken  or  written  word.  Nay,  more,  it  is  not 
even  necessary  that  the  person  to  whom  the  ideas  are  being  communi- 
-cated  should  understand  either  the  spoken,  written  or  gestured  sign. 
So  long  as  a  sign  of  some  sort  stands  for  the  ideas  in  the  mind  oi  him 
who  is  trying  to  communicate  them,  it  constitutes  a  language.  A 
Hottentot  may  try  ever  so  hard  to  communicate  his  ideas  to  me.  He 
lias  a  language,  even  though  I  comprehend  not  an  iota  of  his  vocal 
utterances,  his  graphic  signs  or  his  gesture  movements.  He  has  his 
ideas,  that  is  obvious ;  and  he  has  his  own  particular  symbols  for  them, 
which  he  has  adopted  for  himself.  Those  symbols  constitute  his  lan- 
:guage.  By  means  of  them  he  attempts  to  communicate  his  ideas  to 
another  individual,  whether  that  individual  be  a  human  or  an  animal. 


764  THE   NON-NEURONIC  DISEASES 

Indeed,  he  communicates  the  ideas  to  himself  by  them,  or,  in  other 
words,  he  attaches  to  those  ideas  of  his  own  certain  adventitious,  fixed 
s\Tiibols  which  even  to  himself  he  uses  to  fix  and  recall  the  ideas  nec- 
essary for  the  continuance  of  his  thinking. 

In  its  last  analysis,  then,  language  is  nothing  more  or  less  tJian 
the  symbolising  of  ideas.  This  is  a  most  important  fact  to  grasp  before 
beginning  the  discussion  of  the  disturbances  O'f  language. 

In  the  definition  of  language  two  things  must  be  clearly  empha- 
sized. The  first  is  that  it  is  a  symbol,  a  sign,  a  something  in  place  of 
something  else.  The  symbolizing  is  not  conferred  upon  living  creatures 
from  without,  but  it  springs  originally  from  within.  A  symbol  is  first 
formed  in  the  mind ;  is  first  employed  there ;  and  is  then  expressed 
outwardly.  In  this  way  language  begins  in  animals  and  infants.  Mere 
sounds,  for*  instance,  like  mama  or  papa,  originally  without  meaning 
and  uttered  by  the  infant  in  its  feeble  struggles  to  make  its  little  ideas 
known  to  those  about  it,  have  become  crystallized  into  words.  Origin- 
ally, however,  they  were  nothing  but  sounds  and  meant,  as  symbols  of 
ideas,  nothing  more  or  less  than  the  crow  of  the  cock  or  the  call  of 
the  moose. 

The  so-called  roots  of  civilized  speech  when  traced  back  to  their 
source  reveal  the  fact  that  primitive  language  was  imitative  as  far  as 
possible.  The  savage  who  rubs  two  sticks  together  to  convey  an  idea, 
to  his  fellow  savage  is  employing  a  language  as  much  as  the  dog  who 
barks  and  leads  his  master  to  the  drowning  child,  or  as  that  child  when 
it  cries  and  stretches  out  its  hands  to  the  nursing  bottle. 

All  of  these  movements  and  noises  are  for  the  purpose  of  com- 
municating ideas.  In  time  th.ese  movements  and  noises,  by  repetition^ 
by  the  unconscious  process  of  mutual  agreement,  by  combination  and 
recombination,  become  the  fixed  symbols  of  higher  language.  They 
first  represent  something  in  the  mind  of  the  animal  to  his  own  mind,, 
and  thus  they  become  the  basis  of  his  thinking.  The  capacity  to  form 
and  retain  these  symbols  is  what  distinguishes  man  as  a  higher  think- 
ing animal  than  the  brute.  Babies  cannot  think  like  adults  and  one 
adult  cannot  think  like  another  adult,  largely  because  their  powers  of 
fixing  these  linguistic  symbols  within  their  psychic  mechanism  is  weak. 

Language,  therefore,  as  an  aggregate  oi  symbols  springs  out  of 
thinking  and  in  turn  assists  the  processes  of  thought.  I  hope  the  reader 
has  noted  that  in  the  evolution  of  language  it  is  thought  that  gives  it 
birth.  If  animals  had  no  thoughts,  however  primitive  they  may  be,, 
language  would  never  come  into  existence. 

This  leads  to  the  second  point  that  should  be  emphasized  in  the 
definition  of  language — namely,  that  it  is  for  the  communication  or 
representation  of  ideas.  If  ideas  are  wanting,  there  will  be  no  lan- 
guage. Now  animals  miake  sounds  and  perform  acts  that  are  not  based 
upon  any  ideas,  such,  for  instance,  as  the  thousand  and  one  reflex  acts,, 
the  acts  of  mere  vegetative  life,  that  never  become  language  and  in 
themselves  are  not  in  the  least  linguistic.  They  only  become  linguistic 
the  moment  they  are  made  to  take  the  place  of  an  idea,  the  moment  they 
are  adopted  as  symbols  for  a  thought.     Winking,  for  instance,  is  per- 


THE   NON-NEURONIC  DISEASES  .  J^t^ 

formed  as  a  mere  reflex  act  a  thousand  times  a  day ;  it  is  not  language 
until  it  is  made  to  suggest  some  idea. 

The  essential  point  in  language  then  is  that  it  is  a  symbol  for 
ideas.  As  I  have  said  before,  it  is  perfectly  inconsequential  as  to  what 
the  character  of  the  symbol  may  be,  whether  it  is  known  to  any  other 
than  to  the  one  who  adopts  it,  so  long  as  it  is  a  symbol  and  so  long  as  it 
stands  for  an  idea,  it  is  language. 

This  is  not  the  place  to  go  into  further  detail  in  regard  to  this 
fascinating  subject,  the  development  of  language,  but  I  felt  that  the 
above  brief  notice  of  it  was  necessary  to  emphasize  the  fact,  which  seems 
to  be  lost  sight  of  by  some  physiologists  in  their  discussion  of  the 
cortical  speech  centers,  that  language  is  a  ps}xhic  and  not  a  mere 
physiological  phenomenon.  It  is  the  outward  panorama,  as  it  were,  of 
ideas.  Every  discussion  of  it  and  its  disturbance  involves  a  discussion 
of  the  nature  of  ideas.  These,  as  I  have  shown  elsewhere,  are  what 
we  call  in  modern  physiological  psychology,  psychical  compounds. 
They  represent  combinations  between  psychical  sensations  and  the  feel- 
ings. The  psychical  sensations  and  feelings  are  the  correlates  of  and 
Tiave  as  their  parallel  physiological  bases,  the  five  senses  of  the  body. 
Ideas  being  thus  shown  to  be  complex  and  compound  processes,  it  must 
follow  that  language  based  upon  them  m.ust  have  a  compooind  and 
complex  structure.  It  is  therefore  useless  to  look  for  specific  centers 
in  the  brain  for  the  elaboration  of  psychic  manifestations,  which  in  their 
very  nature  show  that  they  are  compounded  of  many  psycho-physical 
processes.  Physiologists  are  awakening  to  the  fact  that  speech  centers, 
such  as  they  used  to  be  thought  of,  do  not  exist  in  the  brain.  There  are 
groups  of  cells  here  and  there  in  the  cortex  that  undoubtedly  subserve 
the  purpose  of  bringing  together  widely"  divergent  processes  and  so  far 
as  these  groups  of  cells  subserve  the  function  of  symbolizing  ideas  they 
may  be  spoken  of  as  speech  or  language  centers.  These  so-called  speech 
centers  are  available  for  localizing  purposes.  Their  connections  with 
other  centers  are  in  a  few  instances  so  well  known  that  we  can  ofttimes 
localize  a  lesion  very  definitely  when  the  intervening  association  tracts 
are  damaged.  Under  no  circumstances,  however,  are  we  justified  in 
attributing  the  function  of  speech  to  any  one  cortical  area  or  subcortical 
tract. 

Only  by  clearly  recognizing  the  above  described  nature  of  language 
and  its  relation  to  all  of  the  cortical,  and  perhaps  subcortical,  functions 
can  we  explain  some  of  the  strange  phenomena  observed  in  focal 
lesions  which  we  had  expected  from  our  physiology  to  produce  a  defi- 
nite set  of  linguistic  symptoms.  To  account  for  some  of  these  unex- 
pected manifestations,  those  who  ignore  psychology  entirely  and  believe 
that  the  evidences  of  physiology  point  to  special  cortical  spots  as  the 
source  of  such  complicated  psycho-physiological  phenomena  as  speak- 
ing, reading,  writing  are,  have  to  resort  to  some  very  queer  and  illog'- 
ical  reasoning.  Thus  they  talk  about  individual  variations,  contradict- 
ing, as  it  were,  their  own  position  when  they  found  their  physiological 
teachings  upon  such  narrow,  materialistic  bases  as  they  do.  They  say 
one  person  uses  his  visual  memory  more  than  another  in  his  speech; 
another  his  auditorv ;    a  third  his  motor.     All  of  this  is  true  and  in 


766  THE   XOX-XEUKOXIC  DISEASES 

itself  reveals  that  language  is  a  compound,  variable  process,  a  func- 
tional psychosis,  and  not.  as  they  have  just  been  stating,  a  physiological 
manifestation  in  certain  fixed  parts  of  the  cortex.  In  one  sentence  they 
show  that  mind  is  not  an  entity,  that  psychosis  is  not  a  thing,  but  a 
function,  a  process,  an  interplay  between  certain  lower  and  more 
elementary  psycho-physiological  sensations ;  and  yet  in  the  next  sen- 
tence they  try  to  fix  that  mere  function,  process  or  interplay  in  the 
anatomico-physiological  functions  of  a  few  nerve  cells  and  fibres 
grouped  in  so-called  centers.  No  wonder  they  say  with  a  half-surprised 
manner,  "'the  loss  of  a  certain  center  will  cause  a  hardly  noticeable  dis- 
order in  one  and  a  severe  and  persistent  disturbance  in  another."^ 
Elaborate  paradigms  are  constructed  based  upon  the  idea  that  speech 
is  subserved  by  special  cortical  centers,  and  yet  immediately  after  the 
paradigms  it  is  stated  that  partial  lesions  occur  very  often  (a  fact  not 
always  demonstrable,  though  too  often  assumed),  and  that  such  cases 
cannot  be  grouped  in  the  paradigms. 

Disturbances  of  language,  then,  are  psychic  s}'niptoms.  They  are 
not  more  definite  as  localization  symptoms  than  are  some  of  the  illu- 
sions and  hallucinations  previously  referred  to.  Their  definiteness 
occurs  on  account  of  the  sphere  in  which  they  occur — namely,  the  sym- 
bolizing of  ideas.  In  the  manufacture  of  these  symbols,  animals  use 
movements  and  the  secondary  result  of  a  particular  form  of  movement, 
sound.  Behind  all  language,  therefore,  is  some  form  of  motility.  If 
this  motility  involves  the  sound  producing  apparatus,  we  have  loss  of 
articulate  speech.  This  may  be  purely  paralytic.  The  muscles  con- 
cerned may  be  directly  paralyzed  or  immobile.  This  is  a  disturbance 
in  articular  speech.  It  is  called  anartlina  if  it  is  complete;  dysarthria 
if  it  is  incomplete.  The  muscles,  with  their  nerve  supply,  that  are 
involved  are  those  of  the  lips,  tongue,  palate,  larynx  and  respiratory 
apparatus.  Sounds  may  be  made  if  all  of  the  muscles  are  not  paralyzed, 
but  they  cannot  be  articulated  into  definite  forms  to  subserve  the  pur- 
poses of  speech.  When  sounds  cannot  be  produced  the  condition  is 
known  as  aphonia.  A  patient  suft'ering  from  anarthria  need  not  neces- 
sarily be  aphonic.  He  can  make  a  noise,  but  he  can't  speak,  because 
some  of  his  muscles  refuse  to  work. 

The  muscles  by  which  speech  is  articulated  are  innervated  from 
the  nuclei  of  the  medulla,  hence  their  paralysis  is  usually  a  bulbar 
symptom.  But  these  nuclei  are  under  the  control  of  the  higher  centers 
in  the  cortex.  They  may  be  paralyzed,  therefore,  from  disease  in  these 
cortical  centers,  as,  for  instance,  the  facial  and  hypoglossal  near  the 
bottom  of  the  central  convolutions.  As  these  cortical  areas  are  repre- 
sented in  the  opposite  hemisphere  and  the  two  sets  are  intimatelv  con- 
nected by  commissural  tracts,  cortical  paralysis  of  the  muscles  of  articu- 
lation is  not  apt  to  be  permanent.  Symmetrical  disease  in  the  hemi- 
spheres, however,  may  permanently  damage  the  articulation.  This  is 
what  is  known  as  pseudo-bnlhar  paralysis,  because  it  so  closelv  simu- 
lates disease  of  the  medulla. 

All  degrees  of  paralysis  may  occur  from  disease  of  the  bulb. 
The  speech  may  be  only  slightly  deranged,  or  it  may  be  so  profoundly 
afifected  that  nothing  but  sounds  are  heard.     A\'hen'the  lips  are  paraf- 


THE  NON-NEURONIC  DISEASES  76/ 

yzed,  p,  b  and  m  are  sounded  like  f  and  v ;  when  the  tongue  is  affected, 
the  1  and  t  resemble  y  and  th ;  implication  of  the  palare  turns  p  and  b, 
the  explosive  labials,  into  the  continuous  labial  m,  because  the  posterior 
nares  cannot  be  shut  off. 

Other  slighter  forms  of  dysarthria  are  the  conUnent  and  elisive, 
when  the  consonants  and  syllables  are  run  together;  and  the  staccato 
or  scanning  speech^  when  the  syllables  are  unduly  separated  as  one  sep- 
arates them  when  he  is  scanning  a  line  of  poetry.  These  defects  are 
all  self-evident  and  their  examination  needs  no  special  description. 

We  have  just  seen  that  language,  spoken  as  well  as  other  forms  ot 
language,  is  something  more  than  the  utterance  of  noises,  etc.  It  is  a 
symbolic  utterance  of  sound.  The  sound  must  be  made  in  a  particular 
way  to  convey  the  proper  idea.  This  necessitates  the  employment  of  the 
muscles  in  a  particular,  combined  manner.  The  manner  must  be 
thought  out  in  the  brain  before  it  is  put  into  execution.  If  the  word 
to  be  uttered,  the  symbol,  belongs  to  old  and  fixed  language,  the  in- 
dividual's memory  will  be  involved  in  his  thinking  as  to  how  he  should 
put  the  muscles  of  his  vocal  apparatus  to  produce  just  the  sound  he 
wants  to.  It  is  obvious  that  in  this  process,  which  after  long  years  of 
practice  has  become  subconscious  in  part,  a  fine,  delicate  coordinating 
mechanism  is  involved.  The  focus  of  this  mechanism,  or  rather  the 
foci  of  these  mechanisms,  constitute  what  are  called  the  cortical  speech 
centers.  Disease  of  these  centers  causes  a  loss  of  language.  This  is 
known  as  aphasia. 

Aphasia,  then,  does  not  mean  paralysis  in  the  sense  that  anarthria 
does.  It  means  merely  psychic  paralysis  for  language.  It  stands  for  a 
loss  of  the  memory  pictures  of  speech,  the  loss  of  the  power  of  sym- 
bolizing one's  ideas.  As  symbols  are  various,  but  always  involving  a 
motor  idea,  aphasia  is  of  a  varied  type,  but  is  always  related  to  motility 
more  or  less.  Complete  aphasia  would  involve  all  forms  of  symboliza- 
tion  and  as  a  result  would  represent  a  condition  in  which  there  is  no 
language  whatever.  That  would  probably  mean  a  condition  in  which 
there  were  no  ideas,  or  complete  idiocy.  Partial  aphasia  would  mean 
that  the  power  of  symbolizing  one's  thoughts  is  lost  in  one  way  but 
not  in  another. 

Several  forms  of  partial  aphasia  are  now  recognized  clinically, 
though  there  are  doubtless  innumerable  forms  that  are  so  fine  as  to 
quite  escape  ordinary  detection.  Those  that  are  clinically  recognized 
are  motor  or  ataxic  aphasia,  amnesic  aphasia,  alexia  and  agraphia. 
Pantomimic  or  gesture  aphasia  and  paraphasia  should  be  included. 

These  are  all  forms  of  language  defect  and  represent  a  disorder 
in  the  psycho-sensory-motor  mechanism,  that  underlies  the  whole  process 
of  language  production.  There  is,  of  course,  a  parallel  physiological 
sensory  motor  mechanism  in  the  cerebral  cortex,  certain  of  whose 
points  we  can  recognize  in  the  m.otor  speech  center  of  Broca,  the 
sensory  speech  center  of  Wernicke  and  the  centers  for  word-blindness, 
etc.  C3f  these  the  first  is  the  most  definite,  doubtless  because  the  funda- 
mental purpose  of  language  being  the  fixation  and  co^mmunication  of 
ideas  by  symbols  and  symbolization  being  fundamentally  a  motor  and 
emissive  process,  every  form  of  speech  has  in  it  actually,  or  represented 


768  THE  NOX-NEURONIC  DISEASES 

in  it  potentiall}-,  some  form  of  motility.  Even  receptive  speech  and  the 
unuttered  language  of  thinking  are  essentially  emissive  for  it  is  a  process 
wherein  the  mind  communicates  to  itself,  as  it  were,  in  another  form 
its  own  ideas.  As  the  emissive  process  can  only  take  place  over  the 
miotor  pathways,  we  have  in  every  word,  every  form  of  language  the 
motor  element  lurking.  We  have  discovered  that  the  anatomico-physi- 
olc'gical  concomitant  of  tliis  motor  manifestation  resides  in  the  group 
of  cells  known  as  Broca's  center,  and  to  some  extent  all  of  the  motor 
centers.  These  are  in  communication  with  the  hearing  and  visual  and 
touch  centers,  wherein  reside  those  cellular  elements  that  associate 
sounds  and  sights  with  the  muscular  movements  in  such  a  way  as  con- 
stitutes the  aggregate  network  out  of  which  the  linguistic  function  is 
evolved. 

The  interconnections  in  this  basal  sensory  motor  network  is  the 
essential  point  to  note,  for  it  is  upon  them  that  what  wc  call  language 
has  its  foundations.  The  network  may  be  broken  here  or  there  so  that 
there  is  a  partial  rupture  in  the  sensory  motor  complexus,  or  the  group 
of  cells  that  here  and  there  serve  to  unite  the  various  parts  of  the  net 
may  be  obliterated.  In  this  way  we  have  the  partial  and  the  special 
types  of  aphasia  established.  That  there  are  innumerable  types  of 
aphasia,  indicating  covmtless  possible  breaks  in  this  wonderful  com- 
plexus of  sensory  motor  inter-connections  more  than  we  can  now  locate, 
is  hinted  at  in  such  manifestations  as  the  forgetting  of  particular  names, 
of  particular  gestures  and  of  particular  forms  of  print. 

Language  is  the  pro,duct  of  an  associative  process ;  not  of  mere 
cell  activity  per  se.  It  is  a  psychic  phenomenon  resulting  from  inter- 
connections between  sensory  and  motor  elements.  The  so-called  centers 
of  language  are  merely  the  points  at  which  some  of  these  fundamental 
inter-connections  are  most  obviously  brought  about.  Aphasia  is  the 
result  of  a  break  somewhere  in  the  network  of  inter-connections.  If 
the  break  is  at  the  so-called  centers,  the  aphasia  may  be  grossly  and 
wholly  motor  or  sensory  in  type.  If  the  break  is  between  the  centers 
it  may  merely  sever  the  motor  from  the  sensory  side  of  the  complexus, 
or  it  may  sever  one  form  of  motor  from  another  form  of  motor  element 
in  it,  or  one  sensory  from  another  sensory  element  in  it.  As  the  inter- 
connections are  fine  and  innumerable,  so  the  ruptures  may  be  fine  and 
innumerable. 

I  will  now  take  up  and  discuss  a  few  of  the  gross  ruptures  which 
we  recognize  chiefly.  The  reader  will  find  some  assistance  possibly  in 
the  section  devoted  to  the  consideration  of  the  Cerebral  Localizations. 

Motor  Aphasia. — The  term  ataxic  as  applied  to  this  form  of  aphasia 
should  be  dropped,  because  ataxia  can  be  produced  by  sensory  as  well 
as  motor  disturbances.  Motor  aphasia  is  usually  produced  by  a  lesion 
at  the  base  of  the  third,  left  frontal  convolution,  Broca's  center,  in 
right-handed  people.  The  corresponding  area  in  the  opposite  hemi- 
sphere is  the  active  one  in  left-handed  individuals.  Disease  of  one  side 
is  occasionally  compensated  for  by  development  of  the  function  of  the 
other  side,  thus  causing  the  aphasia,  under  certain  conditions,  to  ulti- 
mately pass  away.  Disease  anywhere  in  the  conducting  path  from  the 
center  also  produces  motor  aphasia. 


THE  NON-NEURONIC  DISEASES  769 

Motor  aphasia  is  a  loss  of  voluntary  speech.  There  is  a  distincr 
want  of  memory  pictures  by  which  the  muscular  apparatus  is  put  into 
condition  to  emit  the  desired  sound.  An  aphasic  patient  is  not  speech- 
less. He  can  utter  words  and  often  automatically  can  roll  off  long 
grammatical  sentences.  Verses  that  he  has  memorized  can  often  be 
correctly  recited.  Singing,  which  usually  automatically  sustains  the 
verses,  often  makes  the  task  exceedingly  easy.  Even  a  commonplace 
automatic  conversation  can  be  carried  on  in  mild  cases.  The  moment, 
however,  the  conversation  becomes  voluntary  and  unusual,  it  halts  and 
delays.  Irrelevant  words  and  sentences  are  introduced.  Wrong  words 
are  used.  Words  having  opposite  meaning  from  those  intended  are 
uttered.     Syllables  are  misplaced  and  doubled. 

Complete  motor  aphasia  is  practically  always  accompanied  by  right 
hemiplegia.  Bastian  saw  the  exceptional  instance  in  which  a  left- 
handed  person  experienced  a  lesion  of  the  left  hemisphere  and  had 
right  aphasia  with  right-sided  hemiplegia. 

Sensory  Aphasia,  Word-Deafness. — Here  the  patient  is  in  the  con- 
dition of  a  person  listening  to  an  unknown  foreign  language.  He 
hears  the  sounds  correctly  but  they  mean  nothing  to  him.  They  are 
only  sounds.    There  is  no  actual  deafness. 

This  form  of  aphasia  often  accompanies  the  motor.  It  is  easily 
tested  by  asking  the  patient  to  do  or  say  something.  He  stands  mute. 
He  has  heard  but  he  does  not  comprehend.  Voluntary  speech,  if  this 
amnesic  type  of  aphasia  only  is  present,  is  ready  enough.  Reading  and 
writing,  except  from  dictation,  are  carried  on  normally.  Alexia  and 
agraphia,  however,  are  very  often  present.  The  extent  and  character 
of  the  lesion  determine  this.  The  seat  of  the  disease  is  here  located  in 
the  first,  left  temporal  convolution  in  right-handed  persons.  The  es- 
sential trouble  is  the  loss  of  the  memory  pictures  for  sounded  words. 

Some  impairment  of  speech  may  be  caused  by  this  amnesic  aphasia 
from  its  interference  with  the  processes  of  thought.  Thinking  neces- 
sitates the  use  of  symbols  and  in  higher  language-using  animals,  like 
man,  the  vocal  symbols  are  made  to  serve  the  processes  of  ratiocina- 
tion. When  the  memory  of  these  vocal  symbols  is  gone  it  is  obvious 
that  the  thinking  processes  are  lowered  and  especially  the  utterance  of 
those  processes  in  words  that  must  be  searched  for  partly  in  the 
affected  region.  Mechanical  or  automatic  speech  is  therefore  better 
in  amnesic  aphasics  than  spontaneous,  voluntary  speech ;  and  mere 
spontaneous,  voluntary  speech  is  easier  than  a  conversation,  in  which 
the  mind  is  not  left  so  much  to  its  own  devices.  This  inability  to 
awaken  word  tone  pictures  in  one's  self,  apart  from  the  mere  loss  of 
word-perception,  is  called  amnestic  aphasia.  The  higher  psychic  cen- 
ters are  disconnected  from  the  ordinary  language  centers,  though  audi- 
tory impulses  reach  and  stimulate  the  latter. 

Agraphia. — This  may  occur  alone  but  it  more  generally  accom- 
panies motor  aphasia.  There  is  some  doubt  as  to  the  nature  of  this 
symptom.  It  is  clearly  a  motor  or  psycho-motor  disturbance.  Some 
have  supposed  it  was  due  to  disease  in  Broca's  center,  because  as  they 
say,  internal  motor  vocal  speech  always  precedes  its  outward  expres- 
sion in  writing.    Motor  agraphia,  however,  does  occur  apart  from  ordi- 


770  THE   NON-NEURONIC  DISEASES 

nary  motor  aphasia.  The  trouble,  moreover,  seems  to  be  more  deeply- 
seated  than  would  be  a  mere  loss  of  memory  pictures  for  movements 
in  the  right  arm  and  hand,  for  the  patients  cannot  even  form  the  words 
out  of  lettered  blocks  placed  before  them.  It  probably  represents  a 
much  larger  disconnection  in  the  linguistic  network  than  is  represented 
in  any  one  center  or  single  tract.  No  such  special  center  is  known  to 
exist.  If  inner  speech  precedes  written  speech,  there  may  be  a  discon- 
nection between  Broca's  center  and  that  for  the  hand.  Most  frequently 
agraphia  accompanies  verbal  sensory  aphasia  and  motor  aphasia. 

x^s  I  have  shown,  language  is  practically  always  an  emissive  sen- 
sory-motor phenomenon ;  hence  internal  language  must  somewhat  in- 
volve both  sensory  and  motor  processes  before  it  is  uttered  in  writing 
or  any  other  way.  These  patients  can  very  often  write  from  printed 
copy  though  they  cannot  write  from  diction.  They  do  not,  of  couse, 
understand  or  comprehend  what  they  are  copying.  The  visual  appara- 
tus takes  in  the  letters  on  the  page  and  the  hand  reproduces  them.  The 
patient  is  like  one  who  is  copying  an  unfamiliar,  foreign  language. 

Alexia  or  Word-blindness. — This  may  be  isolated,  though  it  usu- 
ally accompanies  sensory  aphasia.  A  lesion  has  often  been  found  in 
these  cases  in  the  angular  gyrus  in  the  left  Icjiwer  parietal  lobe.  Here 
the  tracts  course  that  connect  the  visual  centers  in  the  occipital  lobe 
with  the  auditory  center  in  the  temporal  lobe.  The  reason  for  the 
frequent  association  of  alexia  and  amnesic  aphasia  is  that  an  internal 
language  must  be  presupposed  before  an  intelligent  comprehension 
of  that  which  comes  in  by  way  of  the  visual  apparatus  can  be  expected. 
These  patients  with  alexia  are  like  persons  reading  an  unknown,  for- 
eign tongue.  They  see  but  they  do  not  comprehend.  Of  course,  writ- 
ing is  impossible  to  them.  This  is  not  the  agraphia  just  described,  for 
spontaneous  writing  and  writing  from  verbal  dictation  (in  isolated 
alexia)  is  easy  enough.  The  alexic  patient  cannot  write  because  the 
graphic  symbols  are  absolutely  unintelligible  to  him.  In  agraphia  the 
disturbance  of  the  comprehension  of  language  precedes  and  prevents 
the  inditing  of  symbols ;  in  alexia  the  disturbance  of  the  comprehension 
of  language  follows  the  writing  instantaneously.  The  latter  is  like  a 
man  trying  to  build  a  brick  wall,  who,  the  moment  he  lays  the  brick 
down  it  ceases  to  be  to  him  a  brick  or  a  wall,  but  something  absolutely 
different  and  irrelevant.  Curiously,  such  patients  can  sometimes  read 
writing  by  tracing  the  outlines  of  the  letter  with  their  finger.  The 
sensory  pathways  of  the  arm  are  here  made  the  connecting  link  be- 
tween the  written  language  and  the  intact  speech  centers. 

Pure  alexia,  as  I  have  been  describing,  is  of  subcortical  origin. 
Right  hemianopsia  for  obvious  anatomical  reasons,  often  accompanies 
pure  alexia. 

Visual  Aphasia.- — -This  is  a  rare  condition  in  which  objects  are 
seen  and  recognized  but  cannot  be  called  by  name,  though  they  can 
be  named  if  in  any  way  they  can  be  perceived  through  the  other  senses. 
Let  such  a  patient  look  at  a  bell,  for  instance,  and  he  cannot  name  it ; 
let  the  bell  be  sounded,  however,  and  he  at  once  states  what  it  is. 

Lesions  in  this  curious  condition  have  been  discovered  at  the 
border  of  the  left  occipital  and  temporal  lobes ;  but  they  have  always 


THE   NON-NEURONIC  DISEASES  77I 

been  extensive  enough  to  implicate  both  tracts  from  the  occipital 
visual  areas  to  the  sensory  speech  center  in  the  temporal  lobe.  Alexia., 
hemianopsia  and  sensory  aphasia  usually  accompany  this  condition, 
Oppenheim  asserts  that  he  finds  this  trouble  not  uncommon  in  otitic 
cerebral  abscess. 

In  tactile  aphasia,  which  is  exceedingly  rare,  objects  that  are 
touched  cannot  be  named.  This  must  not  be  confused  with  astereog- 
nosis. 

No  discussion  of  aphasia  is  complete  without  a  notice  of  the 
disorders  of  pantomime.  These  occur  among  aphasics  and  involve  the 
gesture  language.  Amimia  and  paramimia  have  a  similar  import  to 
aphasia  and  paraphasia.  A  pantomimic  action  is  the  product  of  a  psy- 
chic process.  It  is  therefore  something  more  than  a  mere  emphatic 
gesture.     These  patients  nod  "yes"  when  they  mean  "no." 

The  causes  of  aphasia  may  be  functional  or  organic.  As  I  have 
shown  elsewhere  a  pyschosis  is  the  only  nervous  disease  that  can  be 
strictly  functional  unless  we  include  many  forms  of  reflex  disturb- 
ances under  the  name  functional.  It  is  possible  to  have  a  disorder  in 
the  interplay  and  interconnection  between  perfectly  normal  psycho- 
physical elements.  Among  the  organic  causes  of  aphasia  are  to  be  in- 
cluded the  toxic  causes  that  upset  the  basic  neurones. 

It  is  only  on  the  possibility  of  a  psychosis  being  a  true  functional 
manifestation  that  we  can  explain  the  fact  that  aphasia  may  follow  a 
severe  fright  and  occur  in  hysteric  states.  In  migraine  it  is  probably 
associated  with  vasomotor  disorder.  It,  of  course,  can  be  produced  in 
a  reflex  way.  It  has  thus  been  seen  in  children  as  the  result  of  worms 
and  minor  surgical  operations. 

Exhausted  states  of  the  blood  and  the  nervous  system  may  give 
rise  to  it.  Among  the  toxic  antecedents  are  to  be  recorded  the  acute 
infectious  fevers,  such  as  typhoid,  pneumonia,  scarlatina,  nephritic  con- 
ditions with  uraemia,  carcinoma,  gout  and  in  santonin  poisoning. 

By  far  the  most  common  organic  cause  is  focal  encephalomalacia 
because  it  is  so  frequently  a  cortical  trouble.  Softening  is  more  fre- 
quently a  ca;use  than  is  hemorrhage.  The  middle  cerebral  artery,  espe- 
cially the  left,  that  is  so  frequently  the  seat  of  these  vascular  troubles, 
is  the  artery  that  supplies  the  most  miportant  language-production  re- 
gion of  the  brain.  As  a  rule  "lesions  in  the  deeper  parts,  the  central 
ganglia  and  internal  capsule,  do  not  cause  aphasia.  They  may,  how- 
ever, if  they  are  large  enough  to  compress  the  cortical  areas.  In  uni- 
lateral lesions  that  do  not  compress  these  parts,  the  speech  emissive 
impulses  find  their  way  to  the  opposite  hemisphere  by  way  of  the  cor- 
pus callosum,  and  so  on  outward. 

Cerebral  abscess  may  cause  amnesic  aphasia.  Motor  aphasia  ha« 
followed  abscesses  also  of  traumatic  and  metastatic  origin. 

Pressure  aphasia  may  accompany  suitably  located  intracranial  neo- 
plasms. In  children  tiiberculosis  and  tuberculous  meningitis  are  some- 
times  responsible. 

Gonorrhceal  embolism  has  been  blamed  for  it  by  Pitres  and  Bruns. 
Direct  trauniatistn  is  a  factor  in  the  etiology.  A  congenital  aphasia  has 
been  observed.    It  is  probably  due  to  a  prenatal  or  natal  hemorrhage. 


^^2  THE   XOX-XF.UROXIC  DISEASES 

Toxic  and  fiDictioiial  aphasia  usually  disappear  soon  and  com- 
pletely. As  an  indirect  focal  symptom  it  may  disappear  if  the  original 
cause  changes  so  as  to  relieve  the  pressure  (hemorrhage)  or  obstruc- 
tion (embolism).  Usually  it  requires  .several  weeks  or  months,  though 
a  week  or  so  may  see  it  vanish.  In  children,  there  is  ahvaA's  the  pos- 
sibility of  the  right  hemisphere  taking  up  the  function  when  the  left 
is  damaged  beyond  recovery.  The  nature  of  the  cause  and  its  amena- 
bility to  treatment  obviously  determine  the  prognosis. 

The  treatment,  further  spoken  of  under  the  head  of  cerebral  hem- 
orrhage and  softening,  involves  removal  of  the  cause,  combating  the 
underlying  disease,  and  re-educating  the  patient.  A  correct  diagnosis 
as  to  the  nature  of  the  loss  of  speech  and  a  little  ingenuity  in  setting 
the  linguistic  tasks  for  the  patient  to  practice  dail}'  is  all  that  need  to 
te  suggested  here. 

Motor  Sympto:ms. — Irritative  Symptoms.  Conv^dsions. — These 
may  be  provoked -by  direct  irritation,  as  in  meningitis  or  tumor;  or  by 
the  alteration  of  the  gray  matter  in  regard  to  its  nutrition.  Irritations 
of  the  cortical  motor  zone,  of  course,  affect  the  opposite  side  of  the 
body,  as  all  the  cortico-spinal  motor  tracts  decussate.  As  a  result  tonic 
and  clonic  spasms  occur  which  may  be  limited  to  certain  movements 
or  involve  all  the  movements.  When  the  irritation  is  bilateral,  the 
convulsion  is  general.  In  this  way  we  have  monospasms,  hemispasms 
and  universal  convulsions.  The  movements  may  begin  with  twitchings 
or  they  may  start  in  a  tonic  spasm  and  pass  into  the  clonic  state.  Oft- 
times  a  twitching  will  begin  in  a  certain  small  area  and  then  spread 
gradually  until  a  large  part  or  even  the  whole  body  is  convulsed.  There 
is  no  fixed  rule  as  to  the  succession  of  parts  involved.  Generallv  the 
progress  of  events  can  be  seen  in  the  spasms  to  be  proceeding  up  or 
•down  the  central  convolutions.  Thus  if  the  movement  starts  in  the 
leg,  it  attacks  next  the  arm  and  finally  the  face :  or  if  the  face  is  the 
■earliest  seat  of  the  manifestation,  it  passes  next  to  the  arm  and  finally 
to  the  leg.  A  convulsion  that  starts  in  the  arm  is  apt  to  involve  the 
face  before  it  does  the  leg. 

In  monospasms,  consciousness  is  not  disturbed.  AA'hen,  however, 
the  convulsion  becomes  general,  consciousness  is  usuallv  lost. 

These  localized  monospasms  are  spoken  of  as  partial  or  cortical 
epilepsy.  As  manifestations  of  Jacksonian  epilepsy,  I  have  discussed 
them  elsewhere.  It  is  a  question  whether  all  organic,  gross,  irritative 
lesions  that  provoke  such  monospasms  should  be  regarded  as  epileptic. 
They  are  epileptiform.  They  occur  in  organic  and  functional  troubles. 
Toxic  conditions,  such  as  alcoholism,  ursemia.  saturninism,  seem  to  be 
•capable  of  producing  them,  though  it  is  not  improbable  that  these  are 
merely  organic  also,  being  due  to  hemorrhagic  and  embolic  alterations 
of  a  minute  character. 

A  temporary  paresis  usually  follows  these  manifestations.  If  it 
remains  it  means  that  the  lesion  is  more  than  an  irritative  one.  It  has 
"begun  to  exercise  a  destructive  influence  upon  the  afifected  cortical  area. 

Sensation  is  often  implicated  with  these  irritative  motor  phenom- 
ena. There  may  be  various  parsesthesiae  in  the  limb  that  is  subjected 
to  the  spasm.     It  may  be  only  an  accompan}-ing  symptom  or  it  mav  be 


THE   NOX-XEUROXIC  DISEASES  7/3 

the  sole  symptom  in  the  form  of  an  equivalent.  It  is  now  believed 
that  the  sensory  elements  are  most  intimately  intermingled  with  the 
motor,  or  at  least  are  intimately  interconnected,  so  that  it  may  Aveli  be 
that  the  true  irritative  epilepsies  in  this  case  are  really  sensory  phe- 
nomena with  secondary  motor  manifestations,  even  as  occurs  in  gen- 
eral epilepsy.  Cortical  epilepsy  occurs  from  irritative  subcortical 
lesions  but  disappears  absolutely  when  the  cortex  is  destroyed. 

Choreic  and  athetoid  manifestations  are  irritative  symptoms  but 
they  are  not  believed  to  be  due  to  cortical  irritation.  As  they  usually 
occur  in.  hemiplegic  conditions  they  are  thought  to  depend  upon  the 
irritation  of  the  thalamus.  They  occur  more  frequently  in  disease  of 
the  thalamus  and  are  best  discussed  after  hemiplegia. 

A  tetanoid  spasm  has  been  observed  in  disease  of  the  cerebellum, 
or  other  lesion  that  produces  increased  pressure  beneath  the  tentorium. 
The  head  is  bent  backward  with  opisthotonos,  the  jaws  are  clenched 
and  the  whole  appearance  is  that  of  traumatic  tetanus.  Forced  move- 
ments occur.  It  is  not  known  whether  the  symptom  is  indicative  of 
cerebellar  or  pontile  disease.  The  condition  lasts  sometimes  for  hours, 
though  the  tonic  contraction  is  broken  by  clonic  jerkings. 

General  convulsions,  due  to  disease  of  the  brain,  such  as  tumor, 
embolic  hemiplegia,  and  meningitis,  may  so  closely  simulate  hysteria  as 
to  deserve  the  adjective  hy steroid. 

Paralytic  Symptoms.  Monoplegia.  Hemiplegia. — The  first  great 
characteristic  of  cerebral  paralysis  is  that  it  is  distinctly  of  the  voli- 
tional power  over  the  musculature.  In  diseases  of  the  lower  motor 
segment,  the  paralysis,  of  course,  will  have  all  the  appearance  of  being 
in  the  volitional  sphere,  because  this  segment  lies  between  the  upper  seg- 
ment and  the  musculature,  and  therefore  cuts  off  impulses  passing 
from  one  to  the  other.  In  the  muscles,  however,  that  are  partly  vol- 
untary and  partly  involuntary,  as  for  instance,  the  muscles  of  respira- 
tion and  deglutition,  it  is  rendered  obvious  enough  when  the  volun- 
tary movements  are  impossible  from  upper  segment  disease,  while  the 
involuntary  movements  continue  intact. 

A  second  great  characteristic  of  brain  palsy  is  that,  for  evident 
anatomical  reasons,  the  muscles  are  not  aifected  with  a  true  atrophy. 
Their  nutrition  is  dependent  primarily  upon  the  ganglionic  cells  in  the 
anterior  horns  of  the  cord.  For  the  same  reason  there  is  no  reaction  of 
degeneration  observed  in  cerebral  palsies. 

As  the  upper  or  cerebral  motor  segment  exercises  an  inhibitory 
control  over  the  lower,  when  it  is  diseased,  the  paralysis  is  accompanied 
by  an  increase  of  all  the  reflexes.  This  is  a  third  important  charac- 
teristic of  cerebral  paralysis. 

A  fourth  is  that  the  paralysis  affects  the  movements  of  the  body 
rather  than  the  mere  individual  muscles.  The  areas  of  the  cerebral 
cortex  subserve  facial  movements,  arm  movements,  leg  movements,. 
etc.  A  cerebral  paralysis  never  picks  out  special  muscles,  but  only 
those  muscles  and  their  antagonists  that  normally  are  employed  in  the 
production  of  higher,  purposive  psycho-motor  activities.  This  type  of 
paralysis  is  known  as  monoplegia. 

Cortical  monoplegias  correspond,  as  pointed  out  in  the  section  on 


774  'i'iili   NON-NEUROXIC  DISEASES 

Cerebral  Localization,  with  the  particular  centers  involved  in  the  lesion. 
But  these  centers  have  their  cell  processes  bunched  together,  like  the 
stem  of  a  bouquet,  in  the  internal  capsule  and  so  on  down  to  the  ter- 
mination of  the  pyramidal  tracts  in  the  medulla  and  cord.  Obviously 
the  farther  down  below  the  cortex  the  given  lesion  of  the  same  size 
is  located,  the  more  extensive  will  be  the  paralysis  on  the  opposite 
side  of  the  body.  If  the  lesion  is  in  the  internal  capsule,  for  instance, 
where  the  bundle  is  probably  as  compact  as  anywhere,  the  entire  oppo- 
site half  of  the  body  will  be  paralyzed.  This  is  known  as  hemiplegia. 
If  both  hemispheres  or  their  tracts  are  diseased,  the  hemiplegia  v^^ill 
be  bilateral.  This  condition  is  termed  diplegia.  Between  a  hemiplegia 
and  a  monoplegia,  it  is  clear  that  we  can  have  any  extent  of  palsy, 
according  to  the  particular  location  of  the  lesion. 

Hemiplegia  then  is  the  great,  characteristic  type  of  cerebral  paraly- 
sis. It  involves  the  entire  half  of  the  body.  For  this  reason  it  is  some- 
times spoken  of  as  the  facio-hrachio-criiral  type  of  paralysis.  The  in- 
ability is  most  pronounced  in  those  muscles  and  parts  of  the  body  that 
subserve  the  higher,  complicated  voluntary  movements.  There  is  a 
direct  ratio  between  the  degree  of  intelligence  involved  in  the  normal 
movements  and  the  degree  of  palsy  which  they  have  now  undergone. 
For  this  reason  the  hand  is  more  affected  than  the  foot,  the  arm  more 
than  the  leg,  the  arm  and  leg  more  than  the  face,  the  tongue  and  lower 
part  of  the  face  more  than  the  upper  part  of  the  face,  and  the  upper 
part  of  the  face  more  than  the  great  truncal  muscles. 

With  the  evolution  of  human  intelligence  and  brain  power  there 
is  a  constant  tendency  to  separate  the  actions  of  the  two  sides  of  the 
body.  This  is  shown  in  the  remarkable  feats  accomplished,  as  the  re- 
sult of  practice,  by  pianists  which  ordinary  mortals  cannot  do.  It  has 
been  intimated  that  in  time  we  may  move  each  eye  without  regard  to 
the  other.  At  all  events,  it  is  a  fact  that  the  great  tendency  in  cere- 
bral evolution  is  towards  the  separation  of  the  functions  of  the  hemi- 
spheres. In  those  movements  in  which  this  separation  has  reached  the 
highest  degree  at  the  present  time,  disease  of  one  or  other  hemisphere 
will  be  most,  marked.  Where,  however,  the  movements  are  bilateral 
still,  as  they  are  in  the  movements  of  the  eyeballs  and  the  apparatuses 
of  sound,  deglutition,  and  respiration,  the  paralysis  is  not  so  evident 
because  the  unaffected  hemisphere  takes  up  in  part  the  duties  of  the 
diseased  hemisphere.  In  other  words,  the  bilateral  representation  of 
these  latter  movements  in  the  two  sides  of  the  brain  is  more  positive 
than  it  is  of  the  former  movements.  In  bilateral  lesions,  however,  the 
laryngeal,  deglutitory  and  masticator}-  are  aff'ected  and  we  have  what 
is  termed  pseudo-bidbar  paralysis.  Of  the  trunk  muscles,  the  trape- 
zius is  affected  as  a  rule,  though  the  sterno-mastoid  acts  normally.  In 
a  deep  respiration,  the  paralyzed  side  expands  somewhat  less  than  the 
other  side.' 

The  cases  in  which  hemiplegia  has  occurred  on  the  same  side  as 
the  lesion  are  open  to  grave  doubt.  Most  of  them  were  diagnosed  be- 
fore our  knowledge  of  the  central  nervous  system  was  as  exact  as  it 
is  to-day.  Pressure  by  contrecoup  or  lesions  in  the  opposite  hemisphere, 
or  in  the  pons  and  medulla,  were  not  taken  into  account.     However,  a 


THE  NON-NEURONIC  DISEASES 

FIGURE  187. 


E  G 


775 


-Diagram  of  motor  path  from  right  brain.  The  upper  segment  is  black,  the  lower 
The  nuclei  of  the  motor  cerebral  nerves  are  shown  on  the  left  side  :  on  the  right 
side  the  cerebral  nerves  of  that  side  are  indicated.  A  lesion  at  1  would  cause  upper 
segment  paralysis  in  the  arn?  of  the  opposite  side-cerebral  monoplegia;  at  2,  upper 
segment  paralysis  of  the  whole  opposite  side  of  the  body-hemiplegia ;  at  3.  upper 
segment  paralysis  of  the  opposite  face,  arm,  and  leg.  and  lower  segment  paralysis 
of  the  eye  muscles  on  the  same  side-crossed  paralvsis;  at  4,  upper  segment  paraly- 
sis of  opposite  arm  and  leg,  and  lower  segment  paralysis  of  the  face  and  the  external 
rectus  on  the  same  side-crossed  paralysis:  at  5,  upper  segment  paralysis  of  all  mus- 
cles below  lesion,  and  lower  segment  paralysis  of  muscles  represented  at  level  of 
lesion-spinal  paraplegia;  at  6,  lower  segment  paralysis  of  muscles  localized  at  seat 
of  lesion— anterior  poliomyelitis.     (Van  Gehuehten,  modified.) 


776  THE   XON-XEUROXIC  DISEASES 

congenital  absence  of  the  pyramidal  decussation,  a  developmental 
anomaly,  is  assumed  in  explanation  of  these  homolateral  hemiplegias. 

The  gait  of  a  hemipiegic  is  characteristic.  The  leg  remains  weak 
and  is  dragged  by  the  patient.  The  extensors  of  the  foot  and  toes 
remaining  paralyzed,  the  equino-varus  attitude  is  assumed  and  the 
toes  not  being  lifted  oil  the  floor,  the  foot  is  scraped  outward  in  a 
half  circle  each  time  it  is  moved  forward.  The  flexors  of  the  knee  are 
apt  to  remain  paralyzed  also.  In  the  arm  the  palsy  remains  in  the 
hand  and  fingers,  the  movements  of  the  shoulder  and  elbow  being  par- 
tially regained. 

Though  the  paralysis  is  voluntary,  the  muscles  act  under  certain 
conditions.  Under  strong  emotion,  gesticulation  and  in  associated 
movements  this  is  often  the  case.  Automatic  and  reflex  functions  they 
still  retain. 

The  psychic  or  mental  paralysis  of  Kraftt-Ebing  and  Bruns  is 
due  to  the  dissociation  between  the  cortical  sensory  and  motor  elements. 
Upon  request  the  patient  moves  his  limbs  but  not  of  his  own  purpose 
or  desire. 

Coutractures,  early  and  late,  usually  folloAv  the  cerebral  palsies. 
The  former  develop  in  the  first  few  hours  or  days  after  an  apoplectic 
stroke :  whereas  the  latter  appear  many  weeks  later,  never  before  two 
weeks  from  the  onset  of  the  trouble.  The  former  is  due  to  an  irrita- 
tion of  the  pyramidal  tracts ;  the  latter  are  not  due  to,  though  they  pro- 
ceed in  order  with,  the  corresponding  secondary  degeneration  in  the 
pyramidal  tract.  Adduction,  flexion  in  the  arm,  pronation  in  the  hand, 
and  flexion  in  the  fingers  occur.  The  leg  is  extended  and  the  foot,  as 
I  have  stated  above,  is  in  the  attitude  of  equino-varus.  The  increase 
of  the  contracture  by  sensory  stimulation,  especially  cold,  electricity, 
etc..  its  disappearance  in  sleep,  and  other  factors  indicate  that  it  is  un- 
doubtedly due  to  the  slight  overaction  of  the  lower  motor  segment 
when  the  inhibitory  power  of  the  upper  segment  is  weakened.  This 
explains,  of  course,  the  association  of  an  increased  action  of  the  deep 
reilexes  wnth  these  contractures.  In  some  cases  there  is  a  slight  wasting 
of  the  muscles  from  non-use  but  no  true  atrophy.  What  atrophv  there 
is,  is  probably  due  to  the  absence  of  the  normal  nervous  impulses, 
which  in  themselves  are  somewhat  stimulating  to  the  nutrition  of  the 
muscular  tissues.  In  every  hemipiegic  there  is  some  weakness  in  the 
unparalyzed  side. 

Associated  inoveinents  not  infrequently  occur  in  the  paralvzed 
limbs.  If  the  patient,  for  instance,  grasps  vigorously  with  his  well 
hand  or  suddenly  raises  his  unaffected  arm,  the  same  movement  will 
be  partially  performed  in  the  paralyzed  hand  and  arm. 

The  changes  of  a  trophic  nature  that  are  occasionally  observed 
in  and  about  the  joints  of  hemiplegics  are  supposed  to  be  due  to  neuritic 
or  consecutive  myelitic  changes  and  not  directly  to  the  degeneration 
in  the  pyramidal  tract. 

Alterations  of  local  temperature,  sweating,  oedema,  redness,  etc., 
in  the  paralyzed  limbs  are  sometimes  noted  and  may  be  due  to  vaso- 
motor disturbances  in  the  cortex. 

Hemichorea. — As  a  post-hemiplegic  phenomenon   this   is  not  un- 


THE  NON-NEURONIC  DISEASES 


177 


common ;  as  a  pre-hemiplegic  one  it  is  rare.  According  to  Charcot  it 
is  due  to  a  slow,  progressive  hemorrhage  in  the  optic  thalamus,  irritat- 
ing the  pyramidal  fibres  where  they  course  through  the  internal  cap- 
sule. The  movements  are  jerky,  irregular  and  incoordinated  just  as 
they  are  in  any  chorea.  The  whole  side  or  extremity  is  usually  in- 
volved. 

Athetosis. — In  the  fingers  and  toes  occur,  after  hemiplegia,  espe- 
cially infantile  hemiplegia,  curious,  wavy,  involuntary  movements,  that 
are  the  result  of  irritation  of  the  pyramidal  tract.  The  fingers  undergo 
continuous  polyp-like  slow  extension  and  flexion,  adduction  and  ab- 
duction. They  occur  in  sleep ;  sometimes  only  upon  voluntary  move- 
ment. The  fingers  are  moved  separately,  causing  a  most  grotesque 
and  bizarre  appearance.  Opposite  movements  are  made  in  adjoining 
fingers  simultaneously  sometimes. 

Other  movements  of  irritative  origin  that  are  neither  choreic  nor 
athetoid  are  also  seen  in  conditions  of  hemiplegia.  Among  these  m.ay 
be  cited  the  associated  movements  referred  to  above,  unilateral  tremor 
and  movements  similar  to  those  of  paralysis  agitans  and  disseminated 
sclerosis. 

Alternate  Hemiplegia. — When  the  pyramidal  tract  is  damaged  in 
the  lower  part  of  the  pons,  just  after  the  central  facial  tract  has  decus- 
sated, the  paralysis  will  be  in  the  face  on  the  same  side  as  the  lesion 
but  in  the  limbs  on  the  opposite  side.  In  an  alternate  hemiplegia,  the 
hypoglossus  may  be  paralyzed  on  one  side  and  the  extremities  on  the 
other.     The  tongue  will  thepx  protrude  toward  the  sound  side. 

Conjugate  Deviation  of  the  Head  and  Eyes. — This  is  often  seen 
as  a  symptom  of  brain  disease.  In  cerebral  lesions  the  deviation  is 
toward  the  unparalyzed  side,  or  towards  the  side  of  the  lesion.  The 
muscles  that  draw  the  head  and  eyes  toward  the  hemiplegic  side  are, 
of  course,  weakened  as  the  other  muscles  on  that  side  are.  Spastic 
conditions  naturally  cause  the  deviation  tcr  be  in  the  other  direction  or 
toward  the  spastic  side.  The  reason  is  obvious.  Lesions  of  the  pons 
often  deviate  the  eyes  toward  the  side  opposite  the  lesion,  the  location 
of  the  latter  being  in  the  common  center  for  the  abducens  of  the  same 
side,  and  the  internal  rectus  of  the  opposite  side. 

Sensory  Symptoms. — All  qualities  of  sensation  may  be  impaired 
in  intra-cranial  disease,  especially  the  senses  of  touch  and  position. 
H emiancBSthesia ,  rarely  complete,  occurs  with  lesions  in  the  cortical 
motor  areas.  When  the  sense  of  position  is  disturbed  the  lesion  is 
thought  to  be  in  the  parietal  lobe,  though  there  are  strong  grounds  for 
believing  that  this  disorder  originates  from  disease  limited  to  the  cen- 
tral convolutions.  In  monoplegias  the  motor  and  sensory  phenomena 
are  confined  to  the  same  parts.  Sometimes  the  cortical  motor  zone  and 
other  parts  of  the  cortex  can  be  destroyed  without  loss  of  sensation. 
Wernicke  and  Oppenheim  claim  they  have  observed  a  tactile  paraly- 
sis that  is  a  mental  anaesthesia.  With  the  sensibility  intact  in  the  hand, 
objects  could  not  be  recognized  by  touch.  (See  m.y  views  upon  this 
subject  under  the  head  of  psychic  symptoms,  localization  centers  and 
psychic  blindness.) 

Hemiangesthesia  occurs  on  the  side  opposite  that  of  the  cerebral 


778 


THE   XOX-XEUROXIC  DISEASES 


FIGURE  li 


Position  of  the  fingers  in  athetosis.    (After  Striimpell.) 


THE  NOX-XEUROXIC  DISEASES  779 

lesion.  It  involves  the  entire  skin  and  mucous  surfaces  of  one-half 
of  the  body  when  it  is  complete.  Grasset  claims  that  the  cornea  is  in- 
tact but  that  is  hardly  probable.  The  immediate  cause  of  this  symp- 
tom is,  of  course,  damage  to  the  sensory  conducting  tracts.  Cortical 
hemianaesthesia  is  rare.  The  course  of  the  sensory  tracts  have  been 
traced  in  the  description  of  the  anatomy  of  the  brain. 

The  anaesthesia  is  not  always  the  same  in  all  parts  of  the  affected 
5ide  of  the  body.  It  will  sometimes  be  more  marked  in  one  place  than 
in  another.     All  forms  of  sensation  may  not  be  equallv  involved. 

Hemiansesthesia  is  often  accompanied  by  impairment  of  the  spe- 
cial senses,  the  two  sets  of  pathways  being  contiguous.  Hence  wdth  it 
there  may  be  hemianopsia  or  crossed  amblyopia.  Crossed  ancesthesia 
occurs  in  upper  pontile  lesions,  the  fifth  nerve  being  affected  on  one 
side  and  the  path  from  the  limbs  on  the  other.  Pontile  disease  also 
sometimes  causes  incomplete  bilateral  anaesthesia. 

Sensory  irritation  or  pain  in  the  limbs  often  occurs  when  the  sen- 
sory tracts  are  only  partially  destroyed.  Sometimes  under  these  cir- 
cumstances numbness,  tingling  and  other  paraesthesise  are  observed. 
These  cannot  be  determined  as  tract  or  cortical  symptoms. 

Ataxia  sometimes  occurs  m  the  opposite  extremities  from  disease 
of  the  sensory  cortex  and  the  conducting  tracts. 

In  hemiplegia  and  hemianaesthesia  there  are  apt  to  be  z'asomotor 
and  trophic  symptoms.  In  the  aft'ected  limbs  the  cutaneous  tempera- 
ture is  lowered,  the  parts  are  reddened,  or  cyanotic  and  oedematous. 
In  severe  cases  a  tendency  to  decubitus  is  present.  Skin  eruptions, 
falling  of  the  hair,  and  even  gangrene  have  been  observed.  Slight 
arthropathy  miay  occur. 

Olfactory  Symptoms. — In  examining  the  sense  of  smell  we  are 
wholly  dependent  upon  the  subjective  testimony  of  the  patient.  When 
the  olfactory  nerves  are  affected  by  way  of  the  anterior  nares  we  call 
the  sensation  an  odor ;  when  by  way  of  the  posterior  nares,  it  is  termed 
a  flavor.  As  the  nares  are  innervated  by  the  trigeminal  as  well  as  by 
the  olfactory  nerves,  the  examination  must  be  made  with  substances 
that  affect  only  the  latter  nerve,  such  as  musk,  asafcetida,  oil  of  cloves, 
oil  of  peppermint,  oil  of  lavender,  oil  of  turpentine.  The  substance 
is  simply  held  under  one  nostril,  while  the  other  nostril  is  closed.  Am- 
monia and  acetic  acid  irritate  the  filaments  of  the  fifth  nerve  in  the 
mucous  membrane.  The  sense  in  the  two  nostrils  should  be  com- 
pared and  the  intelligence  of  the  patient  in  regard  to  the  subject  ot 
odors  must  be  given  due  consideration.  There  is  an  olfactory  refiex. 
Disgusting  odors  cause  the  head  to  be  draw^n  awa}'  and  the  mouth  to 
be  retracted.  For  a  description  of  the  olfactory  apparatus,  the  section 
on  the  anatomy  of  the  brain  should  be  consulted. 

Anosmia  or  the  loss  of  the  sense  of  smell  may,  of  course,  occur 
from  local  disease  of  the  mucous  membrane.  As  a  S3'mptora  of  brain 
trouble  it  may  be  due  to  various  traumata,  disease  of  the  bones,  timiors 
in  the  anterior  fossa  of  the  skull,  local  meningitis,  syphilitic  or  other- 
wise. Olfactory  neuritis,  like  optic  neuritis,  may  accompany  brain 
tumor.  Anosmia  has  been  seen  in  tabes  and  as  the  result  of  primary 
atrophy  in  old  age.     It  may  be  bilateral  or  unilateral.     As  a  congeni- 


780  THE   NON-NEURONIC  DISEASES 

tal  condition  it  is  observed  in  idiots.  It  residted  once  from  congeni- 
tal absence  of  the  olfactory  nerves.  Hereditary  anosmia  has  been  re- 
ported. 

Hyperosmia,  or  olfactory  hyper?esthesia,  occurs  in  hysteria  and 
insanity.  It  is  largely  a  psychosis  in  the  olfactory  sphere.  It  is  not 
of  much  clinical  importance. 

Olfactory  parccstheskc  and  hallucinations  occur.  They  have  been 
seen  as  aurje  in  focal  epilepsy  when  the  lesion  was  in  the  temporo- 
sphenoidal  lobe.     They  are  not  common  at  all. 

Optic  Symptoms. — The  optic  apparatus  is  a  part  of  the  brain^ 
as  I  have  explained  in  the  section  upon  anatomy.  It  extends  from 
the  cornea  in  front  to  the  occipital  cortex  behind.  The  neural  part 
includes  that  from  the  retina  to  the  cortical  area  in  the  cuneus.  The 
symptoms  of  disease  in  this  long  tract  are  of  the  greatest  neurological 
importance.  They  group  themselves  naturally  under  the  two  heads  of 
z'isital  disturbances  and  ophthalmoscopic  alterations.  Both  of  these 
sets  of  symptoms  may  be  examined  objectively  but  the  latter  are  more 
accurate  than  the  former  because  they  are  absolutely  unrelated  to  the 
patient's  consciousness.  Among  the  former  are  various  alterations. 
in  the  field  of  vision,  chief  of  which  are  concentric  contraction  of  the 
field,  scotomata  and  hemianopsia.  Psychic  blindness  will  be  included 
in  the  discussion  of  these  visual  symptoms.  Chief  among  the  fundus 
changes^  seen  through  the  ophthalmoscope,  are  the  so-called  "choked 
disc''  or  optic  neuritis,  and  optic  atrophy. 

A'^isuAL  Disturbances. — In  examining  a  patient's  vision  for  neu- 
rological purposes,  it  is  incumbent  to  search  for  refractive  and  other 
errors,  though  this  belongs  especially  to  the  province  of  the  ophthal- 
mologist. In  certain  nervous  conditions  such  as  the  unstable  neu- 
roses, ocular  defects  may,  as  exciting  causes,  set  up  headache  and 
other  symptomatic  troubles.  These  having  been  eliminated,  the  visual 
disturbances  are  to  be  attributed  to  an  intracranial  disorder  of  some 
sort.  We  cannot  always  distinguish  by  these  visual  signs  optic  nerve 
from  cerebral  disease  but  in  regard  to  some  of  them  we  can  draw  all 
but  conclusive  inferences. 

Pupillary  reflex  disorders  may  be  due  to  optic  nerve  disease  and 
hence  the  pupils  should  always  be  examined  also.  The  discussion  of 
the  pupillary  phenomena  naturally  falls  under  the  head  of  disorders  of 
the  third  nerve. 

Concentric  Contraction  of  the  Visual  Field. — The  determination 
of  the  outer  limits  of  the  field  of  vision  for  each  eye  is  accurately  made 
with  a  perimeter.  This  is  not  the  place  to  give  a  minute  description  of 
this  apparatus  and  the  manner  of  using  it.  For  that  the  reader  should 
consult  works  upon  ophthalmology.  Suffice  it  to  say,  however,  that 
it  consists  of  a  semicircular  arc  or  band  which  revolves  upon  a  center, 
so  that  it  can  be  placed  in  the  direction  of  any  meridian.  This  arc  is 
divided  into  degrees  from  zero  at  the  center  to  ninety  at  either  end. 
By  means  of  a  head  rest  the  patient  is  enabled,  with  one  eye  covered,  to- 
place  the  other  eye  in  such  a  position  as  to  fix  its  gaze  upon  a  small 
object  at  the  center  of  the  arc.  While  the  gaze  is  kept  thus  fixed,  a 
small  white  object  is  slid  from  the  outer  end  of  the  arc  towards  the 


THE   XOX-XEUROXIC  DISEASES 


781 


-center.  The  momeiit  the  patient  declares  that  he  sees  it,  the  deo-ree 
on  the  scale  is  noted  and  marks  the  outer  limit  of  the  field  of  vision  in 
that  meridian.  The  process  is  repeated  for  all  meridians  and  the  de- 
crees jotted  down  on  a  chart  upon  which  the  normal  or  averao-e  visual 
field  is  indicated.  By  connecting  these  several  points  on  the  chart 
with  a  continuous  line,  the  visual  field  of  the  patient  is  seen  at  a  o-lance 
and  can  be  compared  with  the  normal  field. 

When  the  white  object,  moving  on  the  arc.  appears  blurred  or 
disappears  entirely,  there  is  a  defect  in   the  field  which  is   termed  a 

FIGURE  189. 


Normal  field  of  vision.     B,  blind  spot  of  ]Mariotte. 


scotoma.  The  head  of  the  optic  nerve,  known  as  the  blind  spot  of 
Mariotte,  and  situated  about  10  degrees  to  the  outer  side  of  the  fixa- 
tion point,  furnishes  a  physiological  scotoma. 

Instead  of  white,  little  objects  of  different  color  may  be  em- 
ployed and  thus  the  color  fields  be  taken  and  compared.  The  perimeter 
shows  that  normally  the  field  for  green  'is  the  smallest.  Then  follow 
in  order,  from  within  outwards,  red,  yellow  and  blue. 

It  should  also  be  noted  that  the  field  of  vision  is  more  extensive 
■externally  than  it  is  internally.  The  outer  part  of  the  retina  is  less 
sensitive  than  the  inner,  and  the  bridge  of  the  nose  cuts  it  off  some- 
what. As  considerable  variations  in  the  field  are  observed  normally, 
in  every  case  of  unilateral  alteration  where  accurate  results  are  desired, 
the  normal  eye  should  also  be  examined  perimetrically  at  the  same 
time. 

In  the  absence  of  a  perimeter,  a  rough  examination  of  the  fields 
may  be  made  in  the  following  manner.  Place  the  patient  with  his 
hack  to  the  window.  Take  a  seat  directly  in  front  of  him  at  a  distance 
of  about  three  feet.  Cover  the  eye  of  the  patient  that  is  not  to  be  ex- 
amined with  a  towel.    Ask  him  to  fix  his  gaze  steadily  upon  the  oppos- 


782  THE   NON-XEURONIC  DISEASES 

ing  eye  of  the  examiner.  The  latter  then  closes  his  other  eye  and  at 
the  same  time  brings  his  finger  along  the  different  horizontal  and  ver- 
tical lines  into  the  field  of  vision,  holding  it  about  half  way  between 
himself  and  the  patient.  For  the  color  fields  a  small  piece  of  green, 
red  or  blue  paper  on  the  end  of  a  pen-holder  may  be  substituted  for  the 
finger.  As  the  finger  or  bit  of  colored  paper  is  gradually  moved  from 
above,  from  below,  or  from  the  side  towards  the  mutual  visual 
axis,  the  patient  is  told  to  say  when  he  first  sees  it.  If  the  patient 
and  examiner  see  it  at  the  same  moment  at  all  points  in  the  edge  of 
the  field,  the  latter  is  normal.  If  the  examiner  sees  it  in  this  line  or 
that  before  the  patient  does,  there  is  a  defect  at  that  point  in  the  pa- 
tient's visual  field. 

A  concentric  contraction  of  the  fields  of  vision  may  take  place  in 
conditions  of  functional  weakness,  like  hysteria  and  neurasthenia,  from 
simple  repetition  of  the  test  or  from  the  attention  being  directed  to  them 
for  a  short  time.  This  is  even  more  marked  when  there  is  a  patholog- 
ical contraction  present.  This  is  not  a  retinal  but  a  central  phenome- 
non, for  if  the  contraction  is  thus  produced  in  one  part  of  the  field  of 
one  eye,  the  corresponding  part  of  the  field  of  the  other  eye  will  be 
seen  to  be  similarly  affected. 

When  the  white  fields  are  contracted,  the  color  fields  are  as  a  rule 
correspondingly  reduced,  so  that  it  may  be  said  that  a  generally  con- 
tracted field  is  a  normal  field  in  miniature  merely. 

Sometimes  there  is  no  contraction  in  the  white  field  while  the 
color  fields  are  markedly  reduced.  The  color  perception  is  generally 
more  easily  blurred  or  destroyed  than  is  the  white.  As  a  rule  it  is  oiily 
necessary  to  test  the  green  and  red  fields  as  they  are  the  smallest  and 
undergo  the  most  diminution  in  morbid  states.  It  must  not  be  forgotten 
that  concentric  contraction  may  occur  slightly  in  myopia,  myosis, 
paresis  of  accommodation  and  with  opaque  corneal  spots.  These  being 
eliminated  as  possible  causes,  we  find  that  this  phenomenon  is  to  be  re- 
garded as  a  sign  of  disease  in  the  retina,  optic  nerve  or  brain. 

Loss  of  sight  anywhere  within  a  visual  field  is  spoken  of  as  a 
scotoma.  Scotomata  may  be  variously  situated  and  of  all  shapes  and 
sizes.  They  may  be  central  or  peripheral.  Concentric  ring  scotomata 
occur  in  hysteria.  They  are  organic  or  functional  in  origin  and  may 
therefore  be  due  to  variously  located  lesions  in  the  optic  apparatus. 
They  may  invade  the  color  fields  as  well  as  the  white.  In  toxic  ambly- 
opia both  eyes  are  affected  and  the  patient  complains  of  misty  vision, 
which  is  due  to  a  central  color (  relative)  scotoma,  especially  for  red 
and  green.  The  fixed  point  is  a  favorite  site  for  scotomata.  The  peri- 
meter aids  one  in  detecting  scotomata,  as  I  have  already  pointed  out. 

Definite  geometric  defects  in  the  visual  fields  are  usually  classed 
under  the  head  of  hemianopsia.  This  is  generally  a  bilateral  blurring 
of  the  half-fields,  though  it  may  be  unilateral.  It  is  easily  enough  ex- 
amined. Often  the  patient  is  all  too  aware  of  it  himself.  All  the  ex- 
aminer has  to  do  is  to  introduce  from  different  sides  some  small  white 
or  colored  object  into  the  visual  field  of  each  eye.  He  may  use  the 
perimeter  if  he  wishes  to  accurately  outline  the  intact  part  of  the  field. 
A  most  remarkable  defect  that  has  been  seen  several  times  is  that  of 


THE   NON-NEURONIC  DISEASES  783 

hemianopsia  for  colors  without  any  change  in  the  white  field.  Usually 
of  course  the  color  fields  are  affected  in  correspondence  with  the  white. 
This  will  be  referred  to  again. 

In  hemianopsia  the  dividing  line  between  the  dark  and  light  part 
of  the  field  generally  passes  through  the  fixation  point  in  the  center. 
It  may  be  horizontal  or  vertical.  In  this  way  we  have  horizontal  and 
vertical  hemianopsia.  The  former  is  almost  always  due  to  retinal 
lesions,  such  as  embolism,  injuries,  etc.  In  vertical  hemianopsia  the 
central  or  dividing  line  generally  passes  a  little  to  one  side  or  around 
the  fixation  point,  leaving  the  central  vision  very  acute.  This  vertical 
hemianopsia  is  spoken  of  as  temporal  when  the  temporal  halves  of  the 
visual  fields  are  dark,  indicating  anaesthesia  in  the  nasal  halves  of  the 
retinse ;  as  nasal  when  the  inner  or  nasal  halves  of  the  fields  are  ob- 
scured, denoting  anaesthesia  in  the  outer  or  temporal  halves  of  the 
retinae ;  as  lateral  or  homonymous  in  which  physiologically  similar 
halves  of  the  field  are  darkened,  as  for  example  the  temporal  half- 
field  of  the  left  eye  and  the  nasal  half-field  of  the  right.  An  incom- 
plete hemianopsia  may  be  sector-like  and  involve  only  a  quadrant,  or 
even  less,  of  one  or  both  fields. 

Of  all  forms  of  hemianopsia  the  vertical  are  the  most  frequent. 
Nasal  hemianopsia  is  exceedmgly  rare  and  is  of  small  practical  inter- 
est. There  is  much  doubt  overhanging  the  inferior  and  superior  hemi- 
anopsias. 

In  addition  to  the  above  conditions,  the  vision  should  always  be 
tested  in  regard  to  its  acuity,  for  which  purpose  test  types  are  em- 
ployed, and  for  the  perception  of  color,  for  which  variously  hued  wools 
are  employed  according  to  the  method  devised  by  Holmgren.  For 
details  in  regard  to  these  tests  works  upon  ophthalmology  should  be 
consulted.  Every  neurologist  should  be  familiar  with  the  use  of  the 
ophthalmoscope.  The  ophihahwscopic  alterations  are  among  the  most 
important  symptoms  that  we  have  of  intracranial  disease.  The  head  of 
the  optic  nerve  is  exposed  to  direct  observation  at  the  fundus  of  the 
eye  and  as  this  so-called  nerve  is  really  a  part  of  the  brain,  in  observ- 
ing its  changes  we  are  observing  the  brain  itself,  as  it  were. 

I  will  now  discuss'  the  localisation  phenomena  of  the  optic  ap- 
paratus, taking  up  the  parts  of  the  latter  in  an  orderly  way  from  the 
optic  disc  backwards,  and  note,  as  far  as  our  present  knowledge  per- 
mits, the  relationship  between  the  special  symptomatology  and  the  site 
of  the  lesion. 

What  may  be  called  associated  changes  in  the  eye,  discoverable 
with  the  ophthalmoscope,  may  at  times  be  most  helpful  in  diagnosing  a 
brain  disease.  These  changes  are  not  due  to  the  brain  trouble  but  are 
merely  collateral  manifestations  of  a  much  more  general  trouble,  of 
which  the  brain  is  the  seat  of  other  manifestations.  For  instance, 
syphilitic  choroiditis  or  tubercles  of  the  choroid  may  confirm  the  diag- 
nosis of  brain  syphilis  or  tubercular  meningitis.  Albuminuric  retinitis 
is  associated  with  an  arterial  degeneration  that  not  infrequently 
eventuates  in  a  cerebral  hemorrhage  or  thrombotic  encephalomalacia. 
Miliary  aneurisms  and  vascular  lesions  of  the  brain  may  legitimately 
be  surmised  when  the  same     conditions  are  observed  in  the  retina. 


784 


THE  XOX-NEURONIC  DISEASES 


Hemorrhages  in  the  retina  and  in  the  pia  mater  have  been  seen  to- 
gether in.  severe  ansemia,  puiura,  leucocytha?mia,  albuminuria,  gout, 
ulcerative  endocarditis  and  septicaemia.  Degeneration  of  the  brain 
sometimes  is  accompanied  by  simple  atrophy  of  the  disc. 

Ncuro-rctinitis  and  optic  atrophy  are  the  chief  ophthalmoscopic 
changes  observable  in  disease  of  the  brain,  because  they  are  consecu- 
tive to  and  dependent  upon  the  latter. 

Optic  neuritis,  papillitis,  neuro-retinitis,  choked  disc  are  all  differ- 
ent names  for  the  same  pathological  process  so  far  as  the  optic  disc 
is  concerned.    A  difference  of  degree  may  be  represented  by  the  terms 

FIGURE  iQo. 


Normal   Fundus   Oculi. 

papillitis  and  choked  disc,  but  the  underlying  process  of  both  is  es- 
sentially the  same. 

As  everyone  knOws  from  his  anatomy  the  optic  nerve  enters  the 
back  of  the  eyeball  through  an  opening  in  the  sclerotic  coat.  Its  fibres 
bend  at  right  angles  like  the  rays  of  the  sun  and  spread  out  on  the 
retina.  That  part  of  the  nerve  which  we  behold  in  the  fundus  as  the 
blind  spot  is  the  papilla.  With  the  ophthalmoscope  w^e  can  see  through 
the  translucent,  radiating  optic  nerve  fibres  the  circular  edge  of  the 
disc.  The  surface  of  the  disc  is  not  uniform.  It  has  usually  a  "physio- 
logical cup"  in  its  center  which  is  rather  pale  from  the  scarcity  or 
absence  of  bloodvessels  in  it.  The  periphery  of  the  disc  is  more  vas- 
cular and  hence  more  rosy  in  tint.  Simple  congestion  of  the  disc  is 
rare  and  of  little  importance.  Much  more  significant  is  the  swelling 
of  the  papilla  and  diminished  translucency  which  it  exhibits  when  there 
is  an  actual  pathological  change.    With  such  a  change,  the  edge  of  the 


THE   XOX-XEUROXIC  DISEASES 


785 


disc  becomes  blurred  and  finally  entirely  obscured.  The  dis- 
tinctness of  the  outline  of  the  disc,  as  affected  by  a  morbid  change, 
undergoes  greater  modification  under  the  direct  than  under 
the  indirect  method  of  examination  with  the  ophthalmoscope. 
Gradually  the  change  involves  the  entire  circumference  of 
the  disc ;  the  swelling  obliterates  the  central  cup  with  a 
mere  trace  of  a  depression  left ;  and  the  vessels,  as  they  course  down 
the  sides  of  the  enlarged  papilla,  diminish  or  disappear  from  view 
because  the  plane  of  their  reflection  has  ceased  to  be  at  right  angles 

FIGURE  191. 


Optic    neuritis    (choked    disc)    in    cerebral   tumor.      (After   Gowers.) 


to  the  line  of  the  examiner's  vision.  The  entire  papilla  assumes  a  red 
or  grayish  red  tint,  increases  to  two  or  three  times  its  normal  diameter 
and  exhibits  in  its  surface  spots  which  are  the  accumulations  of  the 
products  of  degeneration.  Early  in  the  process  the  vessels  are  little 
altered  but  soon  the  veins  become  swollen,  the  arteries  narrow  and  the 
blood  extra vasated. 

The  rapidity  of  the  process  varies  in  difterent  cases.  In  a  few 
days  the  swelling  may  increase  and  measure  six  or  more  diopters  from 
its  blurred  base  to  the  apex.  We  speak  of  it  as  choked  disc  when  it. 
measures  as  much  as  two  diopters.  The  change  may  reach  a  very 
high  degree  of  intensit}-  in  a  couple  of  weeks,  or  it  mav  still  be  chronic 


786 


THE   XOX-NKUROXIC  DISEASES 


and  moderate  after  several  months.  Quick  developments  of  the  disease 
usually  mean  hiijh  intensity  of  it. 

When  the  ])apillitis  subsides  the  arteries  become  more  contracted, 
the  veins  diminish  in  size,  and  the  swelling  after  lingering'  awhile  slowly 
settles  back  revealing  once  more  the  edge  of  the  normal  disc.  Unless 
the  neuritis  has  been  very  moderate,  some  permanent  alterations  re- 
main, consisting  of  new  tissue,  with  a  white  and  atrophied  appearance 
and  associated  damage  to  the  neighboring  edge  of  the  choroid.  This  is 
sometimes  called  consecutive,  or  neuritic,  atrophy.  The  retina  in 
severe  cases  may  have  its  nutrition  affected,  especially  near  the  macula, 
and  this  leads  to  an  appearance  in  it  much  like  that  of  albuminuric 
retinitis. 

Under  the  microscope,  the  papilla  presents  in  its  diseased  state 
all  of  the  usual  changes  observed  in  neuritic  inflammation. 

The  anatomical  cause  of  choked  disc,  as  it  is  seen  for  instance 

FIGURE  192. 


Section  through  a  "choked"   disc  in  brain  tumor.    (After   de  Schweinitz  and 
Randall.) 

in  brain  tumor,  is  obscure.  It  may  be  due  to  one  or  more  conditions. 
It  is  without  doubt  in  the  beginning  a  pure  oedema  of  the  nerve  head 
as  a  part  of  the  inflammatory  process  going  on  inside  of  the  cranium. 
Whether  this  oedema  is  a  mere  mechanical  product,  due  to  compres- 
sion or  the  carrying  of  the  increased  subdural  and  arachnoid  fluids 
along  the  channels  of  the  nerve  to  the  papilla,  or  to  the  irritating  toxic 
qualities  of  that  fluid,  or  to  both  causes  combined,  we  do  not  know 
positively.  The  probability  is  that  the  neuritis  is  due  to  the  descent 
of  the  irritative  influence  which,  when  it  reaches  the  papilla,  sets  up 
an  intense  inflammation.  This  is  aided  by  the  retention  of  the  inflam- 
matory fluids,  carrying  irritating  material,  on  account  of  the  distention 
of  the  sheath.  A  chronic  intracranial  disease  may  cause  an  acute 
optic  neuritis  but  a  chronic  neuritis  never  follows  an  acute  brain  lesion. 
There  is  a  parallelism  between  the  chronicity  of  the  neuritis  and  that  of 
the  cerebral  disease.  Subsidence  of  the  brain  trouble  is  usually  ac- 
companied by  lessening  of  the  neuritic  trouble.  Thus  we  can  follow, 
by  direct  observation  to  a  certain  extent,  the  progress  of  the  intra- 
cranial disease. 


PLATE   III. 

Optic  neuro-papillitis  in  a  case  of  known  cerebral  tumor. 
Drawn  from  life.      (After  Beard.  ) 


788 


THE   NON-NEURONIC  DISEASES 


.seen  in  these  cases,  it  is  to  be  remembered  that  in  chronic  lead  poison- 
ing a  progressive  optic  atrophy  and  ocular  paresis  do  occur. 

Choked  disc,  optic  neuritis,  optic  atrophy  and  toxic  amblyopia 
are  not  very  definite  as  localizing  symptoms.  In  fact  they  belong  to 
the  general  brain  symptoms,  though  they  are  more  definite  than  such 
general  symptoms  as  headache,  vomiting  and  vertigo  previously  dis- 
cussed. 

We  have  now  to  discuss  the  visual  manifestations  by  which  lesions 
can  more  or  less  be  definitely  localized  in  the  optic  tract.  The  reader 
is  again  urged  to  refer  to  the  chapter  upon  the  anatomy  of  the  brain 
where  the  optic  tracts  and  their  decussation  are  described  and  diagram- 
matically  illustrated. 

Behind  the  optic  nerve,  of  whose  diseases  the  etiology  and  symp- 
tomatology we  have  just   been   studying  and   found  to   be  not  very 

FIGURE  193- 


Field  of  Vision  in  Chronic  Lead  Poisoning. 
(Nimier.) 


definite  as  localization  signs,  we  come  to  the  optic  chiasm,  the  optic 
tracts,  the  primary  optic  centers  in  the  inter-  and  mid-brains,  the 
optic  radiations  of  Gratiolet  and  the  occipital  cortex.  The  symptoms 
of  disease  in  any  of  these  parts  of  the  optic  apparatus  are  almost  en- 
tirely visual.  In  other  words  there  need  not  be  with  them  any  oph- 
thalmoscopic alterations  unless  the  optic  nerve  trunk  is  at  the  same 
time  implicated.  A  lesion  of  the  chiasm,  if  of  long  standing,  may, 
however,  set  up  a  descending  atrophy  and  thus  present  a  change  in 
the  appearance  of  the  fundus  oculi. 

The  chiasm  is  affected  generally  by  tumors  of  the  hypophysis 
cerebri.  Syphilitic  and  tuberculous  growths  are  not  uncommon  and 
may  be  inside  or  outside  of  the  chiasm.  Pressure  from  a  neighboring 
pachymeningitis  may  affect  the  commissure.  Other  sources  of  dam- 
age are  internal  hydrocephalus,  distention  of  the  infundibulum  of  the 
third  ventricle  and  vascular  lesions  such   as  interstitial   hemorrhaee 


THE  XOX-XEUROXIC  DISEASES  789 

within  its  mass.    It  has  been  diseased  in  tabetic  atrophy  and  has  been 
the  seat  of  an  interstitial  infiamniation. 

If  the  reader  will  carefully  note  the  course  of  the  optic  fibres 
through  the  chiasm,  he  will  readily  understand  a  bitemporal  hemi- 
anopsia, such  as  is  illustrated  in  the  article  on  acromegaly  in  another 
part  of  the  volume.  The  center  of  the  chiasm  being  most  involved, 
the  mesial  halves  of  the  two  retinge  are  anaesthetic.  Nasal  hemianopsia 
is  exceedingly  rare  and  of  course  would  be  most  likely  a  unilateral 
phenomenon,  whereas  temporal  hemianopsia  is  practically  always 
bilateral.  Amblyopia  occurs  at  first  but  total  blindness  comes  on  sooner 
or  later  from  the  consecutive  atrophy. 

The  optic  tract  behind  the  chiasm  may  be  injured  by  tumors  at 
the  base  of  the  brain  on  the  inner  part  of  the  temporo-sphenoidal  lobe. 
Softening  and  hemorrhage  occasionally,  but  rarely,  damage  the  tract. 
Sometimes  spots  of  disseminated  sclerosis  occur  in  it.  The  crura 
cerebri  may  be  implicated  at  the  same  time.  Within  the  hemisphere 
the  tract  is  hurt  by  softening,  hemorrhage,  tumor  and  various  trau- 
matic lesions. 

A  lesion  that  destroys  a  tract  on  one  side  causes  homonymous 
hemianopsia.  As  I  have  pointed  out  elsewhere  the  line  of  division  in 
these  hemianopsias  is  vertical  and  does  not  pass,  as  a  rule,  through 
the  fixation  point.  It  passes  around  the  latter  so  that  the  central 
acuity  is  not  disturbed.  There  are  many  variations  on  this,  however. 
The  variations  are  probably  due  to  individual  differences  in  the  de- 
cussation of  the  nerve  fibres.  There  is  no  special  localization  valua- 
tion to  be  attached  to  these  differences  in  the  course  of  the  line  of 
division  between  the  light  and  dark  half-fields  through  or  around  the 
fixation  center.  Gowers  says  he  doubts  whether  the  dividing  line  ever 
passes  actually  through  the  fixing  point. 

The  hemianopsia  is  not  always  complete.  A  quadrant  may  repre- 
sent the  blind  area  or  any  sector-like  form.  This  is  to  be  attributed 
to  the  partial  extension  of  the  lesion  in  the  tract  or  visual  centers. 
It  is  very  rare  in  diseases  of  the  tract  where  the  fibres  all  lie  so  close 
together.  It  has  been  seen  in  partial  softening.  Partial  hemianopsia 
is  common  enough,  however,  in  disease  of  the  occipital  lobe. 

In  hemianopsia  there  is  always  some  central  amblyopia,  even  when 
the  division  is  a  considerable  distance  from  the  fixing  point. 

The  light  half  of  the  fields  in  hemianopsia  usually  preserve  their 
normal  boundaries.  \  ery  often,  however,  they  are  contracted  some- 
what, even  when  there  is  no  suspicion  of  a  peripheral  or  ring  neuritis. 

I  have  already  referred  to  the  fact  that  the  color  fields  are  affected 
in  hemianopsia  in  the  same  way  that  the  light  fields  are.  Hemiachrom- 
atopsia  is  a  remarkable  phenomenon  that  has  been  occasionally  seen. 
The  half  fields  for  color  are  aft'ected  while  those  for  ordinary  white 
light  are  intact.  The  division  line  here  seems  to  pass  through  the 
fixation  point.  The  lesion  in  this  case  is  probably  in  the  occipital  lobe. 
Just  where  the  center  that  is  aft'ected  is  located  in  the  lobe  we  do  not 
know. 

Except  as  hemiachromatopsia  (lesion  in  the  occipital  cortex)  and 
with  a  contraction  of  the  tmaft'ected  half  fields  (lesion  probably  in  the 


790  THE   XOX-XEUROXIC  DlSE.vSES 

optic  radiation  near  the  thalamus),  there  is  nothing  distinctive  about 
hemianopsia  by  which  we  can  locaHze  the  lesion  more  definitely  than 
to  say  it  is  in  the  optic  tract  somewhere  between  the  chiasm  and  the 
occipital  cortex.  As  the  connection  between  the  optic  tract  and  third 
nerve  occurs  in  the  primary  optic  centers.  Wilbrand  and  ^^'ernicke 
have  tried  to  make  use  of  this  fact  in  localizing  a  lesion  in  connection 
with  hemianopsia.  If  light  be  thrown  on  the  unaffected  half-field  and 
the  lesion  causing  the  hemianopsia  be  in  front  of,  or  in,  the  primary 
optic  centers,  there  will  be  no  pupillary  response ;  but  if  the  lesion  be 
behind  the  geniculate  and  quadrigeminal  bodies,  there  will  be  a  pupil- 
lary response.  This  does  not  work  out  so  well  clinically,  though 
theoretically  it  is  strictly  correct  if  we  are  sure  of  our  knowledge  in 
regard  to  the  reflex  centers  in  the  primary  optic  nuclei. 

Other  symptoms  added  to  the  hemianopsia  often  enable  us  to 
localize  the  lesion  very  definitely.  Hemianopsia  due  to  lesions  in  the 
optic  tracts  immediately  behind  the  chiasm  is  usually  accompanied  by 
other  cranial  nerve  symptoms.  If  the  lesion  be  in  the  thalamus  or 
external  geniculate  bodies,  the  collateral  symptoms  will  generally  show 
implication  of  the  internal  capsule  and  be  a  hemiplegia  or  hemianses- 
thesia  on  the  same  side  as  the  hemianopsia.  If  the  lesion  is  in  the 
left  hemisphere,  the  visual  paths  are  so  located  that  with  the  hemi- 
anopsia will  probably  be  some  speech  disturbance.  If  the  lesion  is  in 
the  cortical  or  subcortical  fibres,  irritative  signs,  such  as  facial  hallu- 
oinations  which  are  apparently  the  only  symptoms  of  an  irritating 
focus  in  the  visual  center,  will  appear. 

For  obvious  reasons,  reading  is  extremely  difficult  in  right-sided 
hemianopsia.  The  condition,  even  when  slight,  is  usually  recognized 
by  the  patient,  and  yet  a  case  is  recorded  where  the  trouble  was  only 
discovered  by  the  nurse  noting  that  the  patient  never  ate  the  articles 
of  food  placed  upon  one  side  of  the  plate.  Hemianopsia  patients  usu- 
ally carry  their  heads  turned  a  little  toward  the  blind  side.  These 
patients  are  liable  to  accidents. 

Bilateral  hemianopsia,  if  complete,  necessarily  results  in  total 
blindness.  In  this  way  extensive  lesions  in  the  optic  apparatus  behind 
the  primary  centers  cause  complete  loss  of  sight.  Incomplete  bilateral 
hemianopsia,  in  which  central  vision  is  not  lost,  may  not  result  in  total 
blindness,  but  the  orientation,  or  ability  to  distinguish  things  will  be 
greatly  impaired.  Complete  color  blindness  of  apoplectiform  onset, 
iDilateral  hemiachromatopsia,  has  been  seen.  The  ordinary  vision  was 
not  disturbed. 

There  are  no  ophthalmoscopic  changes  in  hemianopsia,  except 
what  may  be  attributed  to  the  causative  lesion,  such  as  a  tumor  or 
associated  hemorrhage. 

Hemianopsia  may  be  transient  or  permanent,  functional  or  toxic. 
It  is  not  at  all  improbable  that  in  some  cases  of  uremic  amaurosis  and 
lead  poisoning,  there  is  a  toxic,  transient,  bilateral  hemianopsia  of 
cortical  origin,  for  the  pupillary  responses  often  remain  normal.  If 
these  are  lost  too  then  the  blindness  is  probably  neuritic  in  origin. 
A  transient  functional  hemianopsia  mav  associate  itself  with  the  scin- 


THE   NON-NEURONIC  DISEASES  791 

tillating  scotomata  of  migraine.  x\s  an  indirect  focal  symptom,  a 
transitory  hemianopsia  has  been  seen  to  follow  an  apoplectic  attack. 

Psychic  Blindness.  This  peculiar  disorder  was  first  observed  by 
Munk  in  animals.  It  has  been  noticed  in  man  also  a  number  of  times. 
Vision  is  not  lost  but  visual  comprehension  is  gone.  Objects,  including 
of  course,  written  word  symbols  are  seen  but  not  recognized.  There 
seems  to  be  a  complete  failure  of  memory  pictures  in  the  visual  sphere. 
A  familiar  person,  a  chair,  a  street  are  clearly  seen  but  they  seem 
perfectly  strange  and  unfamiliar  to  the  patient.  The  patient  sees  with 
his  eyes  but  not  with  his  mind.  This  psychic  blindness  is  not  the 
same  as  visual  aphasia.  Munk  produced  the  condition  in  animals  by 
removing  the  occipital  lobes.  In  man  it  has  usually  been  associated 
with  homonymous  bilateral  hemianopsia  of  one  side.  As  it  does  not 
always  occur  with  hemianopsia,  there  is  doulDt  about  its  being  a  mani- 
festation of  an  occipital  lesion.  This  is  so  frankly  recognized  that 
those  who  have  tried  to  explain  the  phenomenon,  have  adopted  the 
notion  that  there  is  still  a  higher  visual  center,  possibly  in  the  anterior 
part  of  the  occipital  lobe  or  lower  part  of  the  parietal  lobe,  that  re- 
ceives impulses  from  the  occipital  cortex  and  there  gives  them  their 
higher  or  psychic  interpretation.  The  existence  of  this  so-called  higher 
visual  center  is  not  only  hypothetical  but  it  is  unsupported  by  the 
slightest  shadow  of  anatomical  evidence.  It  is  a  sorry  makeshift 
from  one  dilemma  into  another. 

Psychic  blindness  is  a  psychic  manifestation  and  should  be  classi- 
fied under  the  previously  named  psychic  symptoms.  I  mention  it  here 
because  it  happens  to  be  a  psychosis  in  the  visual  sphere.  As  I  have 
stated  at  the  end  of  the  section  on  the  mental  manifestations  of  brain 
disease  it  is  a  crude  conception  of  psychological  phenomena  to  think 
that  they  are  subserved  by  small  cortical  areas  scattered  here  and 
there  throughout  the  brain.  It  belongs  to  the  mode  of  reasoning  adopt- 
ed in  the  phrenology  of  the  long  ago. 

Visual  recognition  is  a  complicated  act.  It  is  the  result  of  a 
combination  among  a  great  many  elementary  psychic  sensations.  These 
psychic  sensations  have  their  physiological  counterparts  in  the  pure 
physiological  visual  sensations  that  are  received  by  the  cortex  of  the 
occipital  lobe.  Simple  psychic  elementary  vision  may  well  be  conceived 
therefore  as  having  its  seat  in  the  occipital  ccJrtex.  But  psychic  ele- 
mentary vision  is  something  very  much  more  simple  than  visual  mem- 
ory and  visual  recognition.  These  are  the  result  of  inter-connections 
between  psychical  compounds  which  are  themselves  made  up  of 
anatomico-psychic  elements.  From  the  very  nature  of  things  there 
cannot  be  a  single  center  for  compound,  complex  psychic  phenomena, 
though  there  may  be  centers  where  the  various  constituent  elements 
are  brought  in  touch  with  one  another,  or  at  least  in  which  certain 
physiological  inter-connections  are  established  from  which  start  the 
various   psychic  manifestations. 

The  whole  doctrine  of  the  cortical  centers  has  up  to  the  present 
time  been  most  crudely  taught  and  only  now  are  we  beginning  to 
realize  that  these  so-called  centers  which  we  have  heretofore  supposed 
subserved   most  pomplicated   psychic   acts,   are  merely   the     starting 


792  THE   XOX-XEURONIC  DISEASES 

points,  the  threshholds,  tlie  central  clearing  houses,  as  it  were,  of  the 
vast  and  intricate  workings  of  the  mind  which  for  its  physical  basis 
requires  the  whole  brain  with  all  its  enormously  inter-connected  parts. 

Psychic  sensation  of  the  elementary  vision  may  have  its  seat  in  the 
occipital  lobe.  Psychic  visual  memory  and  comprehension  is  probably 
coextensive  with  all  of  the  brain  functions. 

J'isiial  haUuciuations  are  psychic  symptoms  that  happen  to  be  in 
the  visual  sphere.  Closely  related  to  them,  if  not  exactly  the  same,  are 
megalopsia,  or  the  apparent  enlargement  of  objects,  and  micropsia, 
or  the  apparent  reduction  m  the  size  of  objects.  These  may  be  due 
to  displacement  of  the  retinal  rods  and  cones.  ]^iore  often,  however, 
they  are  among  the  psychic  phenomena  of  neurasthenia  and  hysteria. 

Monocular  diplopia  seen  in  hysteria  is  a  psychosis.  True  diplopia 
is  a  visual  disturbance  caused  by  paralysis  in  the  ocular  motor  nerves 
and  is  mentioned  elsewhere. 

Hypcrccsthcsia  of  the  retina,  causing  photophobia,  lachrymation 
and  involuntary  closure  of  the  eyelids  may  be  due  to  optic  nerve  hyper- 
sensitiveness.  There  is  reason  to  believe  that  the  fifth  nerve  is  at  the 
bottom  of  photophobia.  It  is  a  suspicious  fact  that  diseases  in  which 
photophobia  is  most  marked  involve  the  structures  that  are  innervated 
by  the  trigeminal  nerve.  There  may  be  a  central  inter-connection, 
however,  between  the  optic  and  the  fifth  nerves. 

GusT.\TORY  Symptoms. — These  are  easily  examined  by  placing 
various  substances  on  the  tongue.  The  four  kinds  of  taste  are  sweet, 
sour,  salty  and  bitter.  Sugar,  vinegar,  salt  and  quinine  may  be  used 
to  test  each  respectively.  Disorders  of  taste  are  usually  due  to  nerve 
diseases  and  have  been  referred  to  under  the  head  of  the  trigeminal 
and  glosso-pharyngeal  nerves.     There  are  hallucinations  of  taste. 

Auditory  Symptoms. — These  are  tested  by  whispering,  after 
closing  the  ear  that  is  not  under  examination,  by  holding  at  different 
distances  a  ticking  watch  and  by  sounding  a  tuning  fork.  A  normal 
person  should  be  employed  as  a  control  test.  Bone  conduction  of 
sound  is  determined  after  closing  the  ears  by  placing  the  watch,  or 
handle  of  the  sounding  tuning  fork  against  the  mastoid  bone  or  be- 
tween the  teeth.  Bone  conduction  is  often  preserved  when  the  mechani- 
cal hearing  is  lost.  When  the  nerves  and  their  centers  are  diseased, 
bone  conduction  is  also  lost. 

Rinne's  test  is  an  excellent  one  to  distinguish  nerve  from  mere  ear 
deafness.  In  a  normal  person  the  vibrating  fork,  after  being  placed 
against  the  bone  and  no  longer  heard,  is  placed  in  front  of  the  ear. 
Its  sound  is  again  heard.  This  occurs  exactly  the  same  way  in  nervous 
impairment  of  audition,  except  when  it  approaches  actual  deafness.  In 
mechanical  impairment,  the  fork  is  not  heard  the  second  time. 

\\'eber's  is  also  a  good  test.  Place  the  sounding  fork  on  the 
frontal  bone  and  it  will  be  heard  as  if  from  a  distance.  The  sound 
will  be  referred  to  both  ears.  If  one  ear  is  then  closed,  the  sound 
will  be  referred  to  that  ear.  When  the  same  test  is  made  upon  a 
patient,  if  the  impairment  of  hearing  is  nervous  the  sound  will  be 
said  to  be  heard  in  the  well  ear ;  if  it  is  due  to  the  sound-conducting 
apparatus,  it  will  be  referred  to  the  diseased  ear. 


THE  NON-XEUROXIC  DISEASES  793 

According  to  Schwabach  the  fork  on  the  head  is  heard  longer  than 
normally  in  disease  of  the  conducting  apparatus,  shorter  than  normally 
in  cerebral  impairment  of  hearing. 

When  there  is  irritability  with  audition,  the  condition  is  some- 
times called  acoustic  hypercesthcsia.  Paracusis  is  where  a  tone  is 
heard  deeper  or  higher  than  it  really  is.  If  the  sound  ear  hears  the 
normal  tone  at  the  same  time,  the  condition  is  called  diplacusis. 

DISEASES  OF  THE  MEMBRANES  OF  THE  BRAIX. 

The  diseases  of  the  intracranial  meninges  are  all  essentially  in- 
flammatory in  type.  The  origin,  course  and  ultimate  results  of  this 
inflammation  may  be  diflierent  in  different  cases  but  its  essential  nature 
is  the  same  in  all.  It  may  be  so  slight,  incipient  or  transient  as  to 
merely  amount  to  a  circulatory  disturbance.  Ansemia  and  hyperaemia 
may  express  the  entire  patholog}'  of  the  case ;  on  the  other  hand  the 
most  violent  characteristics  of  a  severe  inflammation,  simple  or  puru- 
lent, may  constitute  the  disease  process. 

Of  the  three  membranes  the  dura  mater  and  the  pia  mater  are  the 
only  ones  w^hose  inflammation  is  of  clinical  significance.  The  arachnoid 
is  never  diseased  by  itself. 

Ancemia. — This  has  no  clinical  existence  as  a  disease  by  itself,  so 
far  as  we  know.  In  anaemia  of  the  brain,  the  membranes  are  also 
anaemic.     It  cannot  therefore  be  discussed  here. 

Hyperccmia.- — Congestion  is  always  the  first  stage  of  an  inflam- 
mation and  consequently  has  all  of  its  symptoms  in  a  slight  or  transient 
form.  There  may  be  headache,  throbbing  and  full  in  character,  ver- 
tigo, delirium,  convulsions,  and  even  coma  and  death.  These  fulmi- 
nant cases  reveal  an  intense  meningeal  hyperaemia,  which  is  perhaps 
better  described  as  a  rapid,  overwhelming  meningitis.  The  whole  or 
a  part  of  the  membranes  may  be  involved.  When  the  pia  is  impli- 
cated, it  is  a  part  of  congestion  of  the  brain.  When  the  dura  is  the 
seat  of  the  congestion  it  has  the  same  etiology  and  symptomatology 
practically  as  pachymeningitis. 

PACHYMENINGITIS. 

As  the  dura  mater  consists  of  two  layers,  a  thin,  internal,  smooth- 
ly epitheliated  layer  and  an  external,  loose,  periosteal  layer,  either  of 
which  may  be  primarily  inflamed,  we  have  a  pachymeningitis  interna 
and  a  pachymeningitis  externa. 

External  Pachymeningitis.- — This  is  the  most  common  inflam- 
mation of  the  dura.  Generally  it  is  a  secondary  disease  and  is  asso- 
ciated with  surgical  conditions. 

Etiology. — Fractures  of  the  skull,  blows  and  other  injuries  to  the 
head,  with  effusion  of  blood  between  the  bone  and  the  membrane,  are 
the  most  glaring  causes  of  it.  Diseases  of  the  bones  of  the  head, 
caries  and  necrosis  of  the  petrous,  mastoid,  ethmoid  or  outer  table 
even  of  the  squamous  bones  may  light  up  the  inflammation.  Erysipelas, 
otitis  media,   oz^ena   and   other  diseases  mav  cause   it   by  extension. 


794  THE  XOX-XEUROXIC  DISEASES 

Syphilis  and  neoplasms  have  originated  it.  As  a  great  rarity  it  has 
been  seen  to  occur  without  any  traceable  cause.  For  obvious  reasons 
it  is  rare  in  children. 

Pathology. — The  findings  of  the  primar}-  trouble  which  has 
caused  the  pachymeningitis  are  of  course  a  part  of  the  pathology. 
The  dura  itself  exhibits  all  the  changes  of  a  purulent  inflammation.  At 
first  it  is  congested,  red,  oedematous  and  later  on  infiltrated  and  bathed 
in  pus  which  flows  and  accumulates  between  it  and  the  bone.  Oc- 
casionally the  purulent  matter  extends  between  the  two  layers  of  the 
dura  and  even  into  the  arachnoid  beneath  it,  setting  up  a  purulent 
dura-arachnitis.  The  pia  may  become  involved  and  all  the  membranes 
be  glued  together  or  bound  by  adhesions.  Sometimes  the  inflammation 
goes  down  without  the  appearance  of  pus,  in  which  case  it  often  be- 
comes firmly  attached  to  the  skull  and  is  penetrated  by  osteophytic 
growths.  In  syphilitic  cases  the  bones  may  be  greatly  thickened,  the 
pus  large  in  quantity  and  the  membrane  itself  in  a  very  rough  and 
almost  sacculated  condition. 

Symptoms. — These  are  indefinite  because  they  are  obscured  by  the 
svmptoms  of  the  primary  disease  and  because  the  lesion  is  so  out- 
stretched and  variable.  The  discovery  of  the  original  cause  will  often 
enable  the  diagnostician  to  determine  which  of  the  m.ass  of  symptoms 
present  are  to  be  attributed  to  the  meningitis.  Usually  there  is  a 
gradual  onset  of  Iicadache,  fever  and  delirium.  There  are  eompres- 
sion  symptoms,  especially  of  a  hemiplegic  type  if  the  motor  cortex  is 
implicated.  Therefore  convulsions  and  paralyses  are  to  be  looked  for. 
Focal  symptoms  are  rare.  I  once  was  able  to  follow  the  extension 
of  the  brain  compression  by  the  extension  of  the  clot  from  the  hem- 
orrhage, in  the  case  of  a  child  whom  I  saw  fall  several  stories  and 
fracture  its  skull.     Trephining  failed  to  save  life. 

The  course  of  these  cases  is  acute  or  subacute  and  is  largely  due 
to  the  nature  of  the  primary  disease.  As  a  rule  the  prognosis  is  serious 
but  somewhat  better  than  it  is  in  most  of  the  other  forms  of  menin- 
gitis. 

The  treatment  is  entirely  surgical  and  is  largely  the  treatment 
of  the  underlying  cause.  Pus  must  be  evacuated.  If  there  is  reason 
to  believe  that  there  is  no  pus  present,  the  treatment  of  the  mem- 
branous trouble  is  the  same  as  for  an)'  meningitis. 

Pachymeningitis  Interna. — Pathologists  recognize  two  forms  of 
this,  the  purulent  and  the  hemorrhagic.  They  are  both  uncommon, 
especially  the  former.  Some  atithors,  like  Osier,  speak  of  a  pseudo- 
membranous internal  pachymeningitis,  though  it  is  not  usually  recog- 
nized. Osier  saw  it  as  a  secondary  process  in  pneumonia.  Purulent 
internal  pachymeningitis  has  been  seen,  very  rarely,  however,  as  a 
primary  condition.  Generally  it  is  secondary  to  purulent  inflamma- 
tion of  the  pia  or  dura.  Hemorrhagic  internal  pachymeningitis  is  a 
most  interesting  and  remarkable  disease  and  is  still  a  subject  of  much 
debate  among  pathologists.  Some  writers  classify  it  among  the  intra- 
cranial hemorrhages  while  others  still  continue  to  regard  it  as  a  men- 
ingeal inflammation. 

Pachymeningitis  interna  hemorrhagica.     Hccmatoma  of  the  Dura 


THE   NOX-NEURONIC  DISEASES  795 

Mater.  Meningeal  Blood  Tumor. — This  is  a  rare  disease  of  the  dura 
mater,  characterized  especially  by  the  formation  of  an  inflammatory 
membrane  with  hemorrhagic  effusion  upon  its  under  surface.  Whether 
the  hemorrhage  or  the  membranous  deposit  takes  precedence  in  the 
<lisease  process  is  the  question  that  is  still  being  debated.  I  am  in- 
clined to  think  that  the  disease  is  primarily  a  meningitis  of  a  particular 
type  and  that  the  hemorrhage  is  a  secondary  accident,  as  it  were. 
According  to  Gowers,  Prescott  Hewitt,  as  far  back  as  1845,  described 
the  trouble  as  primarily  a  dural  hemorrhage.  Virchow  studied  it 
anew  and  in  1854  demonstrated  that  the  origin  of  it  was  a  particular 
variety  of  pachymeningitis.  This  explanation  satisfied  the  medical 
world  until  Huguenin  recently  revived  Hewitt's  hypothesis  and  ad- 
duced some  evidence  in  support  of  it.  As  the  question  is  still  suh  jttdice, 
the  disease  will  continue  to  be  classified  by  authors  in  accordance  with 
their  individual  confidence  in  the  proofs  of  one  view  or  the  other. 
Etiology. — The  disease  is  very  rare  in  general  practice.  It  is  a 
secondary  condition  and  most  of  the  cases  are  seen  among  the  insane 
in  the  asylums.  It  seems  to  be  consecutive  to  some  forms  of  chronic 
insanity,  especially  chronic  dementia,  general  paresis,  senile  dementia, 
chronic  mania,  chronic  melancholia  and  chronic  epileptic  psychosis. 
It  has  been  seen  to  follow  acute  mania  and  imbecility,  chronic  alcohol- 
ism and  Huntington's  chorea.  Most  of  these  diseases,  it  will  be 
noticed,  are  chronic  hitlammations  and  atrophy  of  the  cerebral  tissue. 
It  has  occurred  secondarily  to  certain  vitiated  and  cachectic  blood 
states,  such  as  is  seen  in  profoimd  anaemia,  in  hemorrhagic  purpura, 
certain  acute  fevers  like  rheumatism  and  smallpox,  in  scurvy,  leukemia, 
and  rarely  syphilis.  It  may  be  observed  in  a  mild  form  in  renal  dis- 
■eases,  chronic  heart  troubles  and  phthisis.  Traumatic  injuries  to  the 
head  may  cause  it.     It  may  occur  as  a  prim.ary  trouble  also. 

Males  are  subject  to  it  more  than  females.  It  is  so  comparatively 
irequent  in  old  age,  especially  with  mental  breakdown,  that  it  is  sup- 
posed to  be  in  part  at  least  the  expression  of  physical  deterioration 
as  much  as  of  actual  disease.  It  occurs  in  infantile  scurvy  though  as  a 
rule   it  is  relatively  infrequent  in  childhood. 

Pathology  and  Pathogenesis. — The  essential  feature  of  dural 
"hsematoma  is  the  formation  of  a  delicate,  vascular  membrane  on  the 
under  surface  of  the  dura  mater  and  between  it  and  the  arachnoid. 
In  about  half  of  the  cases  this  formation  extends  bilaterally  over  both 
Tiemispheres.  In  many  cases,  however,  it  is  limited  in  extent,  spread- 
ing over  only  one  hemisphere  or  part  of  a  hemisphere.  It  may  occur 
at  the  base  of  the  brain,  in  the  middle  and  posterior  fossae  likewise.  It 
is  at  first  a  soft  red  tissue  which  afterwards  becomes  paler  and  harder 
and  more  compact.  It  varies  in  thickness  and  has  a  laminated  con- 
struction with  hemorrhagic  extravasation  between  its  six  or  seven 
layers.  Its  edges  may  be  adherent  and  the  blood-clot  be  inclosed  in 
a  sort  of  sac  arrangement.  Sometimes  these  contain  merely  a  slightly 
colored  serum  with  crystals  of  cholesterine.  Adhesions  between  the 
layers  of  the  membrane  at  a  number  of  places  cause  it  to  have  a 
cystic  appearance.  The  vascular  condition,  its  rich  supply  of  blood- 
vessels  and  the  degeneration  of  the   extravasated  blood,   causes  the 


796  THE   NON-NEURONIC  DISEASES- 

rucldy  tint  in  the  earlier  stages ;  while  development  of  delicate  fibrous- 
tissue  and  other  organization  material  are  responsible  for  its  later 
firmness  and  paleness.  Not  all  cases  present  the  same  exhibition  nor 
does  the  same  case  manifest  exactly  the  same  changes  in  all  parts  o£ 
the  membrane  at  the  same  time.  In  mild  cases,  for  instance,  the  latter 
may  be  like  a  veil  or  delicate  piece  of  lace,  faintly  rose-tinted  and 
easily  pulled  off  from  the  dura.  The  hemorrhages  into  this  may  be 
small  and  punctated,  causing  spots  of  brown,  brownish-red  or  yellow 
here  and  there  according  to  the  age  of  the  extravasation.  On  the  other 
hand  the  disease  process  may  be  so  violent  and  elaborate  that  a  thick, 
many-layered,  intensely  red  and  hard  deposit  is  made.  It  may  cover 
the  brain  like  a  closely-fitting  cap  and  adhere  it  strongly  to  the  men- 
inges. In  such  cases  it  is  difficult  to  pull  it  away  without  tearing- 
off  pieces  of  the  brain  substance.  The  brain  next  to  it  is  usually 
atrophied. 

'  Three  typical  apearances  may  be  noted  in  the  development  of 
this  hematoma.  Some  cases  clearly  show  that  it  consists  of  a  deli- 
cate, inflammatory  or  organization  exudate  into  which  has  penetrated 
numerous  bloodvessels  and  much  granulation  tissue.  In  other  cases. 
there  seems  to  have  been  nothing  but  a  simple  subdural  hemorrhage, 
though,  as  Osier  suggests,  the  membrane  may  have  been  in  existence 
but  was  destroyed  by  the  blood.  In  a  third  set  of  cases  both  vascular 
membrane  and  hemorrhagic  extravasation  seem  to  have  been  developed 
together. 

It  is  owing  to  the  fact  that  the  membane  thus  sometimes  appears 
without  the  evidences  of  hemorrhage,  and  that  at  other  times  the 
hemorrhagic  residua  appear  without  the  evidences  of  the  formation; 
of  a  membrane,  that  so  much  controversy-  has  sprung  up  in  regard 
to  the  primary  nature  of  the  entire  process.  Virchow  adduced  strongs 
proof  that  the  trouble  began  with  internal  pachymeningitis,  that  the 
membrane  was  nothing  but  an  inflammatory  exudate  and  that  the 
presence  of  the  blood  was  a  mere  secondary  phenomenon.  The  etio- 
logy and  course  of  the  disease,  the  appearance  of  the  exudate  without: 
hemorrhagic  extravasation  in  the  light  cases,  and  above  all  the  irregu- 
lar distribution  and  cystic  and  punctated  character  of  the  blood  de- 
posits, as  though  when  fluid  it  found  difficulty  in  spreading  out  evenly 
over  the  surface  of  the  dura,  are  strong  arguments  in  favor  of  Virchow's 
view.  Hence  I  treat  of  the  disease  as  a  form  of  pacliymcniiigitis.  It 
must  be  admitted,  however,  in  all  candor  that  the  position  taken  by 
Huguenin  and  others  is  far  from  being  a  weak  one,  namely,  that  a 
dural  hemorrhage  takes  place  and  that  later  on  the  clot  undergoes 
organization  and  produces  all  the  collateral  appearances  through  irri- 
tation both  of  the  brain  and  dura. 

Symptoms. — The  clinical  picture  of  hsematoma  of  the  brain  is-* 
very  indefinite,  for  its  symptoms  may  range  from  nil  all  the  way  to 
those  of  a  profound  apoplectic  stroke.  They  are  least  marked  or 
absent  entirely  in  the  slight  cases,  whereas  in  the  traumatic  and  other 
cases  they  are  both  severe  and  extensive.  Ofttimes  they  are  marked 
by  the  general  symptoms  of  the  disease  of  which  the  hemorrhagic 
effusion  is  an  accompaniment.    This  is  the  case  in  general  paresis  par- 


THE   NON-XEUROXIC  DISEASES  797 

ticularly.  The  seat  and  character  of  the  lesion,  the  nature  of  the 
associated  disease  or  injury,  and  the  stage  at  which  the  disease  has 
arrived  all  determine  the  general  outlines  of  the  symptomatology. 
When  a  series  of  apoplectiform  seizures  occur,  follozued  by  cerebral 
pressure  symptoms,  in  a  patient  affected  with  any  of  the  diseases 
known  to  be  causative  of  hsematoma,  the  latter  may  be  diagnosed. 
Usually  the  first  symptoms  are  very  gradual  and  insidious,  almost 
prodromal,  in  their  onset.  A  feeling  of  general  distress  and  restless- 
ness, excitement  almost  resembling  delirium,  is  followed  by  an  in- 
creasing headache,  vomiting,  unilateral  epilepiiform  tzvitchings  and 
■coma.  The  patient  emerges  in  rare  cases  from  this  or  he  may  remain 
in  this  state  for  several  days  or  weeks  and  then  die  with  or  without 
another  seizure.  At  times  the  beginning  of  the  trouble  is  a  genuine 
■apoplectic  stroke.  All  of  the  usual  signs  appear,  coma,  paralysis,  con- 
jugate deviation  of  the  eyes,  contraction  of  the  pupils,  retardation  of 
the  pulse,  labored  respiration,  etc.  Vomiting  and  elevation  of  the  tem- 
perature are  not  infrequent.  All  of  the  sym.ptoms  referable  to  unila- 
teral or  bilateral  pressure,  following  a  sudden  access  and  showing  more 
■or  less  of  a  progression,  may  appear  in  different  cases.  The  hemiplegia 
may  be  one-sided  or  double.  Both  it  and  the  monoplegia  are  not  as 
■complete  as  in  ordinary  intracranial  hemorrhage  and  are  often  pre- 
ceded by  local  spasms  and  general  convulsions.  A  liemiparesis  of  one 
side  may  occur  with  marked  contractures  on  the  other.  These  are  all 
often  merely  temporary  phenomena  and  may  appear  with  or  without 
coma.  It  is  very  exceptional  for  the  sensibility  to  be  disturbed. 
Aphasia  and  nystagmus  have  been  seen  in  some  cases.  Choked  disc 
is  rather  a  frequent  manifestation.  The  temperature  may  be  subnor- 
mal but  it  very  often  goes  very  high,  io6  degrees  F.  just  before 
death. 

Diagnosis.- — This  is  always  extremely  difficult.  In  children  it 
is  pretty  nearly  impossible.  The  chief  traits  that  must  be  depended 
upon  are  the  presence  of  injury  (these  cases  usually  present  the  most 
marked  clinical  presentation)  or  disease  with  which  htematoma  is 
known  to  occur,  a  series  of  apoplectiform  seizures  occurring  like  ex- 
acerbations with  remissions  in  a  disease  that  manifests  headache,  ver- 
tigo, choked  disc  and  other  pressure  symptoms,  temporary  or  slight 
monoplegia  or  hemiplegia  followed  and  preceded  by  spasms,  convul- 
sions and  contractures.  The  extensive  involvement  of  the  body  with 
such  paralytic  manifestations,  not  so  profound  as  they  are  in  ordinary 
hemorrhage,  would  be  strongly  suggestive  of  hsematoma. 

Cerebral  glioma  sometimes  presents  itself  in  the  same  way  as 
haematoma.  The  diagnosis  is  then  impossible,  though  a  suspicion  may 
be  aroused  by  the  presence  of  some  mental  or  senile  condition  in  which 
hsematoma  occurs. 

In  ordinary  meningitis  the  diagnosis  is  often  very  difficult.  Haema- 
toma, however,  is  devoid  of  nuchal  rigidity  and  cranial  nerve  (except 
the  optic)  involvement.  In  meningitis  the  remittent  character  of  the 
symptoms,  the  apoplectic  seizures,  the  choked  disc  and  the  intercurrent 
convulsions  do  not  obtain. 

Prognosis. — This  is  bad.     Death  usuallv  occurs  sooner  or  later. 


798  THE   NON-NEUKOXIC  DISEASES 

Treatment. — This  may  have  in  view  the  checking  of  the  inflamma- 
tion and  the  hemorrhages.  In  neither,  however,  is  it  very  successful. 
The  former  suggests  free  purgation  and  diuresis,  the  appHcation  of  the 
ice  bag,  leeches  and  bloodletting  in  robust  individuals.  Counter-irrita- 
tion has  been  tried.  To  check  the  hemorrhage  has  heretofore  proved 
to  be  an  impossible  task,  hence  there  are  no  measures  to  be  recom- 
mended beyond  those  commonly  resorted  to  in  intracranial  hemorrhage. 

In  both  traumatic  and  non-traumatic  hcematoma,  operation  has. 
been  resorted  to  with  a  very  fair  degree  of  success.  Localization 
svmptoms  of  some  degree  of  definiteness  must  be  present.  Dangerous 
compression  of  the  brain  particularly  suggests  the  consideration  of 
surgical  relief. 

LEPTOMEXIXGITIS. 

An  inflammation  of  the  pia  mater  includes  as  a  rule  the  arachnoid 
and  the  cortex,  so  that  the  terms  pia-arachnoiditis  and  meningo-en- 
cephalitis  are  justifi^ed.  In  most  cases  it  is  a  difi^use  condition,  in- 
volving both  the  vertex  and  base  of  the  brain  and  not  infrequently 
even  the  spinal  cord.  Excepting  the  tuberculous  and  syphilitic  types, 
the  vertex  is  afi'ected  in  most  of  the  cases  chiefly.  The  symptoms 
vary  in  accordance  with  the  location  of  the  disease,  but  not  sufficiently 
so  to  establish  that  as  a  basis  of  classification.  Usually  the  disease 
is  acute,  though  it  may  become  chronic.  It  is  highly  doubtful  if  it  is 
very  simple.  Most  generally  it  is  infective  and  purulent.  Sometimes 
it  is  specific  and  epidemic.  Its  symptomatolog}-  is  fairly  uniform  in 
all  types.  No  special  classification  of  it  is  therefore  called  for,  though 
for  convenience  sake  we  may  discuss  separately  Acute  {simple  and 
purulent)  Leptomeningitis,  Epidemic  Cerebrospinal  Leptomeningitis 
and  Tuberculous  Leptomeningitis.  Syphilitic  Meningitis  is  considered 
elsewhere  under  the  head  of  cerebral  syphilis,  and  serous  meningitis  is 
referred  to  under  the  head  of  hydrocephalus.  It  is  misleading  and  in- 
correct to  speak  as  some  authors  do  of  the  brain  condition,  the  so- 
called  "wet-brain,"  of  subacute  alcoholism  as  one  of  serous  meningitis. 
It  is  not  meningitis  at  all  but  a  mere  serous  effusion. 

Acute  (simple  and  purulent)  Leptomeningitis. — It  is  very 
questionable  whether  a  simple,  non-toxic  inflammation  of  the  meninges 
ever  occurs.  The  nearest  approach  to  it  would  seem  to  be  in  some  of 
the  cases  of  Quincke's  hydrocephalus  wherein  the  ependyma  of  the  ven- 
tricles, and  even  the  cortical  meninges,  exhibit  signs  of  a  low  grade  of 
pure  inflammation.  Older  writers  used  to  refer  to  a  smiple  meningitis 
that  was  caused  by  insolation,  mental  strain  and  simple  cerebral  con- 
cussion. In  some  of  these  cases  ^^hich  succumbed  rapidly  to  death, 
nothing  but  intense  congestion  was  discovered.  This,  hovv'ever,  is  not 
accepted  by  many  modern  pathologists  as  proof  positive  of  the  non- 
purulent character  of  these  eases.  They  hold  that  they  are  merely 
foudroyant  cases  that  do  not  reach  the  purulent  stage,  or  are  -not  cases 
of  meningitis  at  all.  Simple  non-purulent  meningitis  is  therefore  de- 
clared to  have  no  existence.  Whether  we  are  yet  in  a  state  of  knowl- 
edge to  adopt  so  radical  a  position  or  not,  we  are  obliged  to  recognize 
that  the  vast  majority  of  all  the  cases  of  leptomeningitis  are  of  septic 


THE  NON-NEURONIC  DISEASES  799 

origin.  The  source  and  nature  of  the  poison  are  different  in  different 
cases.  Usually  it  is  an  infection  carried  to  the  brain  from  some  out- 
side focus  by  way  of  the  blood.  The  meningitis  is  therefore  a  second- 
ary process  except  perhaps  in  the  epidemic  cerebrospinal  form. 

It  is  convenient  to  group  these  various  sources  of  the  infective  pro- 
cess under  several  general  heads.  Traumata,  acute  alcoholism  and 
other  depressing  influences,  and  in  tuberculous  meningitis  even 
heredity,  exercise  an  influence  as  predisposing  factors. 

The  infective  fevers  provoke  leptomeningitis  though  not  as .  fre- 
quently as  the  mere  fibrile  delirium  has  led  many  practitioners  to  sup- 
pose. It  occurs  in  pneumonia,  erysipelas,  septicaemia,  smallpox, 
typhoid,  influenza,  measles,  mumps,  scarlet  fever,  pyaemia,  acute  arti- 
cular rheumatism,  ulcerative  endocarditis,  empyema,  gonorrhoea,  etc. 
The  first  three  give  rise  to  it  more  frequently  than  the  others.  It  has 
been  ascribed  to  actinomycosis  and  is  doubtfully  associated  with  in- 
testinal catarrh.  The  meningitis  due  to  these  causes  is  practically  al- 
ways purulent,  though  the  suppurative  process  may  vary  in  character 
and  severity  according  to  the  particular  microorganism  involved.  It  is 
an  error  to  refer  to  this  form  of  meningitis  as  metastatic.  The  disease 
is  not  transferred.  The  meningitis  is  simply  the  expression  of  a  gen- 
eral infection  of  the  organism  and  may  be  the  only  expression.  A 
pneumococcus  meningitis  has  been  seen  without  any  implication  of  the 
lungs  whatever. 

Injuries  and  diseases  in  the  bones  of  the  skull,  involving  the  men- 
inges are  a  not  uncommon  cause  of  acute  suppurative  leptomeningitis. 
The  injuries  that  directly  involve  the  membranes  and  cause  the  ordi- 
nary form  of  pachymeningitis  are  not  referred  to  here.  Fractures, 
blows,  concussion  may  set  up  a  local  suppuration  with  transmission 
of  the  germs  to  the  pia  mater,  a  sinus  thrombosis  from  the  veins  of 
the  diploe  carrying  the  infection.  Caries  of  the  petrous  part  of  the 
temporal  bone  from  otitis  media,  necrosis  of  the  cribriform  plate  of 
the  ethmoid  and  disease  of  the  cavities  of  the  skull  and  their  bony 
walls  may  light  up  the  meningeal  inflammation. 

Neighboring  foci  of  suppurative  proccesses  must  also  be  held  re- 
sponsible, such  as  chronic  purulent  otitis,  mastoiditis,  disease  of  the 
nasal  cavity,  the  orbit,  the  antrum,  frontal  sinuses,  etc.  Then  again 
the  infection  may  come  in  the  other  direction  from  an  abscess,  a 
tumor,  an  old  hemorrhagic  or  necrotic  focus  in  the  brain.  An  infected 
embolus  from  an  endocarditis  is  a  common  cause  of  The  latter.  A 
puncture  with  a  sound  has  carried  the  disease  from  the  nose  into  the 
cranial  cavity.  Vascular  sheaths  form  another  path  along  which  the 
poison  passes  inward ;  also  the  nerve  sheaths. 

In  certain  diseases  there  is  a  terminal  infection  that  sometimes  re- 
veals itself  in  a  leptomeningitis.  It  is  thus  sometimes  seen  in  chronic 
nephritis,  gout,  valvular  and  muscular  heart  disease,  senile  states, 
arteriosclerosis  and  the  wasting  diseases  of  childhood. 

In  some  cases  the  source  of  the  infection  cannot  be  determined 
and  the  cause  of  the  disease  is  hidden  in  obscurity. 

Thus  it  is  made  clear  that  acute  leptomeningitis  is  a  bacteriological 


800  THE  NON-NEURONIC  DISEASES 

disease,  a  secondary  infective  process  in  most  cases,  with  a  varied 
etiology. 

The  relationship  of  the  disease  to  age,  sex,  climate,  occupation, 
season  and  station  in  life  is  largely  a  matter  of  the  original  source  and 
nature  of  the  primary  infection.  It  may  be  noted,  however,  that  men 
are  slightly  more  affected  by  it  than  are  women,  and  that  it  is  most 
common  in  children  between  the  ages  of  one  and  ten,  since  during  these 
years  the  infective  diseases  are  most  rife  and  disastrous. 

Pathology  and  Pathogenesis. — The  great  pathogenetic  fact  in 
the  development  of  leptomeningitis  is  always  the  presence  of  disease 
germs  or  their  products.  These  may  be  of  various  types  and  may  be 
the  basis  of  a  general  or  a  local  infection.  Somehow  they  get  to  the 
pia-arachnoid  membrane  and  there  set  up  a  typical  mfective  or  puru- 
lent inflammation.  In  some  cases  tiiey  have  been  recovered  from  the 
diseased  membrane  post  mortem ;  in  other  cases  only  the  remains  of 
their  destructive  work  have  been  seen.  It  is  doubtful  if  all  of  the 
germs  that  are  believed  to  give  rise  to  meningitis  will  be  recovered. 
We  are  not  sure  of  the  exact  influence  of  those  that  have  been  so 
far  recovered.  We  dare  not  yet  dogmatize  in  regard  to  the  relative 
importance  of  the  germs  themselves  or  their  biological  products.  In  a 
word,  though  we  have  gotten  so  far  as  to  recognize  acute  leptomenin- 
gitis as  a  germ  disease,  we  are  still  in  the  dark  in  regard  to  many  of  the 
details. 

Direct  examination  of  the  exudate  has  been  rewarded  many  times 
with  the  finding  of  numberless  streptococci  and  staphylococci.  Of 
these  the  former  are  the  more  frequently  met  with.  A  form  of  men- 
ingitis that  occurs  with  pneumonia  and  as  an  independent  affection 
seems  to  be  due  to  the  pneumo coccus  of  Frjenkel.  It  has  been  recov- 
ered many  times  from  the  membrane.  The  meningococcus,  or  diplo- 
coccus  intracellnlavis  of  Weichselbaum,  is  in  all  probability  responsible 
for  some  cases,  especially  of  the  sporadic  and  epidemic  cases  of  cere- 
brospinal meningitis,  though  in  these  have  been  found  other  bacteria 
also.  The  pneumo-bacillus  of  Friedlsender,  the  typhoid  bacillus,  the 
colon  bacillus,  the  gonococcus,  the  tubercle  bacillus,  and  the  staphylo- 
coccus have  all  been  isolated  from  the  diseased  meninges. 

The  streptococcus  is  the  most  important  in  the  pathogenesis  of 
acute  purulent  leptomeningitis.  It  is  the  germ  usually  found  in  those 
cases  due  to  traumata,  chronic  otitis  media,  and  the  septic  processes 
generally ;  in  those  associated  with  ulcerative  endocarditis,  and  those 
due  to  terminal  infection.  The  staphylococci  are  found  in  some  of  the 
last. 

Purulent  inHammation  may  characterize  all  parts  of  the  pia- 
arachnoid  membrane,  though  as  a  rule  it  appears  mostly  on  the  ver- 
tex. It  usually  covers  the  entire  brain,  though  it  may  be  unilateral  or 
even  focal.  It  assumes  the  latter  form  especially  in  those  cases  where 
the  infection  comes  from  some  nearby  suppurating  focus.  It  is  more 
extensive  in  the  general,  infective  cases.  The  pia  is  at  first  congested, 
violently  reddened,  oedematous  and  cloudy.  Gradually  a  purulent  de- 
posit spreads  over  the  sulci,  collections  of  pus  appear  in  spots,  unite 
and  finally  give  to  the  membrane  a  yellowish,  thick,  creamy  appear- 


THE  XOX-XEUROXIC  DISEASES  8oi 

ance.  The  convolutions  are  completely  hidden.  Infiltration  takes 
place  into  the  superficies  of  the  brain  substance ;  small  hemorrhages 
occur;  pus  deposits  in  small  foci;  and  a  general  encephalitic  process 
with  some  atrophy  even  may  appear.  Encephalomalacia  and  abscesses 
are  possible.  Very  prone  is  the  pus  to  deposit  itself  at  the  base  of  the 
brain  in  the  Sylvian  fissure  around  the  chiasm,  beneath  the  cerebel- 
lum and  beside  the  pons.  Sometimes  the  dura  is  implicated.  In  the 
ventricles  there  pours  out  a  sero-purulent  exudate  which  may  so 
distend  them  that  a  distinct  condition  of  hydrocephalus  is  produced. 
The  distension  is  rarely,  however,  as  great  as  it  is  in  the  tuberculosis 
form  of  the  disease.  As  a  very  rare  condition  it  is  said  that  a  puru- 
lent meningitis  may  be  limited  to  the  ventricles  in  childhood.  A  per- 
manent collection  of  fluid  may  be  left  in  the  ventricular  cavities. 

In  many  cases  the  spinal  meninges  are  simultaneously  affected, 
so  that  the  disease  may  be  truthfully  termed  a  cerebrospinal  diffuse 
meningitis.  In  and  about  the  sheaths  of  the  nerve  trunks  the  purulent 
matter  may  sometimes  be  seen. 

Symptoms. — Pathology  and  practical  diagnosis  are  at  logger- 
heads in  regard  to  the  frequency  of  meningitis  in  the  infectious  fevers. 
The  former  finds  it  very  rarely,  the  latter  very  often.  This  discrep- 
ancy is  accounted  for  by  the  fact  that  many  symptoms  of  simple  con- 
gestion as  it  occurs  in  these  fevers  are  like  those  of  a  frank  menin- 
gitis. Mild  delirium,  muscular  twitchings,  spasms  and  retraction  of 
the  neck,  seen  in  typhoid  fever,  for  instance,  are  largely  due  to  the  com- 
hined  effect  of  the  infection,  congestion  and  elevated  temperature 
rather  than  to  an  inflammation  of  the  meninges.  Post  mortem  exam- 
inations show  that  the  latter  is  a  very  rare  complication  of  the  fever. 

The  clinical  picture  of  an  acute  purulent  leptomeningitis  is  a  very 
variable  one,  because  it  is  the  result  of  a  general,  diffuse  lesion  of 
infectious  origin.  Nevertheless  there  is  a  sufficient  degree  of  uni- 
formity about  it  to  establish  a  description  of  the  disease  which  will 
more  or  less  fit  all  cases.  There  are  always  two  sides  to  it.  On  the 
one  hand  are  the  symptoms  that  are  always  characteristic  of  a  general 
iniection ;  on  the  other  are  those  that  indicate  implication  of  the  en- 
tire brain  or  parts  of  it.  The  differences  between  the  various  types 
of.  infection  that  cause  the  meningeal  trouble  produce  differences  in 
many  of  the  details  of  the  general  symptomatology  of  the  infection. 
The  differences  between  the  locations  of  the  main  foci  of  inflamma- 
tion in  different  cases  cause  a  marked  variability  in  many  of  the  cere- 
bral manifestations. 

Some  cases  appear  abruptly  while  others  have  distinct  prodromaia. 
A  feeling  of  general  malaise,  head  soreness,  heavy  feeling  about  the 
-eyes,  vertiginous  distress,  possibly  vomiting,  anorexia  and  general 
irritability  and  uncompanionableness  in  a  few  cases  precede  for  some 
days  the  outbreak  of  the  signs  of  inflammation.  The  prodromata  are 
more  characteristic  of  tuberculous  than  of  the  simple  acute  menin- 
gitis. The  latter  as  a  rule  begins  somewhat  suddenly  with  a  chill,  an 
intense  headache,  a  rise  of  temperature,  a  rapid  pulse  and  all  the  usual 
signs  of  an  acute  infective  process.  If  these  occur  in  the  course  of 
the  same  infective  process  elsewhere  in  the  body,  they  will  be  obscured, 


802  THE   XUX-NEURONIC  DISEASES 

of  course,  by  the  symptoms  of  the  general  febrile  disease.  In  such  a 
case  the  involvement  of  the  meninges  must  be  determined  largely  by 
the  nature  and  location  of  the  original  source  of  infection,  and  its 
probable  influence  in  producing  a  meningitis,  as  well  as  by  the  more 
definitely  localizing  cerebral  manifestations. 

Among  the  latter  headache  easily  takes  the  first  rank.  It  is  a 
sharp,  excruciating  pain  that  appears  with  intense  exacerbations  all 
over  the  head,  though  chiefly  in  the  occipital  and  frontal  regions.  It 
is  never  entirely  absent,  though  at  times  it  may  undergo  a  temporary 
recession  or  remission.  It  is  a  persistent,  stead>-  pain  with  sharp, 
boring,  knife-like  flashes.  Even  stupor  does  not  bring  relief  to  its 
victim  for  in  the  night  when  asleep,  or  later  in  the  disease  when  the 
comatose  condition  comes  on,  he  cries  out  and  seizes  and  grasps  his 
head  with  his  hands  in  manifest  suffering.  In  certain  rare  cases  of 
septicaemic  meningitis,  and  others  due  to  blood  states,  the  disease  has 
been  seen  to  run  its  course  without,  or  with  only  a  slight,  headache. 

J'ouiiting,  of  the  cerebral  type,  is  very  often  present.  It  should 
be  distinguished,  if  possible,  always  from  the  vomiting  that  some- 
times accompanies  the  profound  alimentary  disturbance  caused  by  the 
fever  and  general  infectious  disease.  It  is  sudden,  projectile  and  unin- 
fluenced by  the  presence  or  character  of  the  food  in  the  stomacn. 

With  the  headache  and  vomiting,  there  is  always  more  or  less 
vertigo,  especially  when  the  patient  moves.  Nausea  may  or  may  not 
coexist.  The  bowels  are  generally  constipated  and  there  is  flattening 
of  the  abdomen  with  a  rapid  development  of  an  appearance  of  general 
emaciation. 

]\Iost  cases  are  initiated  with  a  fever  which  in  a  few  days  rises  to 
103  degrees  or  104  degrees  F.,  sometimes  higher.  Just  before  death 
it  may  go  to  108  degrees.  It  may  be  masked  by  the  fever  of  the  pri- 
mary disease.  It  is  an  irregular,  fluctuating  temperature.  In  some 
cases  it  may  be  subnormal,  and  in  a  few  instances  it  is  normal  through- 
out the  entire  course  of  the  disease.  The  usual  febrile  accompani- 
ments such  as  dry  skin,  coated  tongue,  parched  lips,  all  go  with  it. 

The  pulse  is  rapid,  rising  to  160  and  180  before  the  lethal  issue. 
V^ery  often  it  is  slow,  even  as  low  as  40  and  unsteady. 

The  respirations  are  not  often  very  greatly  disturbed.  They  may, 
however,  be  rapid,  irregular,  feeble  and  suddenly  cease.  A  Cheyne- 
Stokes  breathing  is  a  bad  omen.  Aleningitis  of  the  base  of  the  brain 
and  particularly  in  the  posterior  fossa  causes  these  phenomena  most 
markedly. 

The  urine  is  scanty,  high-colored  and  usually  contains  some  albu- 
min. Sometimes  sugar  is  present  in  it.  It  is  purely  a  febrile  urine 
unless  it  partakes  of  the  composition  of  a  urine  that  would  be  ex- 
pected in  the  primitive  disease  underlying  the  meningitis.  The  men- 
ingitis of  the  terminal  stages  of  renal  and  cardiac  affections  must  not 
be  forgotten  in  this  respect.  During  stupor  both  retention  and  in- 
continence of  urine  may  be  expected. 

After  the  headache  perhaps  the  most  characteristic  symptom  of 
meningitis  of  this  type  is  the  delirium.  This  comes  on  early,  as  a  rule 
is  first  noisy   and  excited,  then  becomes   milder  and   muttering   and 


THE   NON-NEURONIC  DISEASES  803 

finally  sinks  into  stupor  and  late  coma.  Sometimes  it  alternates  with 
a  drowsy  or  somnolent  condition.  The  patient  is  dazed  in  it,  it  mani- 
fests itself  in  his  sleep  and  with  it  there  are  evidences  of  distinct  blunt- 
ing of  his  sensorium.  It  usually  accompanies  the  headache  and  wheni 
once  developed  is  more  or  less  persistent  until  the  advent  of  the  coma. 

Hyperccsthesia  of  the  skin  and  of  all  the  sensory  nerves,  particu- 
larly the  optic  and  auditory,  is  very  often  a  pronounced  symptom.  The 
patient  will  complain  of  the  touch  of  the  bed-clothing,  of  a  slight 
draft  of  air,  of  the  light  in  the  room  and  of  every  trivial  noise.  If 
stupid  he  will  suddenly  start  when  touched.  In  quite  deep  stupor  I 
have  seen  the  patient  move  when  touched,  in  a  slow,  reflex,  automatic 
way  that  was  most  weird  and  uncanny.  The  muscles  are  also  hyper- 
sensitive so  that  a  slight  tap  will  set  up  a  most  vigorous  reflex.  The 
so-called  spinal  phenomenon,  which  is  a  sort  of  temporary  opisthotonos, 
is  partly  due  to  muscular  hyperexcitability.  A  light  tap  on  the  lum- 
bar muscles  sets  up  a  spastic  retraction  of  the  column.  Sometimes 
the  muscles  are  permanently  rigid  and  spastic.  This  is  particularly 
the  case  in  the  neck.  The  child  seems  to  have  its  head  drawn  back- 
ward in  an  effort  to  burrow  it  into  the  pillow.  Disease  in  the  pos- 
terior fossa  especially  provokes  this  symptom. 

Another  expression  of  the  general  muscular  rigidity  is  seen  in 
Kernig's  sign.  At  one  time  this  was  supposed  to  be  pathognomonic 
of  meningitis.  It  has  been  seen,  however,  in  many  other  diseases, 
though  it  is  a  valuable  one  in  meningitis.  It  is  easily  tested.  With 
the  patient  sitting  or  lying  on  his  back,  place  the  thighs  at  right  angles 
to  the  body  and  note  how  impossible  it  is  to  completely  extend  the 
legs  upon  the  thighs.  The  sign  may  be  unilateral,  as  I  have  several 
times  seen  it,  or  bilateral  as  it  usually  is.  The  rigidity  and  retraction 
of  the  abdomen  gives  it  the  well  known  scaphoid,  or  boat-like  appear- 
ance. 

All  of  the  nerves  of  the  body,  especially  the  cranial  nerves,  may 
enter  into  the  make-up  of  the  clinical  picture.  Irritability,  rigidity  and 
paralysis  may  be  among  their  exhibitions.  A  certain  amount  of  local- 
ization of  the  lesion  can  be  determined  by  the  general  and  cranial  nerve 
symptoms.  The  latter,  for  instance,  are  more  obvious  in  basal  men- 
ingitis ;  hemiplegic  and  monoplegic  phenomena  in  vertex  meningitis. 
Even  unilateral  hypersesthesia  and  hemiansesthesia  have  been  seen. 

PiipiUary  changes  are  very  frequent  and  important  signs  of  the 
disease.  As  a  rule  the  pupils  are  bilaterally,  very  rarely  unilaterally,, 
contracted  in  the  earlier  stages  of  the  affection ;  dilated  in  the  later. 
Ptosis  and  strabismus,  and  even  nystagmus,  are  present  at  times  and 
easily  accounted  for.  Strabismus  is  particularly  important,  especially" 
if  it  shows  a  tendency  to  be  transient  at  first  or  present  only  on  move- 
ment. 

Implication  of  the  facial  nerve  occurs  often.  The  facial  mus- 
cles are  spasmodic  at  first,  then  rigid  and  later  on  partially  paralyzed. 
Trismus  may  be  present.  The  paralysis  is  of  the  lower  motor  or  peri- 
pheral type  with  partial  reaction  of  degeneration.  Other  motor  craniall 
nerves  may  be  included  as  shown  by  the  difliculty  of  mastication,  of 
swallowing,  of  articulation,  of  vocalization,  and  of  glossal  movement. 


:8o4  THE  NON-NEURONIC  DISEASES 

The  vision  is  sometimes  partially  ali'ected.  Optic  neuritis,  and 
even  atrophy  is  not  uncommon  in  basal  meningitis,  but  it  is  far  less 
frequent  in  the  purulent  meningitis  of  tlie  vertex.  It  is  very  rarely 
complete  enough  to  eventuate  in  a  choked  disc,  and  as  a  result  the 
vision  is  but  little  decreased. 

The  reflexes,  trophic  and  vasomotor  symptoms  are  not  particu- 
larly significant.  The  deep  reflexes  during  the  irritative  stage  are  in- 
creased but  as  stupor  comes  on  they  diminish.  Among  the  vasomotor 
manifestations  is  the  well-known  tache  cerebrale,  of  the  French  authors. 
Drawing  the  thumb  nail  across  the  skin,  a  brilliant  and  more  or  less 
permanent  red  line  is  produced.  This  phenomenon  is  seen  in  so  many 
other  diseases  that  it  has  no  special  value.  In  many  long  running  cases 
there  is  a  strong  tendency  to  the  formation  of  bedsores,  vesicles,  etc. 
Hence  hot  bottles  and  other  irritants  must  be  used  cautiously. 

Early  in  the  disease  general  convulsions  or  even  unilateral  con- 
vulsions may  occur  but  they  are  not  common. 

Diagnosis. — The  diagnosis  of  acute  leptomeningitis  is  not  dif- 
ficult if  the  case  is  a  typical  one  and  not  obscured  by  the  presence  of 
another  more  general  infectious  process.  Mistakes  are  constantly 
made,  however,  as  the  disease  is  rarely  typical,  as  it  is  very  often  asso- 
ciated with  an  over-clouding  septic  process  elsewhere,  and  as  prac- 
titioners too  often  lay  too  much  stress  upon  special  symptoms. 

In  recognizing  the  Tlisease  its  etiology  is  a  matter  of  very  great 
importance.  Not  only  the  disease  itself  is  rendered  probable  but  the 
nature  of  the  inflammation  and  the  location  are  to  be  quite  positively 
inferred  from  the  existence  of  a  general  infection,  like  pneumonia 
.and  septicaemia  or  of  a  neighboring  nidus  of  suppuration  like  chronic 
otitis  or  trauma. 

i,.  The  onset  and  character  of  the  symptoms  should  be  carefully 
noted.  They  appear  somewhat  abruptly  or  rather  acutely  as  signs  of 
an  infective  process :  chill,  fever,  vomiting,  headache,  rapid  pulse,  irreg- 
ular respiration,  constipation,  febrile  urine.  Soon  the  signs  of  cere- 
bral irritation  or  compression  appear :  persistent  headache,  delirium, 
convulsions,  stupor,  retraction  of  the  neck,  contraction  followed  by 
■dilatation  of  the  pupils,  high  temperature  with  slow  pulse  and  irregu- 
lar breathing,  Kernig's  sign,  and  disturbed  vision.  Finally  focal  signs 
and  terminal  coma  make  the  case  plain. 

This  picture  may  vary  in  details  but  in  the  main  it  is  so  charac- 
teristic that  the  presence  of  meningitis  can  hardly  be  overlooked.  The 
greatest  danger  is  that  of  calling  many  diseased  states  and  many 
■other  affections  with  a  symptomatology  which  resembles  in  some  of 
its  features  the  symptomatology  of  meningitis,  the  latter  disease.  For 
this  reason  the  term  meningitis  appears  much  more  frequently  in  clin- 
ical than  in  autopsy  records.  There  is  not  a^  symptom  of  meningitis 
that  does  not  belong  also  to  some  other  disease  prominently,  and  many 
■combinations  of  the  symptoms  are  to  be  seen  in  other  conditions.  All 
■of  which  again  emphasizes  the  fact  that  the  diagnosis  of  acute  menin- 
gitis must  be  made  upon  the  symptomatic  presentation  of  the  case  in 
toto,  and  that  its  differential  diagnosis  from  other  troubles  must  be 
attained  both  by  direct  and  indirect  or  exclusion  methods. 


THE  NON-NEURONIC  DISEASES  805, 

Perhaps  the  commonest  mistake  that  is  made  is  to  diagnose  an: 
incipient  infectious  fever  of  atypical  onset  for  meningitis.  This  error 
is  more  frequent  than  the  reverse,  namely,  the  diagnosing  of  a  men- 
ingitis as  a  simple  infectious  fever.  Typhoid  and  pneumonia  probably 
are  the  leading  culprits  in  this  respect,  though  septicaemia,  pyaemia  or 
any  of  the  other  septic  affections  may  cause  the  error.  If  the  lungs  are 
affected  their  examination,  as  well  as  the  presence  of  all  the  usual 
signs  of  a  pneumonitis,  will  indicate  the  nature  of  the  malady.  Adults,, 
and  especially  children,  have  headache,  delirium,  vomiting,  fever  and 
stupor  as  a  part  of  the  general  infective  process  without  meningitis,, 
hence  the  latter  must  not  be  mf erred  from  these  symptoms  alone.. 
Focal  symptoms,  signs  of  cerebral  irritation,  pupillary  irregularities,, 
twitchings,  convulsive  movements,  optic  neuritis,  progressive  advance- 
ment of  all  these  manifestations  from  a  mere  initial  transiency  to  a 
more  or  less  permanency,  are  the  aids  in  determining  a  meningitis. 
If  the  trouble  be  typhoid  fever  the  rose  spots,  the  characteristic  stools.- 
Ihe  course  of  the  temperature,  the  enlargement  of  the  spleen  and  the 
Widal  blood  test  will  be  present ;  if  meningitis,  the  general  and  focal 
signs  of  this  trouble  will  be  in  evidence.  Jenner  pointed  out  long  ago 
that  simple  febrile  headache  ceases  with  the  onset  of  delirium,  whereas- 
in  meningitis  it  continues  with  the  delirium  and  even  with  the  stupor.. 
Septicaemia  is  to  be  suspected  from  the  absence  of  the  more  charac- 
teristic clinical  picture  of  meningitis,  and  the  presence  of  repeated 
chills,  cutaneous  and  retinal  hemorrhages,  swelling  of  the  joints  and. 
suppurative  processes  generally. 

A  history  of  ear  disease  and  the  examination  of  the  ear  and  mas- 
toid cells  will  help  to  distinguish  a  cerebral  abscess  in  the  posterior 
fossa  from  a  meningitis  m  the  same  locality.  This  distinction  is 
always  difficult,  however,  particularly  as  some  leptomeningitis  may 
accompany  even  an  extradural  abscess.  Much  more  difficult  to  com- 
prehend are  those  cases  of  purulent  otitis  with  cerebral  manifestations 
much  like  those  of  a  meningitis,  which  rapidly  get  well  after  opera- 
tion, followed  by  drainage  of  the  ear  and  mastoid  bone.  A  pyaemia, 
may  explain  some  of  the  symptoms  but  the  occasional  optic  neuritis, 
strabismus,  aphasia  and  other  focal  symptoms  cannot  be  so  accounted 
for ;  and  the  recovery  is  too  rapid  and  complete  to  suspect  the  presence 
of  a  meningeal  inflammation. 

Retraction  of  the  head  is  seen  in  rheuinatisni  of  the  muscles  of  the 
back  of  the  neck  but  the  other  characteristic  signs  of  meningitis,  espe- 
cially the  involvement  of  the  cranial  nerves,  are  wanting, 

Urcemic  poisoning  ofttimes  resembles  an  irritative  meningitis., 
Unlike  the  latter  disease  the  urine  contains  casts  with  the  albumin,  and 
the  focal  symptoms  are  wanting. 

Simple  meningeal  hemorrhage  is  abrupt  in  onset,  apoplectic  in 
character  and  without  the  febrile  and  septic  manifestations. 

Intracranial  tumor  produces  headache,  vertigo,  stupor,  but  not 
the  septic  and  febrile  symptoms.  Choked  disc  and  even  optic  neuritis 
are  comparatively  rare  in  meningitis. 

An  acute  syphilitic  meningitis  may  be  determined  by  the  history 
of  the  infection  and  the  results  of  antispecific  medication. 


8o6  THE  NON-NEUROXIC  DISEASES 

Pscndo-meningitis  is  a  complexus  of  symptoms  which  resembles 
that  of  a  true  meningitis  but  which  upon  autopsy  reveals  no  indica- 
tion of  the  latter.  Congestion,  oedema  and  other  changes  have  been 
noted.  Quincke's  hydrocephalus,  alcoholic,  so-called,  serous  menin- 
gitis or  "wet  brain,"  and  some  other  forms  of  developmental  and 
toxaemic  anomalies  belong  here.  It  is  possible  that  mild  auto-intoxi- 
cation from  gastrointestinal  catarrh  someiimes  causes  these  pseudo- 
meningitic  symptoms  in  children.  In  all  of  these  cases  whether  hydro- 
cephaloid,  encephaloid,  toxaemic  or  congestive,  the  absence  of  the  char- 
acteristic febrile  phenomena,  the  peculiar  history  of  the  cases,  the  non- 
purulent indication  of  the  entire  trouble,  the  absence  of  the  focal  symp- 
toms and  the  non-menmgeal  traits  of  the  disease  in  its  general  course 
are  to  be  made  note  of. 

Some  very  awkward  errors  have  been  committed  between  hysteria 
and  meningitis.  Oppenheim  was  called  to  see  a  woman  who  had  had 
3ier  head  shaved  and  antimonial  ointment  rubbed  on  it,  and  yet  who 
was  out  of  bed,  well  and  attending  to  her  duties  in  a  few  hours.  This 
mistake  is  more  likely  to  occur  between  hysteria  and  tuberculous  men- 
ingitis. A  full  appreciation  of  the  real  nature  of  hysteria,  a  psychosis, 
and  the  detection  of  distinct  organic  symptoms,  such  as  the  fever,  the 
pupillary  changes,  the  optic  neuritis,  the  incontinence  of  urine,  the 
■cutaneous  trophic  lesions,  will  help  to  distinguish  one  disease  from 
the  other.  The  psychic  excitement,  the  psychic  distribution  of  the 
sensory  phenomena  and  paralyses,  the  variability,  and  rapid  change- 
ability of  these  under  psychic  influence  are  unmistakable  in  hysteria. 
The  permanency  of  psychosis  or  psychic  traits  in  the  clinical  picture 
indicate  the  organic  disease.  Errors  are  liable  either  way,  hysteria 
for  meningitis  or  meningitis  for  hysteria. 

During  the  last  few  years  luinhar  puncture  has  been  employed  to 
a  considerable  extent,  in  diagnosing  meningitis.  Beyond  indicating  the 
presence  of  certain  inflammatory  ingredients  in  the  cerebrospinal  fluid, 
and  thereby  demonstrating  the  presence  of  inflammation  somewhere  in 
the  cerebrospinal  canal,  it  cannot  be  said  to  have  proved  itself  a  ver} 
■definite  diagnostic  procedure.  The  risks  attending  it  so  far  outbalance 
the  smallness  and  uncertainty  of  the  knowledge  obtained  by  it,  that  it 
cannot  be  recommended  as  a  routine  method.  In  certain  cases  where 
the  diagnosis  is  absolutely  impossible  by  the  symptoms,  and  it  is  nn- 
perative  that  the  nature  of  the  disease  should  be  definitely  known,  it 
may  be  resorted  to.  The  details  in  regard  to  it  v/ill  be  found  discussed 
in  an  earlier  section  upon  diagnosis  of  diseases  of  the  nervous  sys- 
tem or  of  the  spinal  cord.  The  cerebrospinal  fluid  is  to  be  examined 
physically,  chemically,  microscopically  and  bacteriologically.  The  find- 
ings will  be  uncertain  and  on  account  of  adhesions  here  and  there 
between  the  inflamed  membranes,  shutting  off  parts  of  the  central 
cavity,  nothing  definite  will  be  learned  as  to  the  location  of  the  inflam- 
matory process.  The  chief  information  obtainable  from  the  procedure 
is  in  regard  to  the  bacteria  when  they  are  recovered  from  the  fluid, 
and  the  presence  of  an  actual  inilammatory  lesion.  There  are  no  spe- 
■cial  physical  changes  except  perhaps  a  slight  thickening  and  clouding 
of  the  fluid  in  some  of  the  cases.     The  presence  of  large  numbers  of 


THE  NON-NEURON IC  DISEASES  8o7 

leucocytes  will  indicate  a  purulent  meningitis.  The  bacteria  that  may 
be  isolated  are  especially  the  streptococcus,  the  staphylococcus,  the 
pneumococcus,  the  meningococcus  intracellularis,  the  diplococcus 
lanceolatus  and  the  tubercle  bacillus.  The  albumin  may  be  increased 
and  some  blood  may  be  present. 

Prognosis. — This  is  generally  bad.  Recovery  from  purulent 
meningitis  never  occurs.  Some  simple  forms  have  become  chronic, 
while  a  few  have  recovered.  Gowers,  however,  cites  two  recoveries 
from  the  symptoms  of  meningitis  in  post-puerperal  septicaemia.  The 
difficulty  of  the  diagnosis  always  casts  a  doubt  upon  the  reported  re- 
coveries and  yet  warns  us  never  to  be  too  positive  in  holding  out  an 
unfavorable  prognosis. 

Coma  is  practically  a  fatal  sign.  The  less  acute  the  disease  is 
the  better  the  chance  of  its  becoming  chronic  or  disappearing  entirely. 
If  coma  does  not  come  on  for  three  or  four  weeks,  the  chance  of  es- 
caping death  is  that  much  improved.  Traumatic  cases  and  those  sim- 
ple cases  due  to  adjacent  disease  are  perhaps  the  least  grave.  Sinus 
thrombosis  and  cerebral  abscess  are  not  uncommon  complications  and 
enter  somewhat  into  the  character  of  the  prognosis. 

Treatment. — In  a  disease  so  invariably  fatal  one  approaches  the 
question  of  treatment  with  a  degree  of  hesitancy.  Certain  measures 
and  certain  remedies  have  been  recommended,  and  prophylaxis  is 
always  in  order ;  but  after  all  has  been  done,  it  will  be  found  that  the 
course  of  the  affection  has  been  but  little  modified. 

The  primary  disease  or  source  of  infection  should  always  be 
attended  to,  of  course.  An  otitis  media,  a  diseased  mastoid,  a  puru- 
lent rhinitis,  any  abscess  or  suppurative  focus  in  or  near  the  cranium, 
should  receive  proper  surgical  treatment.  An  incipient  meningitis  may 
be  checked  thus.  Cranial  traumata  should  be  properly  dressed  and 
trephining  should  be  thought  of  in  meningo-encephalitis. 

The  patient  should  be  put  absolutely  at  rest  in  bed  and  all  noise 
and  light  excluded  from  the  room.  The  ventilation  should  be  free ; 
the  diet  should  be  light,  nutritious  and  frequently  given.  If  swallow- 
ing is  difficult,  nutrient  enemata  may  be  resorted  to.  The  temperature 
is  to  be  kept  within  bounds  by  cool  sponging,  and  the  pains  are  to 
be  assuaged  by  opiates,  phenacetine  and  antipyretics.  The  bowels 
should  be  opened  freely  with  calomel  and  salines.  Diuretics  are  also 
commendable. 

The  rationale  of  bloodletting,  counter-irritation,  cold  douching 
of  the  head  for  a  suppurative  process  is  not  very  apparent.  These 
measures  all  have  their  advocates,  however.  Their  employment  en- 
tertains the  attendants  more  than  it  benefits  the  patient. 

In  robust  subjects  and  where  the  disease  has  followed  a  sunstroke, 
mental  shock,  trauma  or  other  cause  of  congestion,  a  few  leeches  may 
be  applied  to  the  mastoid  region.  Not  much  blood  ought  to  be  ab- 
stracted, however.  Most  of  these  patients  are  already  thin  and  anaemic 
and  can  ill  afford  to  lose  any  more  blood.  Cold  may  be  applied  to  the 
head  with  advantage.  The  headache  is  sometimes  relieved  and  the 
temperature  noticeably  lowered.  The  cold  douche,  the  ice  bag.  the 
coiled  tubing  made  to  fit  the  head  like  a  cap  and  to  carry  a  stream  of 


8o8  THE   XON-NEUROXIC  DISEASES 

cold  water  continuously,  or  cracked  ice  in  a  towel,  may  be  used  for 
this  purpose.  Counter-irritation  with  antimonial  ointment  after  shav- 
ing the  head,  the  application  of  vesicants  to  it,  the  use  of  fly-blisters 
or  mustard  to  the  neck  and  similar  measures  have  been  all  recom- 
mended but  are  illogical,  discomforting  to  the  patient  and  without  the 
slightest  ultimate  benefit.  If  it  is  thought  best  to  counter-irritate,  a 
few  light  touches  with  the  Paquelin  cautery  is  the  best  way  to  do  it. 
^^"hile  this  is  being  done,  hot  applications  should  be  applied  to  the 
lower  extremities.  A  treatment  strongly  commended  abroad  is  the 
rubbing  of  the  head  with  a  twenty  per  cent,  iodoform  ointment. 

Internally  iodide  of  potassium,  mercury,  perchloride  of  iron  in 
large  doses,  iodoform,  gr.  vj  to  gr.  xij,  daily,  have  all  their  advocates 
and  are  always  available  for  trial.  The  vomiting  is  coatrolled  usually 
by  dietary  measures,  absolute  quiet  and  the  swallowing  of  pieces  of 
cracked  ice.  It  is  a  cerebral  vomit,  however,  and  is  therefore  abso- 
lutely uncontrollable  until  the  cerebral  excitement  subsides  somewhat. 
Digitalis  may  be  given  to  support  a  weak  pulse.  Salicia  and"  quinine, 
sometimes  given  for  the  elevated  temperature,  do  not  seem  on  that 
account  to  ward  off  in  the  least  the  fatal  issue. 

Surgery  has  been  appealed  to  in  this  disease  witli  some  slight  de- 
gree of  success  apparently.  Ventricular  puncture,  incision  of  the  dura 
and  evacuation  of  the  exudate  in  the  meninges  has  seemed  to  effect 
some  recoveries.  Lumbar  puncture  also  has  been  successfully  em- 
ployed by  Quincke,  Furbringer,  Lichtheim  and  others.  The  spinal 
column  has  been  trephined,  the  dura  incised,  and  drainage  established. 
In  spite  of  the  few  apparent  successes  by  these  various  measures,  they 
are  in  need  of  further  trial  before  a  final  opinion  can  be  passed  as  to- 
their  actual  value  in  the  long  run  of  cases. 

Epidemic  Cerebrospinal  Meningitis. — This  is  sometimes  called 
Spotted  Fever,  occurs  both  epidemically  and  sporadically,  and  is  due 
to  a  special  microorganism.  An  acute  purulent  leptomeningitis  is  its 
most  prominent  lesion  and  the  cause  of  its  leading  symptoms.  Epi- 
demics have  occurred  in  nearly  all  the  countries  of  Europe  and  in  the 
United  States,  causing  great  destruction  of  life.  Four  thousand  peo- 
ple died  of  it  in  Sweden  alone  between  the  years  of  1854  and  i860. 
Severe  outbreaks  took  place  in  the  United  States  from  1805  to  1830, 
in  France  between  1837  and  1850.  in  other  parts  of  Europe  between 
1854  and  1874,  and  in  a  great  many  regions  since  1875.  Maryland  w^as 
visited  by  it  in  1892,  New  York  in  1893,  Boston  in  1898.  Since  the 
first  description  of  it  by  Vieusseux  during  the  outbreak  in  Geneva  in 
1805,  the  disease  has  been  closely  studied  by  Danielson  and  Alann, 
Jackson,  Welch,  Warren,  North,  Stille,  Hirsch,  Councilman,  Mallory, 
Wright  and  others.  Wright's  contributions  to  the  literature  of  the 
subject  are  especially  valuable. 

Etiology. — The  essential  cause  of  the  malady  is  a  specific  germ 
but  there  are  certain  other  moments  that  enter  into  its  etiology  and 
must  be  taken  into  account.  Children  constitute  the  majority  of  its 
victims,  though  it  may  occur  at  any  age.  In  civil  life  children  and 
young  adults  manifest  a  particular  susceptibility.  Of  course,  adults 
make  up  the  list  of  cases  when  it  occurs  m  militarv     life.     In     some 


THE   XOX-XEUROXIC  DISEASES  809 

epidemics  adults  have  escaped  entirely.  Males  outnumber  females 
somewhat.  Cold  and  temperate  climates  constitute  its  favored  locali- 
ties, and  the  Spring  and  Winter  its  choice  seasons.  Endemic  influ- 
ences are  practically  nil,  as  the  disease  is  seen  to  break  out  in  widely 
separated  and  most  dissimilar  localities.  It  does  not  seem  to  be  directly 
contagious  nor  invited  by  personal  habits  or  characteristics.  Unsani- 
tary surroundings,  crowding  together,  as  in  tenement  houses  or  mili- 
tary barracks,  the  squalor  and  wretchedness  of  the  cities,  seem  to 
foster  it.  Babes  nursing  sick  mothers  have  escaped ;  attendants  upon 
the  sick  are  rarely  attacked ;  and  the  handling  of  the  clothing  and 
excretions  of  the  sufferers  does  not  seem  to  be  particularly  danger- 
ous. Over-exertion,  all  conditions  of  bodily  and  mental  depression, 
association  with  pigs  and  dogs  afflicted  with  a  similar  affection,  as 
noted  in  some  of  the  Irish  epidemics,  predispose  to  it.  Immunity  is 
not  conferred  against  a  second  attack.  Country  districts  are  not  ex- 
empt, and  the  disease  very  often  returns  in  the  same  locality. 

Pathology  and  Pathogenesis. — As  a  rule  the  intracranial  find- 
ings are  about  the  same  as  those  described  under  the  previous  section 
headed  acute  purulent  meningitis.  The  pia-arachnoid  is  soft,  red,  con- 
gested, opaque  and  filled  with  a  creamy,  purulent  exudate  over  the 
entire  brain,  but  especially  at  the  base.  The  convolutions  of  the  hem- 
ispheres, the  basal  structures  and  the  roots  of  the  cranial  nerves  are 
bathed  in  the  pus  and  hugged  by  the  intensely  congested  membrane. 
By  the  fibrino-purulent  exudate  the  meninges  are  thickened  not  only 
at  the  base  of  the  brain  and  vertex  but  up  and  down  the  posterior  sur- 
face of  the  cord  also,  especially  in  the  dorsal  and  lumbar  regions.  In 
the  more  chronic  cases  patches  of  scattered  yellow  indicate  the  earlier 
presence  of  the  exudate.  The  ventricles  are  dilated,  sometimes  to  an 
enormous  extent.  Pus  appears  in  them  as  well  as  in  the  posterior 
horns  of  the  cord.  The  neighboring  brain  substance  is  softened  and 
damaged,  compressed  by  the  thickened  meninges  on  one  side  and  the 
dilated  ventricles  on  the  other,  and  reveals  foci  of  old  hemorrhagic 
extravasation  and  even  of  sharp  meningo-encephalitis.  Small  abscesses 
may  be  present  also.  All  of  the  cranial  nerves,  but  especially  the  optic, 
the  trigeminus,  the  facial  and  the  auditoiy,  and  all  of  the  spinal  nerves, 
may  be  found  imbedded  in  and  infiltrated  by  the  exudate.  The 
labyrinth  as  a  consequence  may  become  involved.  Otitis  media  with 
perforation,  irido-choroiditis  and  panophthalmitis  may  all  follow.  In 
other  parts  of  the  body  signs  of  bronchopneumonia,  pleuritis,  enlarge- 
ment of  the  spleen,  acute  nephritis,  swelling  of  the  intestinal  follicles 
and  disease  of  the  joints  may  be  observed. 

In  some  cases  death  takes  place  so  swiftly  that  none  of  these  con- 
ditions have  had  time  to  make  their  appearance,  and  therefore,  there 
are  no  post  mortem  findings.  In  light  cases  sometimes  only  congestion 
of  the  meninges  and  a  mere  trace  of  an  exudate  are  to  be  discovered. 
There  is  much  variation  in  this  respect  and  so  wide  are  the  differ- 
ences that  the  disease  has  actually  been  classified  in  types,  such  as  the 
malignant,  the  mild  and  the  aborted,  the  acute,  intermittent  and  chronic. 

A  microscopic  and  bacteriological  examination  of  the  exudate  has 
latelv  given  us  most  valuable  information  as  to  the  probable  cause  of 


8lO  THE   XOX-NEURONIC  DISEASES 

the  disease.  Polynuclear  leucocytes  are  found  closely  packed  in  the 
fibrinous  material,  also  cells  two  to  eight  times  the  diameter 
of  a  leucocyte.  In  variable  number  many  diplococci  also  are  found,  the 
most  frequent  one  being  the  diplococcus  intracelUdaris  meningitidis. 
described  by  Weichselbaum  in  1887.  The  polynuclear  leucocytes  are 
almost  constantly  the  habitat  of  this  microorganism.  Many  believe 
that  is  the  cause  of  spotted  fever  because  it  is  so  constantly  observed. 
Other  microorganisms  that  provoke  or  at  least  one  associated  with 
acute  purulent  meningitis  have  also  not  infrequently  been  seen,  so  that 
some  pathologists  still  mamtain  that  we  are  not  yet  in  a  position  to 
affirm  positively  that  the  diplococcus  intracellularis  is  the  cause  of 
cerebrospinal  fever.  It  is  not  like  Fra^nkel's  pneumococcus,  though 
the  latter  has  often  been  associated  with  it  in  this  and  other  forms  of 
acute  meningitis.  In  tuberculous  meningitis,  and  even  in  the  nasal 
mucous  membrane  of  perfectly  healthy  children,  the  Weichselbaum 
diplococcus  has  been  observed. 

Further  study  of  the  bacteriology  of  this  form  of  meningitis  would 
seem  to  be  desirable  therefore  before  its  pathogenesis  can  be  dogma- 
tized upon. 

Symptoms. — As  the  clinical  picture  is  such  a  varied  one  it  will 
be  well  perhaps  to  describe  a  typical  case  and  discuss  its  main  symp- 
toms in  detail  first,  and  then  enumerate  and  point  out  the  differences  in 
the  recognized  types  afterwards. 

There  are  two  great  groups  of  clinical  signs  of  the  disease  in 
every  case.  The  first  are  those  of  the  general  profound  toxcsmia  and 
constitutional  malady ;  the  second  are  those  that  belong  to  the  meitin- 
geal  inflamination  and  some  complicating  features. 

The  period  of  incubation  of  the  germ  is  unknown  and  the  prod- 
romata  are  not  usually  very  prominent.  Most  cases  begin  abruptly  or 
if  there  are  premonitory  indications,  they  consist  of  the  usual  feeling 
of  malaise,  slight  headache,  backache,  dullness,  nausea,  constipation 
and  anorexia.  Much  more  commonly  there  is  a  chill,  a  sudden  access 
of  fever,  vomiting  and  a  severe  headache.  The  scene  opens  just  as 
nearly  all  of  the  infectious  fevers  do.  Vertigo,  restlessness,  insomnia, 
and  general  convulsions  may  be  added  to  it.  In  a  day  or  so  the  men- 
ingitic  symptoms  begin  to  declare  themselves.  The  headache  increases 
and  becomes  intense,  especially  in  the  occipital  region  and  down  the 
back  of  the  neck.  The  temperature  steadily  rises  to  100  degrees  or  102 
degrees,  and  the  pulse  becomes  rapid  and  irregular.  Both  run  a  varied 
and  irregular  course.  With  the  pain  in  the  back  of  the  neck,  the  mus- 
cles become  rigid  and  there  is  marked  nuchal  retraction.  This  has 
been  so  extreme  that  the  head  hung  back  between  the  shoulder  blades. 
The  spine  gradually  becomes  arched  so  that  there  is  opisthotonos. 
Orthotonos  is  probably  more  frequent  than  opisthotonos.  Pains  and 
rigidity,  severe  in  type,  appear  in  the  limbs.  Every  touch  to  the 
patient,  every  effort  to  move  him  causes  him  to  cry  out  with  the 
agony.  He  writhes,  his  face  becomes  contracted  and  he  shows  in  an 
unmistakable  manner  that  he  is  in  extreme  pain.  Trismus,  abdominal 
retraction,  strabismus  and  a  general  muscular  rigidity  so  that  the  pa- 
tient can  be  lifted  like  a  statue,  are  all  present.    The  maxillary,  spinal- 


THE  NON-NEURONIC  DISEASES  8il 

truncal  and  leg  and  arm  muscles  are  all  involved  and  reveal,  with  the 
tenderness  and  shooting  pains,  without  ever  passing  into  paralysis,  the 
•typical  picture  of  cerebral  and  spinal  meningitis  with  implication  of 
the  cranial  and  spinal  nerve  roots.  The  sensorium  for  a  time  is  clear 
but  soon  delirium  and  a  clouding  of  the  faculties  add  themselves  to 
-the  complexus  of  manifestations.  The  cephalalgia  continues,  the  fever 
exacerbates  and  a  wald  and  maniacal  delirium  seizes  the  patient.  He 
Taves  and  strikes  out  and  becomes  a  perfect  fury.  The  delirium  is  a 
gradual  and  early  manifestation.  In  the  beginning,  it  is  associated 
with  violent  erotic  or  sexual  excitement.  In  a  few  days  it  exhausts 
itself  and  sinks  rapidly  into  the  stupor  and  comatose  condition.  Just 
tefore  death,  w^hich  occurs  in  these  cases  in  from  ten  days  to  a  couple 
of  weeks,  the  fever,  which  has  been  very  erratic,  suddenly  rises  to  io6 
degrees  or  io8  degrees,  the  pulse  becomes  small,  feeble  and  irregular, 
the  respirations  grow  labored  and  assume  the  Cheyne-Stokes  tvpe  or 
sighing  characteristic,  and  the  coma  becomes  profound  and  complete. 
Among  the  other  symptoms  are  to  be  noted  the  coated  tongue, 
foul  breath  and  constipation.  There  is  retention  and  incontinence  of 
urine.  Some  albuminuria  is  present ;  sometimes  glycosuria.  The 
urine  at  first  is  typically  a  febrile  urine  but  later  it  is  apt  to  be  exces- 
sive in  amount.  The  spleen  is  almost  constantly  enlarged,  though  on 
account  of  the  pain  cannot  generally  be  palpated. 

Later  manifestations  are  of  a  paralytic  and  trophic  character.  The 
"name  of  the  disease,  spotted  fever,  is  given  on  account  of  the  marked 
'Cutaneous  symptoms.  They  are  not  a  constant  feature  of  the  disease, 
liowxver.  The  skin  may  be  merely  erythematous  or  mottled.  Rose 
spots,  as  in  typhoid  fever,  sometimes  are  present ;  at  other  times  only 
petechia  and  scattered  purple  spots  are  to  be  seen.  Herpes  occurs 
more  frequently  than  it  does  in  pneumonia  or  intermittent  fever.  Other 
-cutaneous  manifestations  that  have  been  noted  are  erythema  nodosum, 
■ecthyma,  urticaria  and  pemphigus.  Gangrene  of  the  skin  has  been  a 
'"are  observation.  Other  complications  of  the  meningitis  are  conjunc- 
tivitis, a  neuroparalytic  keratitis,  chemosis,  mydriasis,  optic  neuritis, 
strabismus,  facial  paresis  and  deafness.  The  implication  of  the  cra- 
nial nerves,  of  course,  explains  these  symptoms.  Purulent  irido- 
choroiditis  is  a  particularly  frequent  trouble,  and  is  in  all  probability 
the  result  of  metastasis.  Amaurosis  is  its  ultimate  result.  Aphasia  has 
T)een  seen. 

General  convulsfons  are  not  common  except  in  children.  Hemi- 
plegia and  monoplegia  may  be  present  but  hidden  by  the  clouded  con- 
sciousness. Paraplegia,  loss  of  patella  reflex  (increased  usually  at 
first),  paralysis  of  the  sphincter  vesicae  and  girdle  pains  indicate  the 
disease  process  in  the  cord.  Bedsores,  joint  troubles  and  extreme 
■emaciation  occur  in  the  protracted  cases. 

As  these  symptoms  are  not  alw^ays  the  same  in  all  cases,  as  not 
all  cases  are  fatal  by  any  means,  and  as  the  disease  runs  a  course  any-    . 
M^here  from  a  few  hours  to  several  months,  clinicians  have  established 
the  following  types : 

I.  The  Malignant  or  Fulminant  Form. — This  may  appear  epi- 
demically or  sporadically.     The  disease  seems  to  burst  out  all  at  once. 


8l2  THE   XOX-XEUROXIC  DISEASES 

The  chills,  headache,  fever,  vomiling,  delirium,  somnolence,  convul- 
sions, spasms,  rigidity  and  terminal  coma  appear  suddenly  and  ruit 
their  course  in  a  few  hours.  The  onset,  the  development  and  the  termi- 
nation are  swift  and  terrible.  In  one  case  the  whole  gamut  of  symp- 
toms from  start  to  finish  was  run  in  five  hours.  Other  cases  have  died 
in  twenty- four'  hours  or  less.  Truly  may  these  cases  be  styled  apo- 
plectic. 

2.  The  Ordinary  Form. — This  has  been  described. 

3.  The  Rudimentary  or  Abortive  Form. — These  cases  are  very 
confusing  when  they  occur  sporadically,  though  during  an  epidemic 
they  may  be  correctly  recognized.  The  symptoms  are  all  mild  and  in- 
definite. The  headache  and  backache  are  slight.  Possibly  there  is  some- 
restlessness,  irritability,  insomnia  or  dullness.  There  may  be  nausea. 
The  nuchal  muscles  may  seem  a  little  stiff.  Fever  is  slight  or  absent. 
Two  classes  of  these  cases  are  recognized.  In  one  the  symptoms  be- 
gin abruptly  and  with  considerable  severity,  but  in  a  few  days  they- 
die  out  or  subside  to  almost  nothing.  In  the  other  they  are  never  more- 
than  slight  and  the  cases  are  entirely  ambulatory. 

4.  Intermittent  Form. — These  are  protracted  cases,  often  run- 
ning many  months  with  complete  intermissions  or  marked  remissions- 
in  all  of  their  symptoms.  They  may  even  appear  as  quotidian,  tertian 
and  other  types.  Some  cases  run  a  steady,  severe  course  at  first,  and 
then  pass  into  convalescence  as  an  intermittent  disease.  Pyjemia  rather 
than  malaria  is  the  suggestive  feature  about  the  fever. 

5.  Chronic  Form. — This  is  frequent  according  to  Heubner^ 
\\'ith  a  very  variable  symptomatology,  these  cases  run  along,  now  up,. 
now  down,  but  never  intermittent,  for  three  and  six  months.  Intense 
marasmus  usually  supervenes.  As  Osier  says,  it  is  not  improbable  that 
hydrocephalus  or  intracranial  abscess  is  at  the  bottom  of  these. 

Diagnosis. — The  diagnosis  of  epidemic  cerebrospinal  meningitis 
offers  the  greatest  difficulties  only  when  the  case  is  a  sporadic  one,  or 
in  those  cases  that  now  and  then  continue  to  break  out  in  a  locality 
where  the  epidemic  has  prevailed.  If  the  complete  picture  of  the  dis- 
ease is  kept  well  in  mind,  the  general  septic  febrile  process,  the  charac- 
teristic cerebral  and  spinal  meningitic  manifestations,  the  marked 
cutaneous  exhibitions  and  the  frequent  complications,  such  as  pleurisy^ 
broncho-pneumonia,  pericarditis,  parotitis  and  implication  of  the  artic- 
ular joints,  I  think  one  will  have  little  trouble  in  making  a  diagnosis,, 
even  though  all  of  these  indications  are  not  present  at  the  same  time.. 
The  history  of  the  case  must  be  always  given  due  weight.  Perchance 
the  patient  has  had  the  disease  before,  or  there  has  been  a  recent  epi- 
demic in  the  vicinity.  If  the  epidemic  is  raging  at  the  time,  there  is 
no  doubt  about  the  diagnosis  whatever. 

Sporadic  cases  are  hard  to  distinguish  sometimes,  especially  when, 
protracted  and  not  very  violent,  from  tuberculous  meningitis.  Tuber- 
culosis elsewhere  or  in  the  family  is  suggestive  of  the  latter.  ^Slore- 
over  the  spinal  symptoms  are  not  so  prominent,  whereas  the  mental  are 
slightly  more  so  in  the  tuberculous  disease  of  the  membranes.  The 
herpes  and  other  skin  manifestations,  the  enlarged  spleen,  the  com- 
plications, speak  for  the  epidemic  disease,  or  at  least  they  are  not  the 


THE   NON-NEURONIC  DISEASES  813 

-same  as  they  are  in  tuberculous  infection.  Lumbar  puncture  and  the 
iinding  of  the  specific  micrococci  or  bacilH  olTers  the  crucial  test  of 
"the  true  nature  of  the  trouble. 

Atypical  forms  of  typhoid  fever  and  cerebrospinal  meningitis  may 
be  confounded  with  each  other.  In  the  former  the  temperature  runs 
-a  different  course,  there  aie  loose  stools  with  tympanites  and  an  ab- 
-sence  of  the  herpes,  joint  troubles  and  characteristically  combined  cere- 
bral and  spinal  meningitis  manifestations.  Here  again  lumbar  punc- 
ture comes  to  our  rescue. 

PneuniGcoccus  meningitis,  which  may  occur  either  alone  or  as 
an  accompaniment  of  pneumonia,  is  sometimes  very  like  the  epidemic 
iorm.  According  to  Leichtenstern,  with  the  former  the  contraction  of 
the  muscles  of  the  neck  is  often  wanting,  while  in  the  latter  it  is  inva- 
iriably  present.  The  former  quickly  leads  to  delirium  and  coma,  whereas 
in  the  latter  the  sensorium  is  clear  for  a  long  time  or  even  throughout 
"the  entire  course  of  the  disease.  The  former  is  rapidly  fatal,  the  latter 
-IS  frequently  recovered  from.  In  the  former,  symptoms  pointing  to 
-a  wide  extension  of  the  meningeal  infection  of  the  brain  and  cord,  in- 
volving the  spinal  and  cranial  nerve  roots,  are  less  pronounced  or  even 
■absent  as  compared  with  the  same  symptoms  in  the  latter.  Lumbar 
puncture  may  settle  the  question  to  a  large  extent  by  discovering  the 
pneumococcus  in  the  one  case  or  the  diplococcus  intracellularis  in  the 
other. 

Epidemic  cerebrospinal  meningitis  has  some  imitations  in  small- 
pox, tetanus,  uraemic  coma,  acute  articular  rheumatism  and  hysteria. 
A  careful  consideration  of  the  history,  a  thorough  examination  of  the 
patient  and  the  recollection  of  the  clinical  picture,  in  toto,  of  the  spe- 
-cific  meningitis  will  enable  one  to  avoid  error  in  the  dift'erential  diag- 
Tiosis. 

Prognosis. — This  is  always  serious  but  not  necessarily  bad.  In 
-epidemics  the  mortality  ranges  from  twenty  to  seventy-five  per  cent. 
In  children  it  is  more  fatal  than  in  adults.  Early  in  the  epidemics 
severe  cases  predominate,  later  on  the  mild  cases  are  in  the  majority. 
~Very  rapid  or  very  protracted  cases  are  not  hopeful.  Mild  cases  that 
Tun  a  medium  course  offer  the  best  outlook.  They  often  get  well, 
though  usually  leaving  some  defect  or  complication,  such  as  blind- 
"ness  or  deafness,  which  are  apt  to  be  permanent  if  they  show  no  signs 
■of  receding  in  the,  first  three  months  after  the  outbreak  of  the  dis- 
••ease.  Deep  coma,  repeated  convulsions  and  high  fever  are  bad  omens. 
Existing  complications  such  as  pneumonia,  endocarditis,  and  pericar- 
-ditis  add  to  the  gravity  of  the  prognosis.  Fulminant  cases  destroy  the 
patient  in  a  few  hours  or  a  day  or  two.  Ordinary  cases  run  an  irregu- 
lar course,  as  a  rule,  of  two  or  three  weeks.  Protracted  cases  may 
•continue  for  many  weeks.  Chronic  cases  may  not  be  free  from  signs 
■of  the  disease  for  five  or  six  months.  Sequelae  are  unfortunately  com- 
mon. Death  is  caused  by  exhaustion,  decubitus,  marasmus  in  chronic 
•cases ;  by  the  intense  intoxication  with  asphyxia  and  annihilation  of  all 
the  vital  processes  in  the  acute  and  fulminant  cases. 

Treatment. — There  is  no  specific  remedy  for  the  disease.  After 
placing  him  in  the  best  hygienic  environment,  the  most  we  can  do  for 


8l4  THE   NON-NEURONIC  DISEASES 

the  patient  is  to  sustain  his  strength,  ameHorate  his  siififerings  and  com- 
bat some  of  the  symptoms.  Opium  usually  has  to  be  given  freely.. 
Morphia  administered  hypodermically  is  the  best.  Mercury,  iodide  of 
potassium,  salicylate  of  sodium,  ergot,  belladonna,  calabar  bean,  quinine 
in  large  doses,  digitalis,  benzoate  of  sodium,  chloral,  potassium  bromide 
and  alcohol  are  some  of  the  remedies  that  have  been  recommended 
for  both  the  disease  in  general  and  to  meet  special  indications.  The 
long  and  varied  list  of  them,  and  the  continued  high  mortality  of  the 
disease,  demonstrate  how  futile  is  practically  all  of  our  therapy  in  re- 
lation to  it. 

In  regard  to  bloodletting,  hydrotherapy,  counter-irritation  and  the 
application  of  cold  to  the  head  and  spine,  the  same  principles  are  ap- 
plicable here  that  I  suggested  under  the  head  of  acute  purulent  menin- 
gitis. Hot  baths  have  lately  been  very  favorably  recommended,  as  also 
has  lumbar  puncture. 

Plain,  nutritious  diet,  of  milk  and  strong  broths  especially,  must 
be  given  during  the  fever.  The  stomach  tube  may  have  to  be  em- 
ployed if  swallowing  is  difficult.  Stimulants  are  needed  regularly  in 
most  cases. 

The  residual  symptoms  call  for  no  special  treatment. 

Tuberculous  Meningitis. — This  is  a  form  of  meningitis  that 
generally  runs  a  subacute  course,  is  due  to  a  specific  germ  and  occurs 
mostly  in  children.  It  used  to  be  spoken  of  entirely,  and  is  even  still 
sometimes  referred  to,  as  acute  hydrocephalus,  or  "water  on  the 
brain."  Basilar  meningitis  is  another  of  its  more  popular  synonyms. 
Though  its  study  really  dates  from  the  observations  of  Robert  Wright, 
of  Edinburgh,  in  1768,  our  accurate  knowledge  of  it  was  laid  down 
by  Gerhard,  of  Philadelphia,  in  1832  and  1833.  It  has  a  few  distinctive 
features  that  warrant  its  discussion  in  a  section  by  itself,  though  in 
the  main  it  is  the  same  in  all  respects,  except  etiology,  as  all  the  other 
forms  of  leptomeningitis. 

Etiology. — The  essential  cause  of  the  disease  is  the  tubercle 
bacillus.  This  usually  enters  the  circulation  from  a  tuberculous  lesion 
somewhere  else  in  the  body,  lungs,  joints,  intestines,  and  so  reaches  the 
base  of  the  brain  where  it  sets  up  its  specific  inflammation.  It  is  thus 
a  secondary  disease,  or  infection.  There  are  cases  in  which  both 
during  life  and  after  death  no  primary  focus  can  be  discovered.  It  is 
always  highly  probable  that  the  latter  has  been  overlooked  for  a  com- 
plete examination  grossly  and  minutely  of  all  the  tissues  of  the  body  is  a 
very  difficult  task.  Nevertheless  it  may  be  true,  as  believed  by  some 
authorities,  that  in  a  few  instances  the  disease  may  be  primary  in  the 
brain,  the  bacilli  entering  the  cranium  by  way  of  the  nose  and  cribri- 
form plate  of  the  ethmoid  bone. 

A  certain  amount  of  predisposition  towards  the  disease  is  shown 
in  the  fact  that  it  attacks  preferably  individuals  of  a  certain  age.  It 
is  frequent  in  children,  rare  in  adults.  It  is  scarcely  ever  seen  during 
the  first  year  of  life.  Most  cases  occur  between  two  and  ten  years  of 
age.  The  majority  of  those  that  I  have  seen,  have  been  about  four 
and  six  years  of  age.  It  occasionally  breaks  out  in  early  adult  years. 
It  is  exceedingly  infrequent  after  forty.     Every  explanation  hitherto 


THE  NON-XEURONIC  DISEASES  815 

offered  to  account  for  the  predominance  of  the  disease  in  childhood  is 
entirely  hypothetical.  Some  thnik  it  is  due  to  the  relative  rapidity  of  the 
vital  processes  in  the  growing  brain  of  the  child;  others  hold  that  it 
has  relationship  to  the  frequency  of  alimentary  tuberculosis  in  children. 
It  has  frequently  been  charged  to  the  ingestion  of  tubercle-infected 
milk.  The  eruptive  fevers,  especially  measles,  have  in  a  considerable 
number  of  my  cases  immediately  preceded  its  revelation.  These  may  act 
along  with  such  assigned  subsidiary  causes,  as  cranial  traumata,  ex- 
cessive emotional  excitement,  mental  strain  and  alcoholism  in  dimin- 
ishing the  individual's  general  power  of  resistence.  The  bronchial  trou- 
bles of  measles  and  pertussis  may  open  the  gateway  for  the  infected 
air  to  scatter  the  germs  into  the  circulation.  Males  suffer  more  than 
females. 

Pathology  and  Pathogenesis. — The  disease  may  appear  any- 
where in  the  meninges  of  the  brain  and  spinal  cord.  In  fact  many 
of  the  cases  are  cerebrospinal  meningitis  with  the  cerebral  manifes- 
tations masking  the  spinal.  The  favorite  seat  of  the  trouble  seems  to  be 
the  base  of  the  brain,  hence  the  name  basilar  meningitis.  In  the  vicin- 
ity of  the  great  vessels  found  here,  the  arteries  branching  off'  from  the 
anterior  middle  and  posterior  cerebrals,  the  pia  is  inflamed,  granular 
and  covered  with  an  exudate.  Around  the  optic  chiasm,  in  the  inter- 
peduncular space,  up  along  the  Sylvian  fossae,  beneath  the  medulla 
oblongata  and  cerebellum,  and  even  in  some  cases  up  on  the  convexity 
of  the  hemispheres  and  down  along  the  spinal  cord,  the  meninges  are 
thickened,  opaque  and  covered  with  the  gelatinous  effusion.  There 
turbidity,  matting  together  and  nodular  contents  are  unmistakable. 
x\ll  along  the  vessels,  especially  at  the  points  of  their  bifurcation,  or 
branching,  are  found  the  miliary  tubercles  which  caused  Guersant  in 
1827  to  use  the  name  granular  meningitis.  Sometimes  these  coalesce 
and  form  larger  tuberculous  nodules.  In  these  are  found  the  specific 
bacilli  of  tuberculosis.  By  stripping  off'  the  membrane  and  holding  it 
up  before  a  bright  light  the  tubercles  become  very  evident.  They  are 
seen  to  be  imbedded  in  the  exudate  and  also  where  there  are  no  signs 
of  inflammation.  They  are  identical  in  structure  with  the  same  sort  of 
tubercles  found  elsewhere  in  the  bod}^  They  may  be  very  numerous  or 
only  few  and  widely  scattered.  The  dura  may  be  invaded  by  them, 
especially  in  the  region  of  the  middle  meningeal  artery.  They  are 
sometimes  seen  in  the  tunica  intima  of  the  arteries  in  conjunction  with 
an  endarteritis  and  a  proliferation  of  the  adventitia.  In  such  cases 
the  calibre  of  the  vessel  may  be  diminished  and  a  thrombosis  occur. 
The  choroid  plexus  is  usually  included  in  the  infection,  and  the  nodules, 
with  redness  and  the  exudate,  are  seen  scattered  along  the  sheaths 
of  the  cranial  nerves.  The  neighboring  brain  substance  is  always  more 
or  less  implicated  so  that  the  condition  partakes  of  the  nature  of  a 
meningo-encephalitis.  It  is  injected,  infiltrated  with  leucocytes,  oedema- 
tous,  softened  in  spots  and  punctated  with  small  hemorrhagic  foci. 
Spots  of  softening  from  tuberculous  arteritis  also  appear  in  the  basal 
ganglia,  cerebral  peduncles  and  the  spinal  cord,  even  in  some  cases  as 
far  as  the  filum  terminale.  The  ventricles  are  usually  dilated  and  full 
of  turbid  fluid,  producing  a  condition  of  internal  hydrocephalus.    The 


8l6  THE  NOX-NEURONIC  DISEASES 

ependyma  is  softened  and  diseased.  The  fornix  and  septum  lucidum 
are  often  broken  down.  As  is  usually  the  case  in  hydrocephalus  with 
ventricular  pressure  the  cerebral  convolutions  are  compressed  and 
flattened  and  the  sulci  are  partially  or  completely  obliterated.  Such 
is  the  pathological  picture  of  an  ordinary  case  of  tuberculous  menin- 
gitis. There  are  cases,  however,  which  are  swift  and  fulminant  in 
which  not  much  more  than  the  presence  of  the  tubercles  and  intense 
congestion  can  be  discovered.  In  other  cases  the  disease  runs  such  a 
prolonged  course  that  a  superficial,  strata-like  exudate  with  spots  of 
caseation  and  other  evidences  of  old  or  chronic  inflammation  are  all 
that  is  to  be  seen. 

Symptoms. — Clinically  tuberculous  meningitis  assumes  a  varied 
guise.  It  is  an  infectious  disease  usually  with  more  or  less  prominent 
symptoms  of  local  lesions  in  other  parts  of  the  body  as  well  as  in  the 
brain.  On  this  account  we  usually  find  the  trouble  in  weak,  puny,  pale, 
anaemic,  ailing  and  badly-nourished  individuals,  who  at  the  same  time 
have  a  diseased  lung,  joint,  ear  or  lymph  glands.  The  general  debili- 
tated physique  and  its  functional  inadequacies  present  their  own  par- 
ticular symptomatology.  The  local  nidus  of  the  disease  adds  its  quota 
to  the  tout  ensemble  of  the  clinical  picture.  In  the  midst  of  all  this 
the  clinical  signs  of  the  meningitis  must  be  traced  out  ere  a  diagno- 
sis of  the  latter  can  be  assumed.  To  add  still  more  to  the  difficulty, 
the  meningitis  itself  may  be  a  very  diffuse  or  limited  lesion,  involv- 
ing large  or  small  areas  of  functional  brain  substance;  it  may  be  a 
rapid  and  stormy  process,  or  a  quiet,  progressive  inflammation,  each 
with  its  own  variety  of  symptoms ;  and  finally  it  may  im- 
plicate such  functionally  dissimilar  elements,  in  such  a  variable 
way  that  nothing  definite  can  seem  to  be  made  out  of  the 
complex,  clinical  presentation.  In  view  of  all  these  difficulties  it  is 
not  surprising  that  the  trouble  is  so  often  overlooked  or  not  recog- 
nized until  coma  and  death  are  close  at  hand.  The  natural  hesitancy. 
born  of  a  desire  to  avoid,  if  possible,  the  final  confirmation  of  so  sad 
and  fatal  an  affliction,  clouds  the  physician's  best  judgment  even  when 
it  is  struggling  in  the  midst  of  one  of  the  most  difficult  diagnostic  prob- 
lems that  medicine  sometimes  offers. 

One  should  approach  the  diagnosis  of  tuberculous  meningitis 
therefore  carefully,  with  a  clear  and  unbiased  reasoning  faculty,  and 
wath  a  perfect  mental  conception  of  what  a  typical  case  should  look 
like.  For  there  is  a  clinical  picture  of  tuberculous  meningitis  that  is 
sufficiently  distinct  and  uniform  to  warrant  its  being  described  as  a 
disease  per  se,  however  surrounded  or  clouded  it  may  be  by  other  man- 
ifestations. So  clear  and  distinct  is  this  portraiture  that  many  divide  ft 
into  three  periods,  the  prodromal,  the  irritative  and  the  paralytic,  and 
give  a  special  description  of  each  of  them. 

Premonitions  of  tuberculous  meningitis  may  occur  weeks  and 
months  before  it  frankly  announces  its  presence.  They  are  sometimes 
very  marked  and  in  none  but  a  tyro  would  fail  to  awaken  a  strong  sus- 
picion. At  other  times  they  are  so  slight  and  evanescent  that  their 
significance  is  hardly  appreciable  until  the  disease  is  sufficiently  ad- 
A^anced  to  make  a  diagnosis  a  comparatively  easy  matter.     The  child's 


THE  NON-NEURONIC  DISEASES  817 

disposition  indicates  a  cliange.  It  is  somewhat  fretful  and  irritable 
and  cross.  It  seems  to  be  subject  to  spells  and  paroxysmal  outbreaks 
of  crying  and  worrying.  In  the  intervals  it  may  appear  somewhat  in- 
different  or  unsocial  and  dull.  As  these  changes  often  follow  an 
attack  of  measles  or  other  disease  or  are  associated  with  some  cachectic 
condition,  they  are  attributed  to  general  ill  health.  After  awhile  attacks 
of  headache  appear  at  various  intervals  and  the  child  complains  of  the 
acuteness  and  darting  character  of  the  pain.  In  one  case  the  parents 
noted  months  before  an  unsteadiness  of  gait  which  they  attributed  to 
convalescent  weakness.  In  sleep  the  threatened  victim  is  restless,  tosses 
about,  talks,  has  terrifying  dreams  and  cries  out  now  and  then  or  sud- 
denly wakens  up  with  a  start.  As  the  case  advances  the  headache  be- 
comes excruciating  and  unnervmg.  Periodical  at  first,  it  is  now  more 
or  less  persistent  with  intolerable  exacerbations.  The  little  patient 
seizes  his  head  with  his  two  hands  and  screams  with  the  agony.  He 
instinctively  avoids  the  light  and  the  slightest  noise  rouses  him  into  a 
frenzy.  A  mild  delirium  now  begins  to  assert  itself  and  with  it  an  un- 
conquerable insomnia.  Unexpected  and  unaccountable  attacks  of  vom- 
iting take  place.  The  appetite  is  lost.  Constipation  is  troublesome. 
Emaciation  shows  itself.  Occasionally  there  will  be  a  slight,  irregular 
elevation  of  the  temperature. 

Many  cases  seem  to  glide  gradually  from  the  prodromal  condi- 
tion into  the  easily  recognized  state  of  the  disease.  In  other  cases, 
however,  perhaps  the  majority,  after  a  few  weeks  of  these  indefinite, 
transient  exhibitions  of  peevishness,  headache,  fever  and  vomiting,  the 
child  suddenly  becomes  violently  ill.  There  is  a  chill  or  a  convulsion, 
with  violent  vomiting,  sudden  rise  of  temperature,  int'ense  headache 
and  many  of  the  signs  that  accompany  the  outbreak  of  all  the  infec- 
tious fevers.  Ofttimes  over-exertion  at  play,  exposure  to  the  hot  sun, 
or  indiscretion  in  eating  seems  to  precipitate  the  attack.  Unless  he  is 
suspicious  and  guarded,  the  physician  will  be  very  liable  to  ply  reme- 
dies to  correct  the  supposed  indigestion  and  offer  a  favorable  prognosis. 
It  is  a  matter  of  profound  chagrin  and  sorrow  to  the  attendant,  as  I 
have  several  times  witnessed,  when  at  the  end  of  ten  days  or  a  couple 
•of  weeks  coma  comes  on  in  spite  of  all  his  treatment  and  hopeful  prom- 
ises, and  the  patient  dies  while  he  is  forced  to  admit  that  if  he  had 
only  been  more  studious  of  the  case  he  might  have  recognized  the  pre- 
Tnonitory  signs  many  weeks  before. 

The  temperature  rises  to  103  degrees.  The  pulse  becomes  rapid 
and  then  slower.  The  respirations  do  not  change  mttch.  The  sen- 
sorium  remains  for  a  while  clear  and  the.  headache  grows  more  in- 
tense. A  short,  sharp,  distressing  cry,  the  so-called  hydrocephalic  cry, 
is  vented  now  and  then.  The  sleep  is  broken  and  fretful,  or  there  may 
he  insomnia.  The  muscles  begin  to  twitch  and  start.  The  pupils  are 
contracted.  Vertigo  is  complained  of.  Light  and  sound  are  absolutely 
unbearable.  Delirium  alternates  with  somnolence.  The  teeth  are 
ground  together  and  the  head  is  burrowed  into  the  pillow.  This  is  the 
so-called  stage  of  irritation.  The  motor  and  sensory  manifestations 
of  it  are  striking  and  characteristic.  The  hypercesthesia,  both  of  the 
general  and  special  senses,  is  all  but  too  obvious.     The  patient  resents 


8l8  THE   XON-NEURONIC  DISEASES 

every  touch  upon  his  skin  and  muscular  tissues.  He  doesn't  want  to 
be  moved.  He  begs  simply  to  be  left  alone  free  from  contact  as  much 
as  possible  of  bedding  and  clothing.  Following  the  early  transitory 
twitchings,  the  muscles  of  the  neck,  face,  back,  arms  and  legs  become 
rigid.  Before  the  coniractures  become  marked  the  reflexes  are  notice- 
ably exaggerated  and  Kernigs  sign  is  pronounced.  Trismus  is  pres- 
ent. The  back  is  bowed  in  opisthotonos.  The  abdomen,  is  hard  and 
retracted.  The  arms  and  legs  and  hands  and  feet  are  all  more  or  less 
flexed,  rigid  and  contractured.  In  this  stage  general  or  partial  con- 
zulsions  may  occur  or  epileptiform  attacks,  or  brief  tetanic  contrac- 
tions in  the  entire  musculature  of  the  body. 

Gradually  these  symptoms  lead  into  the  stage  when  stupor  reveals 
the  exhausted  and  hydrocephalic  conditions  of  the  encephalon.  All 
signs  of  irritation  subside  and  the  patient  lies  still,  dull,  apathetic  and 
uncomplaining.  He  may  utter  an  occasio>ial  cry  or  there  may  be  a 
slight  convulsive  zvave  pass  over  the  body  but  as  a  rule  all  is  still.  The 
coma  is  clearly  deepening  and  the  earlier  suffering  is  being  replaced 
bv  an  appearance  of  death.  The  pupils  are  now  dilated  and  unequal. 
Fision  is  obscured,  or  at  least  there  is  no  reflex  response  as  in  health. 
The  eyeballs  are  rolled  from  one  side  to  the  other.  Strabismus  is  pres- 
ent ;  sometimes  a  condition  not  unlike  nystagmus.  In  a  little  while 
signs  of  optic  neuritis  or  choked  disc  may  appear  at  the  fundus.  Oc- 
casionally a  tuberculous  choroiditis  can  be  made  out.  Respirations  be- 
come sighing.  The  temperature  fluctuates  widely  even  from  day  to 
day.  The  pulse  usually  drops  below  the  normal.  The  skin  is  erythe- 
matous in  patches  and  if  rubbed  with  the  finger  nail  exhibits  the  un- 
important tdclve  ccrebrale  of  the  French  writers.  The  bowels  are  still 
obstinately  constipated  and  the  abdomen  is  boat-shaped. 

Gradually  from  this  stage  the  patient  passes  into  the  final  or 
paralytic  stage  in  which  paralysis,  not  complete,  however,  of  the  cra- 
nial nerves  and  of  special  groups  of  muscles,  and  coma  constitute  the 
predominant  symptoms.  An  occasional  twitch  or  convulsion  may  occur 
and  with  a  great  effort  the  child  may  be  aroused.  As  a  rule,  however, 
intense  coma,  immobility  with  contracture  or  relaxation  and  a  general 
collapsed  typhoid  state  is  the  condition  present.  After  awhile  the 
patient  cannot  be  roused  at  all.  Involuntary  evacuations  of  the  bowels 
and  bladder  take  place.  The  pulse  becomes  rapid  and  feeble.  A  lotv 
delirium  may  continue.  The  temperature  falls  to  subnormal,  even  to 
94  or  93  degrees,  rising  suddenly  to  io6  or  io8  degrees  just  before 
death,  which  occurs  usually  from  two  to  three  weeks  after  the  onset 
of  the  malady. 

In  adults  the  disease  may  appear  abruptly,  run  a  violent  course 
with  exaggeration  of  all  the  symptoms  and  terminate  in  death  in  a  few 
days.  Children  also  are  occasionally  attacked  this  way.  More  often, 
however,  in  children  the  disease  runs  a  more  protracted,  irregular 
course.  Even  remissions  occur  that  raise  false  hopes  of  recovery;  In 
these  cases  monoplegias,  hemiplegias,  aphasia,  Jacksonian  epileptiform 
phenomena,  rigidity  followed  by  temporary  relaxation  or  permanent 
contractures,  tremors,  athetoid,  cataleptoid  and  tetanic  conditions  need 
not  surprise   one  if  they   appear.     A  moment's  consideration  of   the 


THE  XOX-NEURO^'IC  DISEASES  SlQ 

lesion  and  its  location,  the  thickenings,  the  arteritis,  the  hemorrhages;, 
thromboses  and  foci  of  softening  in  and  about  the  area  supplied  hy 
the  middle  cerebral  artery  will  explain  them. 

Diagnosis. — In  a  frank  case,  the  diagnosis  of  tuberculous  menin- 
gitis is  not  a  matter  of  great  difficulty.  The  discovery  of  a  tuberculous 
focus  somewhere  else  in  the  body,  the  prodromal  historv,  the  onset, 
course  and  character  of  the  symptoms  present,  if  carefully  analyzed  and 
properly  valued  in  their  various  relationships,  will  afford  an  outline 
picture  that  can  easily  be  recognized.  And  yet,  as  I  have  said  before, 
sometimes  the  diagnosis  is  a  most  diiffcult  matter  on  account  of  the 
irregularity  of  the. symptomatology  of  the  meningitic  trouble,  and  espe- 
cially on  account  of  the  masking  of  the  case  by  the  symptoms  of  the 
complications  that  are  often  present.  Lianhar  pimcture  is  usually  con- 
clusive even  though  the  bacilli  are  not  always  recovered.  The  menin- 
gitic character  of  the  tluid,  the  evidence  of  IcHCocytosis,  its  ready 
coagulability,  its  high  pressure,  its  cloud)^  purulent  appearance  though 
it  may  be  clear,  are  all  confirmatory  when  the  symptoms  point  in  the 
least  toward  tuberculosis. 

The  trismus  in  some  cases  may  cause  them  to  be  mistaken  for 
f eta II us.  The  history  of  an  injury  determines  the  latter,  however. 
Typhoid  fever  and  other  infectious  diseases,  gastrointestinal  catarrh, 
ansemia,  hemicrania  may  be  confused  with  the  early  stages  of  menin- 
gitis. Care  in  eliciting  the  minute  history  of  the  case  and  in  the  personal 
examination  of  the  patient  will  forestall  error.  The  same  may  be 
said  of  general  miliary  tuberculosis  which  may  or  may  not  have  men- 
ingitis associated  with  it.  Sometimes,  when  meningitis  seems  to  be 
the  only  affection  present,  its  tuberculous  nature  can  be  suspected  when 
the  prodromal  stage  is  prolonged  and  preceded  even  by  weeks  and 
months  of  transient  premonitions,  when  the  temperature  is  moderately 
raised,  when  its  entire  course  lacks  violence  and  great  severity,  when 
tuberculous  choroiditis  can  be  discovered  and  when  the  disease  occurs 
in  a  child. 

Prognosis. — This  is  decidedly  bad.  The  reported  recoveries  have 
probably  been  cases  that  were  erroneously  diagnosed,  in  spite  of  the 
fact  that  a  few  such  cases  have  been  put  upon  record  by  reliable  author- 
ities. I  have  never  seen  a  recovery  in  a  positive  case  of  the  disease. 
Freyhan,  according  to  Oppenheim.  had  a  case  recover  even  after  the 
tubercle  bacilli  had  been  secured  from  the  cerebrospinal  fluid.  The 
possible  contingencies  surrounding  such  a  case  are  so  numerous,  that 
in  view  of  the  almost  constant  fatality  of  the  disease,  one  may  be  ex- 
cused for  retaining  a  doubt  in  regard  to  it.  The  disease  runs  a  more- 
typical  course  in  children  than  it  does  in  adults.  It  may  be  latent  or 
be  quite  over-shadowed  by  the  primary  trouble  for  a  long  time.  As; 
a  local  meningitis  of  the  vertex,  it  may  cause  only  aphasia,  hemiplegia,, 
Jacksonian  manifestations,  merely  to  become  generalized  years  later:. 
It  is  believed  that  some  of  the  so-called'  aborted  cases  are  due  to  tuber- 
cular intoxication  of  the  brain  rather  than  a  true  meningitis. 

Treatment. — Prophylaxis  is  important.  Tuberculous  foci  should' 
always  be  removed  from  other  parts  of  the  body,  surgically  or  other- 


820  THE   XOX-XEURONIC  DISEASES 

wise,  if  possible.  A  tuberculous  child  should  be  treated  on  general 
principles  with  fresh  air,  good  food,  nutritious  diet,  careful  nursing, 
cod  liver  oil,  and  tonics. 

The  administration  of  large  doses  of  potassium  iodide  ( 600  grains 
a  day  in  one  case  that  recovered)  and  symptomatic  treatment  bounds 
our  therapy  in  this  intractable  disease. 

Surgical  measures  such  as  ventricular  tapping  as  a  palliative,  tre- 
phining and  subarachnoid  drainage  and  lumbar  puncture  as  radical, 
have  been  tried  with  a  modicum  of  success.  More  experience  will  be 
needed  before  final  judgment  can  be  passed  upon  the  operative  treat- 
ment of  tuberculous  meningitis. 

Chroxic  IMexixgitis. — Except  as  a  syphilitic  product,  chronic 
meningitis,  is  rare,  much  more  so  clinically  than  pathologically,  though 
in  general  practice  it  is  often  diagnosed  in  headache,  after  isolation  and 
following  injuries  to  the  head.  It  may  occur  at  the  vertex.  On  the 
autopsy  table  it  is  more  often  seen  at  the  base.  It  plays  a  role  in  the 
production  of  intense  h3-drocephalus  by  reason  of  the  adhesions  it 
causes  and  the  closure  of  the  inter^-entricular  openings.  Its  symptom- 
atology is  usually  slight  or  nil.  The  symptoms  often  attributed  to  it 
are  mostly  due  to  compression,  congestion  and  other  disturbances  of 
the  brain  substance,  especially  the  cortex. 

In  alcoholic  subjects  there  is  a  condition  that  is  sometimes  spoken 
of  as  serous  meningitis.  Inflammation  is  not  present,  however.  The 
headache,  slight  delirium,  mental  failure  and  tendency  to  optic  neuritis 
are  due  to  congestion  mereh*.  Intoxication  of  the  brain  elements  is 
also  probably  responsible  in  part  for  the  symptoms.  Multiple  neuritis 
and  hepatic  engorgement  often  complicate  these  cases. 

Chronic  syphilitic  meningitis  has  been  spoken  of  under  the  head 
of  syphilis  of  the  central  nervous  system.  There  are  many  forms  of 
obscure  basal  meningitis  in  children  as  well  as  in  adults,  which  run 
an  irregular  course  and  are  probably  due  to  inherited  syphilis. 

Chronic  ossifying  meningitis  is  a  pathological  curiosity  that  has 
iDeen  seen  in  some  old  cases  of  persistent  headache,  epilepsy  and  in- 
-Sanity. 

There  is  a  chronic  infantile  tucningitis,  the  non-tuberculous  pos- 
terior meningitis  of  infants  that  is  of  considerable  interest.  It  is  somie- 
times  associated  wdth  syphilis  and  may  cause  a  severe  hydrocephalus. 
Its  chief  symptom  is  retraction  of  the  head,  so  that  it  has  even  been 
called  the  "cer^-ical  opisthotonos  of  infants.*'  The  posterior  fossa  of 
the  skull  is  its  choice  location.  Sometimes  its  onset  is  sudden;  at 
other  times  it  is  gradual.  Fever,  vomiting,  rigidity  of  the  limbs  and 
convulsions  have  all  been  pointed  out  in  connection  with  it  by  Gee  and 
Barlow.  The  retraction  of  the  head  may  be  intermittent.  Palsy  is 
rare.  Sometimes  there  are  strabismus  and  nystagmus.  The  head  be- 
comes hydrocephalic  in  size  after  a  time  in  some  cases.  Recover}^  or 
death  may  take  place  in  from  a  month  to  a  year  or  a  3^ear  and  a  half. 
Sometimes  weeks  before  death,  the  child  passes  into  a  state  of  stupor 
or  coma.  Antisyphilitic  treatment  should  always  be  given  a  trial  in 
these  cases. 


THE  NON-NEURONIC  DISEASES  82I 


CIRCULATORY  DISEASES  OF  THE  BRAIN. 

From  clinical  as  well  as  experimental  observation  we  know  that 
the  brain  is  very  susceptible  of  the  slightest  change  in  its  circulation. 
Just  how  this  is  we  are  not  always  able  to  determine.  Its  functional 
integrity  is  clearly  dependent  upon  the  quality  and  quantity  of  blood 
flowing  through  it,  upon  the  blood  pressure,  and  upon  the  velocity  of 
the  flow.  The  relative  importance  of  these  various  factors  is  still  un- 
known to  us.  In  the  older  pathology  mere  blood  pressure  and  quan- 
tity of  blood  constituted  a  basis  whereon  were  erected  elaborate  -clin- 
ical descriptions  and  symptomatic  differentiations.  It  is  probable  that 
in  an  organ  so  highly  vascularized  as  the  brain  is  and  with  such  a  rich 
anastomosis  between  all  parts  of  its  main  circulatory  apparatus,  the 
changes  of  pressure  and  amount  of  blood  would  have  to  be  compara- 
tively gross  to  effect  marked  changes  in  the  cerebral  symptomatology. 
As  a  sort  of  reaction  to  this  coarse  and  largely  hypothetical  clinico- 
pathology  of  the  past,  it  is  now  denied  by  many  that  any  changes, 
capable  of  being  observed  at  the  bedside,  take  place  in  the  mere  pres- 
sure of  the  blood  or  the  quantity  circulating  through  the  brain.  This 
is  perhaps  an  extreme  in  the  opposite  direction,  though  it  is  a  whole- 
some protest  to  the  many  fine  focal  and  generalized  distinctions  that 
used  to  be  made  in  the  symptomatology  erected  upon  the  old  hypo- 
thetical pathology. 

There  are  symptomatic  manifestations,  however,  that  are  clearly 
due  to  circulatory  disturbances.  In  accounting  for  these,  modern 
pathology  lays  the  greater  stress  upon  the  quality  of  the  blood  and  the 
velocity  of  its  flow  in  the  capillaries.  The  composition  of  the  blood 
we  know  is  subject  to  great  variations.  Its  corpuscular  richness,  its 
chemical  and  bacteriological  ingredients,  its  endogenous  and  exogenous 
contents,  its  gases,  its  specific  gravity  and  physical  state  are  all  finer 
factors  in  influencing  the  delicate  activities  of  the  cerebral  neurones, 
it  would  seem,  than  are  the  mere  pressure  and  quantity  of  the  fluid. 
Moreover  the  rapidity  of  flow  depending  largely  upon  the  tension  of 
the  vascular  walls,  and  causing  a  correspondingly  swift  removal  of 
deleterious  products  of  metabolism  and  conveyance  to  the  nerve  cells 
of  stimulating,  nutritious  pabulum  would  also  appear  to  be  a  more  in- 
fluential factor.  These  facts  are  supported  by  experimental  research 
and  dovetail  better  with  what  we  know  nowadays  of  cerebral  physiol- 
ogy and  pathology  than  the  old  theories  based  upon  mere  hyperemia 
and  ansemia.  They  are  founded  upon  better  proofs  than  the  mere 
post  mortem  macroscopic  appearances  of  the  brain.  The  latter,  it  is 
now  recognized,  are  to  a  large  extent  due  to  such  post  mortem  influ- 
ences as  the  position  of  the  corpse,  pressure  about  the  neck,  time  of 
examination,  etc. 

Ante  mortem  appearances  of  the  face  and  skin  have  too  long  been 
adopted  as  arguments  for  a  similar  condition  in  the  intracranial  tis- 
sues. There  is  no  assurety  that  they  are  the  same,  and  some  facts  even 
intimate  that  they  rarely  are.  Facial  pallor  during  life  and  cerebral 
pallor  after  death,  do  not  by  any  means  prove  that  the  brain  was  in 


822  THE   XO-\"--\EURO.\IC  DISEASES 

like  condition  while  the  patient  was  alive  and  manifesting  the  symp- 
toms supposed  to  de  due  to  them. 

Notwithstanding  our  symptomatology  of  cerebral  anaemia  and 
hypersemia  is  based  upon  clinical  and  experimental  observations,  fur- 
ther studies  are  needed  to  determine  just  ho\\-  much  is  due  to  each  of 
the  respective  factors  that  always  more  or  less  accompany  these  circu- 
latory conditions,  namely,  the  quantity  of  the  blood,  its  quality,  the' 
pressure  of  its  column,  and  the  swiftness  of  its  flow.  Until  we  learn 
more  about  these,  we  will  still  have  to  treat  of  the  clinical  manifesta- 
tion3  under  the  two  general  heads  of  cerebral  anccmia  and  cerebral- 
hyperccmia. 

CEREBRAL  AX.E:AIIA. 

It  is  perfectly  reasonable  to  suppose  that  under  certain  conditions 
the  quantity  of  blood  in  the  brain  may  be  diminished,  even  consider- 
ably, below  the  normal.  \Miat  is  the  normal  for  any  one  particular 
individual  and  how  far  below  the  normal  can  the  quantity  of  intra- 
cranial blood  of  that  individual  be  reduced  before  the  brain  manifests 
it  outwardly?  Who  can  tell?  Hence  when  we  outline  a  symptoma- 
tology for  cerebral  angemia,  it  must  not  be  imagined  that  we  attribute 
the  symptoms  entirely  to  the  mere  want  of  blood.  Other  unknown  fac- 
tors are  undoubtedly  at  work,  such  as,  for  instance,  the  nutritive  pov- 
erty of  the  blood,  its  altered  composition,  the  shock  caused  by  the  sud- 
den disturbance  in  its  flow  and  the  diminished  pressure  in  some  cases  in 
the  blood-vessels. 

Etiology. — So  far  as  we  know,  cerebral  anaemia  is  both  a  local 
and  general  condition  and  may  be  dependent  upon  both  local  and  gen- 
eral causes.  An  embolus,  for  instance,  causes  a  local  anaemia,  followed 
by  other  changes  in  the  brain ;  a  cachetic  state  of  the  constitution  may 
be  accompanied  by  deficient  and  bad  blood  supply.  The  anaemia  ma}- 
therefore  be  primary  or  secondary.  The  immediate  and  remote  causes 
of  the  condition  are  therefore  innumerable  and  I  can  only  mention  a 
few  by  way  of  illustration. 

Severe  hemorrhage  in  some  other  part  of  the  body,  or  even  in 
the  brain  itself,  may  provoke  a  symptomatic  anaemia.  The  coma  of 
hemorrhagic  apoplexy  is  believed  to  be  due  partly  to  the  sudden  anaemia 
of  the  cortex  caused  by  the  local  loss  of  blood  and  certainly  in  sud- 
den and  profound  hemorrhages  from  the  lungs,  stomach,  bowels, 
uterus,  syncope  and  other  signs  of  severe  cerebral  auEemia  are  often 
observed.  The  sudden  withdrawal  of  ascitic  fluid,  paracentesis  of  the 
abdomen,  precipitate  parturition,  abrupt  disturbance  of  the  heart  ac- 
tion from  valvular  or  other  form  of  disease,  violent  cupping,  nervous 
collapse  as  seen  in  simple  swooning,  may  suddenly  diminish  the  amount 
■of  blood  flowing  to  the  brain.  The  same  condition  as  a  continuous  one 
follows  probably  the  exhaustive  febrile  diseases,  cardiac  weak- 
ness, partial  obstruction  by  tumor,  aneurism  and  diseased 
blood  vessels,  and  hydrocephalic  conditions.  Pressure  upon 
or  ligature  of  the  carotid  produces  signs  of  transient  cerebral  anaemia, 
^'asomotor  spasm  and  anaemia  have  been  blamed  for  certain  forms 
of  migrainous  headache  and  epileptiform  phenomena.     It  is  thus  seen 


THE   NON-NEURONIC  DISEASES  823 

that  a  great  variety  of  causes,  mechanical  and  physiological,  sudden 
and  gradual,  may  be  blamed  for  the  intracranial  disturbance.  Let  me 
repeat,  however,  that  simply  the  diminution  alone  in  the  intracranial 
quantity  of  blood  is  not  to  be  regarded  as  the  whole  of  the  pathology 
of  the  trouble,  or  as  the  sole  cause  of  its  symptomatic  exhibitions. 

Pathology  and  Pathogenesis. — Macroscopicaily  the  brain  looks 
pale  and  whitish.  There  is  a  noticeable  deficiency  in  the  number  of 
puncta  vasculosa  in  the  white  substance.  The  gray  matter  looks  whiter 
than  it  should  and  its  vascularity  seems  diminished.  The  membranes 
are  pale  and  there  is  an  effusion  of  serum  in  the  pia  mater.  Both  inside 
and  outside  of  the  ventricles  the  cerebrospinal  fluid  is  slightly  in- 
creased. Paleness  and  excessive  moisture  are  the  chief  gross  appear- 
ances. Microscopically  the  nerve  cells  are  said  to  be  changed,  are  un- 
duly translucent  or  granular ;  while  the  vascular  walls  are  somewhat 
degenerated  and  thickened  in  some  cases.  These  appearances  may  be 
general  throughout  the  brain  or  local,  according  to  the  nature  of  the 
primary  cause. 

Symptoms. — These  are  practically  the  same  for  all  cases,  though 
in  detail  they  will  vary  widely,  according  to  whether  the  ansemia  is 
general  or  local,  primary  or  secondary,  slight  or  severe.  A 
simple  attack  of  syncope  illustrates  well  the  main  features 
of  the  clinical  picture.  The  patient,  suddenly  or  gradually, 
experiences  a  sinking  sensation,  his  head  gets  light,  spots 
float  before  his  eyes  or  his  vision  gets  clouded,  he  feels  dissy  and  sud- 
denly weak,  his  heart  seems  to  flutter,  his  breathing  is  somewhat  sigh- 
ing and  heavy,  his  ears  buzz,  he  is  nauseated  and  may  even  vomit.  He 
falls  or  is  quickly  placed  upon  a  chair  or  couch.  His  eyes  close  and 
his  consciousness  vanishes.  In  a  few  moments  he  comes  to,  is  dazed 
or  slightly  delirious,  manifests  apathy  and  a  desire  for  sleep.  The 
pupils  are  contracted  though  later  on  they  may  be  dilated.  In  severer 
cases,  such  as  follow  sudden  loss  of  blood,  the  symptoms  are  more 
swift  in  onset  and  more  profound.  There  is  a  sudden  flash  of  light 
before  the  eyes,  followed  by  darkness,  a  quick  loss  of  consciousness, 
vomiting  and  falling.  The  pulse  is  weak  and  hurried;  the  respiratious 
are  labored,  shallow  and  sighing;  the  skin  is  moist  and  cool,  and  the 
piipils  are  dilated.  The  reflc.ves  are  all  anmdlcd,  the  pulse  grows 
slower  and  feebler  and  in  some  cases  the  patient  dies  in  a  convulsion. 
In  other  cases  spasms  pass  over  the  body  and  the  patient  awakens 
momentarily  delirious  and  complaining  of  severe  headache.  Some- 
times the  consciousness  vanishes  only  when  the  patient  attempts  to 
sit  up,  being  present  as  long  as  he  keeps  the  recumbent  position.  I 
had  a  case  of  profound  neurasthenic  anaemia  in  a  woman  who  while 
perfectly  flat  on  the  back  swooned  away  every  few  moments.  Some 
of  the  severe  hemorrhagic  cases  may  continue  from  several  minutes 
only  to  an  hour.  They  are  dangerously  near  death  and  one  cannot 
at  times  foretell  the  outcome. 

In  general  chronic  anaemia  there  is  a  general  sluggishness  of  the 
cerebral  processes  with  a  tendency  to  functional  vagaries,  parcesthesia 
and  even  hallncinations.  Irritable  weakness  of  the  nerve  elements  is 
the  nearest  we  can  come  to  an  explanation  of  the  pathogenetic  phe- 


824  THE  XOX-XEUROXIC  DISEASES 

nomena.  These  patients  are  drowsy,  indifferent,  lack  initiative  force 
and  staying  qualities.  Their  memories  are  weak,  the  volition  lacks 
vigor,  the  imagination  and  intellect  will  only  work  under  a  vigorous 
spurring.  They  are  prone  to  sleep  and  yawn  and  are  regarded  as  splen- 
did illustrations  of  laziness.  Everything  but  to  sit  and  read,  is  an 
effort  to  them,  especially  all  mental  exertion.  Sometimes  they  arouse 
into  tremendous  irritability  and  excitement  over  trivialities  and  com- 
plain of  every  noise  and  unusual  ray  of  light.  They  are  decidedly 
neurasthenic.  Heaviness  of  the  head,  insomnia  at  night,  occasional 
spells  of  syncope,  mistiness  before  the  eyes  and  vertigo  upon  every  sud- 
den movement,  all  relieved  by  lying  down,  are  the  lot  of  these  suffer- 
ers of  anaemia  from  chlorosis,  frequent  hemorrhages,  pernicious 
anaimia  and  similar  causes. 

Marshall  Hall  has  applied  the  adjective  hydrocephaloid  or  hydroen- 
cephaloid  to  a  type  of  cerebral  anaemia  seen  in  children  with 
prolonged  diarrhoea.  The  patient  lies  in  a  semicomatose  condition  with 
eyes  partially  open,  pupils  contracted,  fontanelle  depressed,  with 
symptoms  later  on  resembling  those  of  basilar  meningitis,  such  as 
dilatation  of  the  pupils,  convulsions,  strabismus,  retraction  of  the  head 
and  death  in  profound  coma. 

Anaemia  is  probably  at  the  bottom  of  the  cases  in  which  delirium 
is  associated  with  marasmus  and  extreme  inanition.  In  the  cases 
which  in  the  past  have  been  spoken  of  as  oedema  of  the  brain,  ansemia 
is  in  all  likelihood  the  fundamental  pathological  basis  of  the  symptoms. 

As  a  part  of  the  anaemic  state,  malnutrition  and  intoxication,  as 
I  have  already  intimated,  may  play  the  chief  role. 

DiAGXosis. — Is  easy  when  all  attendant  circumstances  are  taken 
into  account.  The  immediate  cause,  the  underlying  cachexia,  the  char- 
acter and  distribution  of  the  general  symptoms  in  general  ansemia,  and 
focal  symptoms  in  local  anaemia,  and  the  absence  of  all  other  signs  of 
organic  disease  of  the  brain  will  form  the  basis  of  a  correct  diagnosis- 
Congestion  of  the  brain  may  in  a  few  instances  simulate  anaemia,  and 
organic  disease  may  have  anaemia  as  a  part  of  its  pathological  com- 
plexus.    These,  however,  with  care  are  easily  differentiated. 

Progxosis. — This  is  generally  favorable  in  mild  cases.  Cases 
due  to  heart  lesions,  exhaustive  hemorrhages  and  other  grave  condi- 
tions, with  coma,  are  dangerous  and  too  often  fatal.  Serious  signs 
of  trouble  are  convulsions,  pupillary  dilatation  and  light  iridoplegia. 
The  hydrocephaloid  cases  of  children  are  usually  favorable  under 
prompt  and  proper  treatment.  Visual  disorders  sometimes  remain 
after  severe  anaemic  spells. 

Treatmext. — First  and  foremost  is  to  force  the  blood  back  into 
the  brain  as  quickly  and  judiciously  as  possible.  In  acute  cases  the 
patient  should  be  placed  with  the  head  downwards.  In  chronic  cases, 
I  usually  always  have  them  occupy  a  bed  with  the  foot  of  it  slightly 
elevated  on  bricks.  In  the  acute  cases  the  limbs  may  be  slightly  bound 
or  an  Esmarch  bandage  may  be  temporarily  applied.  Transfusion  may 
have  to  be  employed  in  some  cases.  The  cause  of  and  character  of 
the  attack  must  always  be  taken  mto  account.  If  the  heart  has  sud- 
denly failed,  proper  stimulants  in  the  way  of  alcohol,  ammonia  salts^ 


THE   XOX-XEUROXIC  DISEASES  82 ^ 

aromatic  spirits  of  ammonia,  must  be  administered.  If  thei;e  is  a 
vasomotor  spasm,  amyl  nitrite  and  nitrogl3-cerin  are  called  for.  A 
few  drops  of  the  former  may  be  inhaled  from  a  handkerchief,  while 
the  latter  is  to  be  given  hypodermically.  They  should  not,  of  course, 
be  given  together. 

Cold  and  heat  to  the  skin,  tickling,  faradization,  sinapisms,  am- 
monia inhaFations  may  do  in  most  cases  of  simple  syncope. 

Artificial  respiration  may  be  required  in  some  severe  cases. 

The  general  management  of  the  cases  involves  the  treatment  of 
the  primary  disease  and  the  improvement  of  the  general  anaemic  con- 
dition. The  focal  anaemias  are  referred  to  under  the  head  of  cerebral 
softening  or  encephalomalacia. 

CEREBRAL  HYPEREMIA. 

The  statements  previously  made  in  regard  to  the  possibility  and 
frequency  of  circulatory  disturbances  in  the  brain  apply  to  hyperaemia 
as  well  as  to  anaemia.  In  the  past  too  much  was  assumed  and  too 
definite  a  description  of  the  symptomatology  of  a  supposed  cerebral 
congestion  was  promulgated.  Actual  facts  were  wanting  and  theories 
ran  riot.  On  the  other  hand  to-day  in  some  quarters  there  is  too 
strenuous  a  denial  that  cerebral  congestion  ever  occurs  or  presents  dis- 
tinctive symptoms.  Both  logic  and  data  proclaim  that  the  condition 
does  sometimes  occur  and  that  certain  special  manifestations  are  the 
direct  outgrowth  of  the  condition.  \\'e  can  therefore  reasonably  oc- 
cupy a  middle  ground  and  wait  for  further  observations  to  clear  up 
many  things  that  are  still  unaccountable. 

The  essential  fact  in  cerebral  hyperaemia  is,  of  course,  the  exces- 
sive amount  of  blood  in  the  cerebral  vessels.  This  tells,  however,  only 
a  part  of  the  story.  Much  is  still  within  the  dark  in  regard  to  the 
mechanism  of  the  production  of  this  congestion  and  in  regard  to  asso- 
ciated conditions  upon  which  the  symptoms  may  depend  for  aught  we 
know,  such  as  the  composition  of  the  blood,  the  speed  of  its  flow,  the 
influence  of  its  altered  pressure,  etc.  Changes  of  quantity  alone  are 
gross  and  unsatisfactory  grounds  whereon  to  explain  the  delicate 
changes  of  nervous  activity. 

It  has  been  declared  that  there  is  a  permanent  form  of  cerebral 
congestion  caused  by  continuous  mental  exertion,  by  certain  constitu- 
tional plethora  and  by  some  other  conditions.  This  is  very  question- 
able, however,  and  even  were  the  possibility  and  probability  of  such  to 
be  granted,  it  would  still  be  hard  to  say  what  in  any  particular  indi- 
vidual should  be  the  normal  quantity  of  the  blood  in  the  encephalon  and 
at  what  point  it  ceases  to  be  normal  and  becomes  abnormal  or  true 
hyperaemia.  Clinically  we  are  much  more  concerned  about  the  tem- 
porary or  transient  cerebral  congestions,  as  the}'  at  least  exhibit 
lines  of  demarkation,  coarse  to  be  sure  at  times,  whereby  we  can 
distinguish  the  normal  from  the  abnormal. 

Temporary  hyperaemia  of  the  brain  may  be  active  and  arterial,  or 
passive  and  venous.  The  former  is  often  the  beginning  of  an  inflam- 
mation ;  the  latter  is  frequently  recognized  as  hypostatic  congestion. 


826  THE  NOX-XEURO-XIC  DISEASES 

Etiology. — The  causes  of  active  congestion  of  the  brain  are  both 
numerous  and  diverse.  Among  them  we  recognize  a  general  plethoric 
condition  that  is  disturbed  and  sends  a  flush  of  blood  to  the  head ;  the 
beginning  of  certain  febrile  states  with  its  varied  agents  such  as  in- 
fection, elevated  temperature,  nervous  irritability ;  cardiac  over-activity 
from  whatever  cause,  organic  or  functional ;  cold  to  the  skin  and  a  con- 
traction of  the  peripheral  arterioles ;  a  dilatation  of  the  arterioles  of 
the  brain  by  certain  drugs  such  as  amyl  nitrite,  nitroglycerin  and  alco- 
hol, possibly  by  mental  emotion  and  other  nervous  influences,  as  in 
neurasthenia,  hysteria  and  perhaps  in  certain  vasoneurotic  diseases 
like  exopththalmic  goitre ;  suppression  of  certain  customary  discharges  ; 
strains  and  violent  muscular  exertion,  etc.  Insolation  symptoms  have 
been  attributed  to  cerebral  congestion. 

Any  mechanical  obstruction  to  the  return  flow  of  blood  from  the 
head  will  cause  passive  cerebral  congestion.  It  is  generally  therefore 
a  chronic  condition  and  is  seen  sometimes  in  tumors  of  the  neck,  new 
growths  in  the  mediastinum,  in  pulmonary  emphysema  and  in  uncom- 
pensated mitral  stenosis.  Tight  bands  about  the  neck,  collars,  strain- 
ing, coughing,  sneezing,  playing  upon  wind  instruments,  and  other 
severe  muscular  effort  may  cause  a  temporary  congestion  or  intensify 
one  already  produced  by  other  factors.  In  addition  to  the  obstruc- 
tions thus  caused  in  the  superior  vena  cava  and  veins  of  the  neck, 
the  sinuses  and  veins  of  the  intracranium  itself  may  be  blocked  by 
thrombosis  and  other  pathological  conditions.  In  certain  states  of  the 
constitution,  even  the  retention  of  the  horizontal  attitude  may  delay 
the  return  of  the  blood. 

Pathology  axd  Pathogenesis.  —  The  post-mortem  findings  in 
cerebral  hyperaemia  are  so  indefinite  that  one  can  hardly  construct  a 
pathological  picture.  The  contents  of  the  vessels  vary  enormously 
and  quickl}-  by  both  ante  and  post-mortem  changes  in  position  and  as 
a  result  of  other  unknown  factors.  In  suffocation,  for  example,  the 
veins  are  clearly  engorged  and  yet  after  death  the  brain  is  found  to 
be  anaemic.  Active  hyperaemia  is  practically  never  seen  after  death 
and  so  long  as  it  does  not  run  into  inflammation,  it  leaves  no  signs  of 
its  former  presence.  In  a  few  cases  the  veins  of  the  cortex  have  been 
distended  and  the  arteries  at  the  base  and  about  the  Sylvian  fissure 
were  full  of  blood.  Mere  post-mortem,  gravitation  may  have  had  some- 
thing to  do  with  this :  it  is  certainly  no  evidence  of  what  mav  have 
been  the  condition  during  life.  In  some  cases  there  are  bulgings  of  • 
the  vessels,  blood  pigment  in  the  sheaths  and  minute  spots  of  extrava- 
sation. The  value  of  these  as  findings  is  uncertain.  In  a  word  then, 
there  is  no  known  definite,  uniform  pathology  of  cerebral  hyperaemia. 

Symptoms. — Leube  believes  that  it  is  not  possible  to  make  a 
diagnosis  of  pure  cerebral  congestion,  as  he  contends  that  the  symp- 
toms usually  attributed  to  it  are  of  toxic  origin.  Osier  declares  that 
as  a  separate  clinical  entity,  congestion  of  the  brain  rarely  comes  un- 
der observation.  Its  symptomatology  is  certainly  very  obscure  and 
indefinite.  Some  writers  have  associated  it  with  throbbing  headache, 
delirium,  fever,  insomnia  and  convulsions.  Mental  activity  and  ex- 
citement, even  mania,  have  been  attributed  to  it.     On  the  other  hand 


THE   NON-NEUROXIC  DISEASES  827 

it  has  been  blamed  for  torpor,  dullness  of  intellect  and  terminal  coma. 
All  grades  of  cases  are  supposed  to  exist.  In  some  the  face  merely 
Pushes  up  and  feels  hot,  the  conjunctiva  betome  red,  the  temples  throb, 
the  eyes  flicker,  the  head  aches  a  little,  the  mind  is  dazed  and  more  or 
less  nausea  and  dizziness  are  present.  A  full  meal,  an  alcoholic  drink 
■or  a  sudden  muscular  exertion  will  in  neurotic  and  predisposed  plethoric 
people  produce  such  a  general  exhibition.  In  severer  cases,  con- 
sciousness may  be  profoundly  disturbed.  Mania  and  fever  are  said 
to  occur.  Meningitis  seems  to  be  about  to  declare  itself  when  after  a 
short  time  all  of  the  symptoms  gradually  or  suddenly  subside.  Para- 
lytic  and  apoplectic  forms  of  the  trouble  have  been  related.  Hemi- 
plegia, aphasia,  unilateral  convulsions  and  death  have  been  credited  to 
it  because,  forsooth,  no  changes  of  any  sort  were  to  be  discovered  in 
the  autopsy.  I  am  inclined  to  think  that  some  form  of  virulent  intox- 
ication, such  as  we  see  in  some  forms  of  Landry's  paralysis  and 
delirium  grave,  rather  than  mere  congestion  is  the  pathogenetic  ele- 
ment in  these  cases. 

Stupor,  insomnia,  mental  dullness,  confusion  of  niind  are  among 
the  manifestations  that  have  been  assigned  to  passive  congestion. 
These  are  all  uncertain,  however,  and  it  is  to  be  remembered  always 
that  the  symptoms  may  belong  to  the  original  disease,  as,  for  instance, 
the  tumor,  the  heart  disease,  upon  which  the  hypostatic  congestion  in 
-part,  depends. 

Prognosis. — This  is  favorable  so  long  as  the  case  is  one  merely 
of  congestion.  If  there  is  disease  of  the  heart,  of  the  arterial  walls, 
liemorrhages,  embolus,  thrombosis  and  other  complications  may  arise 
or  already  be  present  that  will  make  the  outlook  in  cerebral  congestion 
a  matter  of  some  serious  moment.  Passive  congestion  takes  its  prog- 
nosis from  the  cause  upon  which  it  depends.  It  is  bad,  of  course,  in 
tumors,  aneurisms  and  valvular  lesions  of  the  heart. 

Treatment. — Prophylaxis  is  important ;  stimulants,  over-exertion, 
-exposure,  mental  excitement  and  dissipation  and  excesses  of  all  kinds 
must  be  avoided.  The  life  must  be  a  regular  tonic  one,  including  sys- 
tematic exercise,  plain,  light  food,  plenty  of  sleep  and  fresh  air,  with 
attention  to  all  the  functions  of  the  skin,  bowels  and  kidneys.  It  must 
Tdc  even  in  all  things.  Sudden  changes  are  provocative  of  congestion 
In  those  who  are  predisposed. 

In  the  attack  the  patient  should  not  lie  down.  The  bowels  should 
be  acted  upon  promptly  by  an  enema,  calomel  or  even  croton  oil. 
The  head  should  be  rendered  cool  with  an  ice  bag  or  cold  water  coil, 
while  the  feet  are  placed  in  hot  water  alone  or  with  mustard,  or  wrap- 
ped in  hot  cloths.  Cupping  to  the  sides  of  the  spine,  mustard  to  the 
nape  of  the  neck  or  leeches  to  the  temples,  mastoid  bones  or  back  of 
the  neck  should  be  though  of.  Venesection  may  be  advisable,  if  the 
Tieart  action  and  general  strength  do  not  contraindicate  it.  Medicines 
are  of  little  avail,  though  ergot  and  aconite  have  been  used. 

The  other  treatment  of  the  trouble,  whether  active  or  passive,  in- 
cludes symptomatic  measures  and  means  to  remove  the  underlying 
•cause  so  far  as  that  is  possible. 


828  THE   XON-XEUROXIC  DISEASES 

CEREBRAL  HEMORRHAGE. 

An  intracranial  hemorrhage  may  occur  into  the  membranes  of 
the  brain  {meningeal  hemorrhage)  or  into  the  substance  of  the  brain 
{cerebral,  medullary,  pontile  or  cerebellar  hemorrhage). 

Cerebral  hemorrhage  is  the  most  frequent  and  the  form  that  is 
meant  when  the  term  hemorrhagic  apoplexy  is  used.  The  other  forms- 
of  the  trouble  will  be  found  discussed  under  appropriate  headings  else- 
where. 

Etiology. — Disease  of  the  bloodvessels  underlies  cerebral  hemor- 
rhage, hence  all  factors  that  tend  to  the  development  of  such  a  disease 
and  all  agents  that  cause  a  sudden  rupture  in  the  diseased  vessel  wall 
constitute  its  chief  etiological  forces.  The  former  may  be  referred  to- 
as  the  predisposing  causes,  the  latter  as  the  exciting. 
Among  the  former  age,  sex,  climate,  heredity,  previous  state- 
of  health  and  mode  of  life,  exercise  a  significant  influence. 
Hemorrhage  may  occur  at  any  age  but  is  most  frequent  at  that  time  of 
life  when  the  bloodvessels  are  subjected  to  strains  which  their  debil- 
itated and  diseased  condition  renders  them  less  able  to  withstand. 
Four-fifths  of  all  the  cases  therefore  occur  after  forty  years  of  age 
and  the  liability  to  it  increases  with  each  decade  thereafter  until  about 
the  age  of  eighty  when  it  seems  to  diminish  markedly.  Between  the 
ages  of  ten  and  fifty  an  apoplectic  stroke  from  hemorrhage  is  a  com- 
parative rarity.  The  accidents  of  birth  increase  slightly  the  liability 
of  infants.  In  extreme  old  age  it  is  not  so  frequent  as  is  commonly 
supposed,  most  of  the  strokes  then  being  due  to  thrombosis  and  sec- 
ondary emboli  from  disease  of  the  vessels.  Men,  on  account  of  their 
more  strenuous  lives  and  greater  addiction  to  alcohol,  are  somewhat 
more  attacked  by  it  than  women.  The  occurrence  of  more  cases  in- 
the  haunts  of  civilization,  among  peoples  living  in  the  temperate  zone, 
in  cold  weather  and  at  high  altitudes  is  easily  accounted  for.  Strain 
and  strenuosity  are  here  more  in  evidence  and  all  those  predisposing" 
and  exciting  influences  about  to  be  mentioned. 

It  has  long  been  imagined  that  a  tendency  to  apoplexy  ran  in  cer- 
tain families.  There  is  indeed  a  slight  hereditary  influence  exerted 
through  the  vascular  system.  It  is  about  equal  in  significance  with  that 
other  time-honored  notion  that  apoplectic  individuals  possess  a  partic- 
ular type  of  constitution,  including  a  short,  stocky  neck,  a  florid  coun- 
tenance and  a  stout,  plethoric  body.  As  many  cases  are  due  to  arterio- 
sclerosis, those  factors  that  tend  to  the  production  of  this  condition  are- 
important.  They  include  the  abuse  of  alcohol,  syphilis,  gout,  over- 
indulgence in  eating  with  lack  of  exercise,  over-exertion  and  similar 
agencies.  Intoxications  and  infections  predispose  to  hemorrhage.  It 
has  followed  lead  poisoning,  rheumatism,  the  acute  infectious  fevers. 
Certain  conditions  of  the  blood  as  in  purpura,  profound  and  pernicious 
anaemia,  leukaemia  favor  multiple  cerebral  hemorrhage.  Nephritis 
with  hypertrophy  of  the  left  ventricle  of  the  heart,  especially  if  uncom- 
pensated, must  be  closely  watched  as  a  particularly  influential  factor. 
Arteritis,  atheroma  of  the  arteries,  miliary  aneurisms,  and  a  fatty  con- 
dition of  the  vessels  are  all  elements  in  the  causation  of  cerebral  hem- 


THE  XOX-XEUROXIC  DISEASES  829 

orrhage.  Numerous  are  the  causes  therefore  of  arterial  disease.  This 
condition  alone,  however,  probably  never  provokes  a  hemorrhage. 
Some  sudden  strain  or  other  exciting  cause  must  usually  operate  in 
conjunction  with  the  disease  of  the  arterial  system.  Among  such  ex- 
-citing  causes,  numerous  as  they  are,  may  be  mentioned  sudden  phys- 
ical exertion,  like  running  for  a  car,  climbing  a  steep  hill  or  riding 
horseback,  sudden  anger,  violent  coitus,  cold  bathing,  coughing  as  in 
pertussis,  or  the  overloading  of  the  stomach  with  food  and  drink  and 
5training  at  stool.  I  have  seen  it  follow  a  late  hearty  supper  after 
which  the  patient  had  retired  and  gone  to  sleep.  In  these  cases  it  may 
be  true,  as  Gowers  suggests,  that  the  recumbent  posture  retards  the 
flow  of  the  blood  from  the  brain.-  Injuries  to  the  head  may  in  excep- 
iional  cases  provoke  a  cerebral  as  well  as  meningeal  hemorrhage. 

To  sum  up  then,  the  varied  etiology  of  cerebral  hemorrhage  mz.\ 
be  classified  under  the  two  great  sets  of  causes,  the  predisposing  and 
the  exciting.  The  former  include  certain  familial  and  temperamental 
traits,  certain  constitutional  cachexias  and  diseases,  and  certain  definite 
pathological  changes  in  the  walls  of  the  arteries  ;  the  latter  take  cog- 
nizance of  a  thousand  and  one  physical  and  mental  strains  and  shocks. 

Pathology  and  Pathogenesis. — The  pathology  of  cerebral 
hemorrhage  resolves  itself  entirely  into  the  disease  of  the  bloodvessels. 

Atheroma  is  the  most  common  affection  of  the  cerebral  arterial 
system.  It  aft'ects,  however,  the  larger  vessels  only  and  is  observed  in 
about  one-fifth  of  all  the  cases.  It  leads  indirectly  to  the  hemorrhage 
by  impairing  the  resiliency  of  the  vascular  walls. 

Degenerative  arteritis  leading  to  the  formation  of  niiliary  aneur- 
isms is  the  immediate  cause  of  the  majority  of  hemorrhages.  These 
minute  dilatations  measure  from  i-ioo  to  1-25  inch  (one-fourth  to  one 
millimetre)  in  diameter,  rarely  number  more  than  a  hundred,  ^nd  ap- 
pear most  numerous  on  the  arterioles  supplying  the  central  ganglia. 
There  is  some  doubt  as  to  the  exact  nature  of  their  origin.  They  are 
certainly  not  inflammatory.  Charcot  thought  they  were  associated 
with  a  periarteritis  and  were  due  to  changes  in  the  adventitia.  Later 
investigators  believed  that  the  alterations  were  in  the  intima.  The 
probability  is,  from  the  most  recent  studies,  that  the  muscular  coat  is 
the  primary  seat  of  the  disease  process.  This  atrophies  and  disinte- 
grates, ultimately  causing  the  entire  vessel  wall  to  be  degenerated  and 
excavated.  The  periarteritis  noted  by  Charcot  is  in  all  likelihood  a 
secondary  process.  These  little  fusiform  and  sacculated  bodies  are 
not  encountered  as  a  rule  prior  to  the  fortieth  year ;  after  that  they  in- 
crease in  number  with  each  advancing  year,  showing  that  they  belong 
■exclusively  to  the  degenerative  period  of  life.  They  must  not  be  con- 
fused with  simple  excavation  of  the  lymph  sheath  from  an  effusion  of 
hlood.  Arteriosclerosis  may  or  may  not  be  associated  with  them. 
AVhile  in  the  great  majority  of  cases  their  rupture  is  the  immediate 
-source  of  the  hemorrhage,  they  are  not  an  absolute  requisite  for  such 
a  disaster. 

Fatty  degeneration  of  the  walls  of  the  cerebral  arterioles  occurs 
in  marasmus,  post-infective  states,  leucocythjemia,  purpura  and  similar 
■diseases  and  is  sometimes  a  cause  of  hemonhage. 


830  THE  NON-XEURONIC  DISEASES 

Small  hemorrhages  undoubtedly  occur  sometimes  as  the  result  of 
mere  diapedesis,  the  walls  of  the  vessels  having  been  rendered  more 
permeable  in  renal  disease,  severe  anjemia,  and  various  infections  and 
intoxications. 

The  location  of  the  hemorrhage  is  a  matter  of  some  moment.  The 
most  common  is  in  and  about  the  basal  ganglia.  In  seventy-five  per 
cent,  of  all  cases  miliary  aneurisms  develop  most  profusely  upon  the 
Iciiticulo-striatc  and  leniicnlo-ophc  arteries.  After  the  middle  cere- 
bral arteries,  the  anterior  cerebral  and  posterior  cerebral  are  most 
affected. 

Twenty  per  cent,  of  all  the  hemorrhages  within  the  cranium  occur 
in  the  vicinity  of  the  corpus  striatum.  _^The  favorite  locations  in  order 
after  this  are  the  meninges  and  cortex,  optic  thalamus,  internal  and 
external  capsules,  centrum  ovale.  The  size  and  arrangement  of  the 
arteries  in  these  respective  areas  have  muc)i  to  do  in  determining  their 
relative  importance.  The  cortical  arteries,  for  instance,  are  abund- 
ant and  richly  terminated  in  a  network,  whereas  the  central  arteries 
are  pure  terminal  arteries  of  large  calibre  and  spring  from  their  parent 
stem  at  right  angles.  This  makes  a  difference  in  the  pressure  to  which 
they  are  relatively  exposed. 

The  hemorrhage  may  be  small  and  limited  to  the  striate  body  or 
internal  capsule ;  more  generall}-  it  extends,  if  large,  somewhat  into- 
the  centrum  ovale,  the  lateral  ventricle  or  the  insula.  It  is  rare  for  a 
hemorrhage  to  be  confined  to  the  centrum,  or  to  originate  in  the  ven- 
tricle. The  blood  in  ventricular  hemorrhage  may  flow  into  all  of  the 
ventricles  and  form  a  perfect  mould  of  them  This  is  the  apoplexie 
foudroyante  of  the  French  authors. 

In  ordinarv  cerebral  hemorrhage  the  clot  varies  greatly  in  size 
and  shape.  In  insular  hemorrhage  it  may  attain  the  size  of  a  man's- 
fist  and  be  irregularly  round  in  shape :  in  cortical  hemorrhage  it  may 
be  flat  and  dift\ise  though  it  is  more  often  small  and  multiple.  In  the 
various  diatheses  and  post-infectious  states  it  is  apt  to  be  small  and 
multiple.  In  a  few  days  the  clot  begins  to  soften,  changes  begin  to 
take  place  in  and  about  it,  inflammation  occurs  around  the  apoplectic 
area  and  a  wall  is  created  inclosing  it  in  a  cyst  along  about  the  twen- 
tieth or  thirtieth  day.  The  contents  of  the  cyst  undergo  further  de- 
generative changes,  a  transparent  fluid  fills  it  and  perhaps  fibrous  tra- 
beculas  run  across  it.  The  age  of  the  lesion  can  be  fairly  well  deter- 
mined by  the  decoloration  of  the  exudate,  the  swelling,  the  atrophy  of 
the  red  corpuscles  and  the  nature  of  the  pigment.  On  the  third  day 
appear  only  cells  with  blood-corpuscles.  Free  pigment  is  seen  about 
the  eighteenth  day  and  after  the  sixtieth.  It  takes  about  four  weeks 
for  the  cyst  to  form,' and  ten  days  more  for  it  to  begin  to  contract. 
Complete  cicatrization  is  rare.  Either  a  small  cyst  remains  with  semi- 
fluid contents  or  in  the  event  of  no  cyst  having  formed  the  connective 
tissue  proliferates  and  a  small  pigmented  scar  is  left. 

Secondary  degenerations  begin  about  the  tenth  or  fourteenth  day 
and  vary,  according  to  the  location  of  the  hemorrhage  and  the  particu- 
lar cells  and  their  axones  that  have  been  damaged.  In  old  hemiplegic 
cases  thev  have  been  seen  to  extend  nearlv  all  the  wav  down  the  cord. 


THE  XOX-XEUEOXIC  DISEASES  831 

Symptoms. — There  may  be  slight  premonitions  of  cerebral  hem- 
orrhage, though  as  a  rule  prodromata  are  more  common  in  embolism 
and  thrombosis.  The  patient  may  experience  a  little  dizziness,  full 
feeling  in  the  head,  headache  with  epislaxis  and  disturbed  heart  action, 
and  bad  dreams  at  night.  A  little  numbness  of  the  hand  and  foot  of  one 
side  may  be  complained  of.  All  this  is  rare,  however,  in  hemorrhage. 
As  a  rule  the  patient  is  stricken  suddenly  while  he  is  at  his  usual  avoca- 
tions or  after  some  unwonted  mental  or  physical  strain.  The  stroke 
having  occurred,  its  symptomatology  ma}'  be  conveniently  studied 
under  two  groups  of  phenomena — namely,  those  of  the  actual  apoplectic 
insult  and  those  of  the  resulting  paralysis.  Usually  suddenly,  some- 
times gradually,  the  patient  is  rendered  unconscious.  He  falls  or  is 
caught  in  time  to  be  assisted  to  a  couch.  The  coma  is  in  a  fcAv  minutes 
profound  and  the  patient  resembles  an  individual  in  the  deepest  slum- 
ber. He  cannot  be  aroused.  His  breathing  is  heav}-  and  slow.  The 
cheeks  puff  in  and  out  with  the  respirations.  The  latter  are  noisv  and 
stertorous  and  may  even  assume  the  Cheyne-Stokes  character.  The 
chest  movements  are  restricted,  especially  on  the  side  that  is  paralyzed. 
The  face  appears  flushed,  sometimes  cyanotic.  The  pupils  are  dilated 
and  unequal  and  in  the  coma  irresponsive  to  light.  The  limbs  are  limp 
and  dead.  If  they  are  slightly  raised  and  then  released,  it  will  be 
noticed  that  they  fall  heavily  on  the  paralyzed  side,  but  somewhat  more 
slowly  on  the  opposite  side.  The  paralysis  is  positively  flaccid  and  the 
deep  reflexes  are  absent,  as  w^ell  as  the  cutaneous  peripheral  reflexes. 
In  most  cases,  especially  the  foudoyant  apoplexies,  the  coma  pre- 
cedes the  paralysis.  In  other  cases  the  gradual  approach  of  the  paraly- 
sis is  accompanied  a  little  later  by  unconsciousness.  In  rare  instances 
there  may  be  little  or  no  unconsciousness  or  the  patient  may  awake 
from  a  nap  to  find  himself  hemiplegic.  Swallowing  is  not  performed 
in  the  comatose  stage  and  is  extremely  difficult  even  after  the  return  of 
consciousness.  Involuntary  micturition  and  evacuation  of  the  bowels 
sometimes  occur  in  the  coma.  The  piilse  is  generally  tense,  full  and 
slow.  The  temperature  is  normal  or  subnormal.  The  head  and  eyes 
are  strongly  turned  toward  the  side  of  the  lesion.  In  some  cases  gen- 
eralized convulsive  movements  occur.  Gradually  in  the  course  of  a  few 
hours,  or  even  sooner,  the  coma  wears  away,  the  patient  opens  his 
eyes,  tries  to  speak,  and  exhibits  emotion  upon  the  realization  that  he 
is  paralyzed.  Such  in  brief  is  the  clinical  picture  of  the  average  stroke 
of  apoplexy.     Some  of  its  details  are  deserving  of  further  discussion. 

As  I  have  already  intimated,  the  sudden  unconsciousness  is  th*e 
most  striking  feature.  Its  association  with  the  paralysis  makes  it 
pathognomonic  of  cerebral  hemorrhage.  It  varies  in  depth  and  dura- 
tion and  bears  no  proportional  relationship  to  the  paralysis.  It  may  be 
very  slight,  while  the  latter  is  severe.  Its  onset  is  often  immediately 
preceded  bv  intense  vertigo,  headache,  fullness  of  the  head  and  blurring 
of  the  vision.  Things  swim  before  the  eyes  and  the  world  seems  to  be 
going  topsv-turv\-.  It  usually  lasts  from  a  few  minutes  to  a  few  hours. 
The  "restoration  to  consciousness  is  more  or  less  rapid  and  complete, 
though  a  state  of  somnolence  may  follow  for  some  time.  The  coma 
is  beheved  to  be  due  to  the  sudden  disturbance  of     the     circulation, 


832  THE   NOX-XEUKOXIC  DISEASES 

(anaemia)  and  to  the  molecular  concussion  throughout  the  entire  brain, 
provoked  by  the  abrupt  outpouring  of  the  blood. 

The  paralysis,  like  the  coma,  varies  in  different  patients  according 
to  the  extent,  location  and  rapidity  of  the  hemorrhage.  It  is  always 
of  the  hcmiplegic  or  facio-hrachio-crural  type  and  is  on  the  opposite 
side  of  the  body  from  that  of  the  hemorrhage.  It  involves  most  the 
finer  complicated  movements,  hence  the  hand  and  arm  are  more  affected 
than  the  foot  and  leg,  and  both  extremities  more  than  the  face.  Mus- 
cles that  have  a  bilateral  representation  in  the  brain  and  work  on  both 
sides  of  the  body  in  unison  are  but  little  affected ;  hence  the  respiratory 
muscles,  those  of  the  abdomen  and  of  the  eyes  soon  recover  from  the 
first  shock.  Dysarthria  may  occur  from  the  implication  of  the  finer 
movements  of  tlie  muscles  of  articulation.  This  must  be  carefully  dis- 
tinguished from  the  aphasia  that  occurs  in  right-sided  hemiplegia. 
The  lower  part  of  the  face  is  always  more  involved  than  the  upper,  a 
differential  indication  of  facial  palsy  of  central  origin.  The  face  is 
asymmetrical,  the  corner  of  the  mouth  droops,  the  naso-labial  crease  is 
obliterated  and  the  saliva  oozes  out  on  the  paralyzed  side.  Deglutition 
is  difficult.    The  laryngeal  muscles  are  not  particularly  involved. 

\Y\t\\  the  onset  of  the  coma  the  temperature  usually  falls  one  or 
two  degrees.  In  a  few  hours  it  rises  to  normal  or  even  passes  the  nor- 
mal point.  On  the  paralyzed  side  the  temperature  is  usually  higher 
than  on  the  other  side.  If  the  temperature  remains  subnormal,  or,  on 
the  other  hand,  if  it  takes  a  rapid  rise  to  102  degrees  or  103  degrees  F., 
the  coma  continuing,  death  is  near  at  hand.  Just  before  the  fatal  issue 
the  temperature  may  sink  again. 

Vomiting  occurs  in  cerebellar  hemorrhage,  but  very  rarely  in 
cerebral  hemorrhage. 

The  conjugate  deviation  of  the  head  and  eyes  in  the  majority  of 
cases  is  toward  the  side  of  the  hemorrhage.  In  other  words,  the  patient 
seems  to  stare  in  the  direction  of  the  lesion.  In  exceptional  cases,  es- 
pecially when  there  are  unilateral  convulsions  or  spasms,  or  when  early 
rigidity  occurs,  the  conjugate  deviation  of  the  head  and  eyes  may  be 
away  from  the  lesion  and  toward  the  paralyzed  side,  or  more  accurate- 
ly, convulsed  side.  As  a  rule  this  symptom  disappears  with  the  wear- 
ing away  of  the  coma. 

For  the  first  day  or  so  the  amount  of  urine  passed  may  be  larger 
than  normal  and  it  may  contain  albtimin  and  sugar. 

The  sequence  of  events  in  and  immediately  after  the  stage  of  seiz- 
ure varies  considerably  in  different  individuals  and  depends  upon  the 
extent  and  severit}'  of  the  hemorrhage.  In  a  few  rapidly  fatal  cases, 
especially  when  the  blood  has  broken  into  the  ventricles,  the  patient 
fails  to  emerge  from  the  coma,  the  respiration  assumes  the  Cheyne- 
Stokes  character,  the  temperature  ascends  to  103  degrees  F.  or  higher, 
the  pulse  beats  violently  and  the  patient  dies  in  a  day  or  two  wnth 
hypostatic  pneumonia.  In  another  class  of  cases,  fatal  but  more  tardily 
so,  consciousness  returns  partially,  mild  delirium  occurs,  with  head- 
ache, restlessness  and  anxiety.  With  the  reaction  period  setting  in  in 
about  forty-eight  hours  and  continuing  for  a  week  or  more,  the  tem- 
perature, after  remaining  normal   for  a  time,  rises,   and  pneumonia 


THE  NON-XEURONIC  DISEASES  833 

develops  and  kills  the  patient  in  a  state  of  unconsciousness.  These 
cases  may  last  even  as  long  as  two  months.  F.arly  ngidity  develops  in 
their  paralyzed  limbs,  serious  trophic  changes  occur,  such  as  sloughing 
and  vesicular  formations,  and  perhaps  the  congestion  at  the  bases  of 
the  lungs.  In  the  favorable  cases,  which  happily  constitute  the  larger 
number,  the  initial  coma  disappears  in  a  few  hours,  leaving  the  mind 
entirely  unaffected,  or  at  the  worst  only  weak  and  confused.  The 
deviation  of  the  eyes  and  the  temporar}'  ptosis  pass  away  with  the 
coma,  the  sound  side  of  the  body  resumes  its  proper  activity,  the 
paralyzed  side  shows  a  slight  tendency  toAvard  rigidity  with  return  or 
even  slight  increase  of  the  deep  reflexes,  the  temperature,  the  pupils  and 
respirations  return  to  their  normal  condition.  A  slight  febrile  reaction 
with  some  temporary  constitutional  disturbance  accompanying  the  in- 
flammatory changes  in  the  apoplectic  area,  and  the  absorption  of  the 
blood  may  occur  in  a  week  or  so  and  then  pass  away,  leaving  as  the 
prominent  and  almost  sole  constituent  of  the  clinical  picture  the  hemi- 
plegia with  aphasia  when  it  is  on  the  right  side  in  right-handed  individ- 
uals, or  without  aphasia  when  it  is  on  the  left  side. 

Complete  hemiplegia  is  of  the  facio-brachio-crural  type  and  in- 
volves the  arm  more  than  the  leg,  and  the  leg  more  than  the  face.  In 
partial  hemiplegia  any  one  of  these  members  may  be  the  seat  of  the 
paralysis.  So  dominant  and  all-engrossing  is  this  one  symptom  of  this 
so-called  chronic  stage  of  the  disease,  that  the  patient  is  in  common 
parlance  referred  to  as  a  "hemiplegic."  He  enters  upon  this  role 
usually  about  a  month  after  the  stroke  and  when  all  of  the  other  symp- 
toms have  vanished  or  diminished  to  such  a  degree  as  to  be  quite  un- 
noticeable. 

It  is  usually  stated  that  the  ends  of  the  extremities  are  more  dis- 
tinctly aft'ected  with  paralysis  than  are  the  segments  nearer  the  trunk. 
The  difference  is  only  apparent,  however,  because  in  this  as  in  all 
cerebral  palsies  the  more  the  movements  are  complicated  and  the  more 
the}'-  are  related  to  the  higher  intelligence  normally,  the  more  they  are 
affected  when  paralyzed.  The  loss  of  power  moreover  involves  seg- 
ments of  the  body  rather  than  individual  muscles ;  movements  rather 
than  special  anatomical  structures  merely. 

A'lovements  that  normally  depend  upon  muscles  that  act  bilaterally, 
such  as  those  of  respiration,  phonation  and  facial  expression,  are  but 
slightly,  if  at  all,  affected.  Each  side  here  is  probably  better  repre- 
sented bilaterally  in  the  brain  than  are  the  movements  of  the  arms 
and  legs.  That  there  is  some  bilateral  representation  of  the  latter  in 
the  cortex  is  shown  by  their  tendency  to  act  together  in  untrained  nor- 
mal individuals,  and  by  the  fact  that  even  in  true  hemiplegia  some 
weakness  is  observed  on  the  sound  side.  The  movements  of  the  lower 
part  of  the  face,  as  in  all  central  facial  palsies,  are  more  involved  than 
those  of  the  upper  part.  The  frontal  muscles  and  the  orbiculares  palpe- 
brarum continue  to  act,  while  the  cheek,  the  side  of  the  nose  and  the 
corner  of  the  mouth  are  almost  or  quite  immovable.  The  tongue  is  pro- 
truded towards  the  paralyzed  side  because  the  involvement  of  the  mus- 
cle on  that  side  of  it  leaves  the  muscle  of  the  other  side  without  its  noi-- 


834  THE   XON-XEURONIC  DISEASES 

nial  opposition.     The  soft  palate  may  be  slightly  pendant,  but  the  mus- 
cles of  deglutition  are  not  seriously  involved. 

On  account  of  the  paralysis  of  the  tongue,  lips,  cheek,  etc.,  there 
is  a  true  paralytic  dysarthria,  which  must  not  be  confused  with  the 
disturbance  of  speech  known  as  aphasia.  I  have  seen  such  an  error 
made.  In  aphasia  wrong  words  or  no  words  at  all  are  uttered  ;  the 
few  that  may  be  employed  are  not  affected  in  any  way  by  articulation ; 
the  trouble  is  one  of  psychic  origin  rather  than  of  mere  muscular  in- 
efficiency. On  the  other  hand,  in  paralytic  dysarthria  there  is  no  lack 
of  W'Ords  and  speech,  no  utterance  of  wrong  words,  but  rather  a  bad 
and  inefficient  articulation  of  them.  The  trapezius  is  liable  to  be 
included  in  the  paralysis.  Certain  automatic  movements,  like  crying 
and  laughing,  are  usually  performed  when  the  face  cannot  be  moved 
voluntarily. 

The  paralysis  in  the  limbs  may  be  partial  or  couiplcte.  In  the  for- 
mer condition  a  slight  degree  of  activity  in  certain  directions  is  re- 
tained. The  fingers  in  a  few  days  or  weeks  can  be  slowly  and  partially 
flexed ;  the  arm  can  be  slightly  bent  at  the  elbow ;  and  the  whole 
extremity  can  be  drawn  over  towards  the  body.  The  movements  are 
all  feeble  and  sluggish,  however,  and  performed  clearly  with  a  heroic 
efifort.  The  flexors,  as  a  rule,  show  more  of  a  tendency  to  recover  than 
do  the  extensors.  A  great  number  of  variations  obtain  in  regard  to  the 
distribution  of  the  paralysis.  As  a  rule  the  leg  recovers  much  more 
than  the  arm  and  nearly  always  so  much  that  walking  after  a  fashion 
is  possible.  In  many  cases  only  the  face  and  arm  remain  paralyzed. 
In  others  the  face  recovers  and  the  arm  remains  paralyzed  more  than 
the  leg.  It  is  very  rare  for  the  face  and  arm  to  escape  or  recover 
while  the  leg  alone  remains  involved.  In  mild  cases  many  kinds  of 
coarse  work  can  be  done  with  the  hemiplegic  hand  and  arm ;  usually 
the  finer  kinds  of  work  requiring  nice  adjustment  and  coordination, 
such  as  w-riting,  pla3dng  upon  musical  instruments,  etc.,  are  impossible 
or  extremely  difficult.  It  is  rare  for  these  finer  movements  ever  to 
become  possible  again  unless  the  case  has  been  unusually  mild  and  a 
complete  recovery  obtained.  The  inability  to  write  must  be  carefully 
examined  in  some  cases  so  as  not  to  be  confused  with  agraphia.  The 
distinction  is  usually  easily  made  and  demands  only  a  little  ingenuity  in 
applying  the  proper  tests. 

The  gait  of  the  hemiplegic  is  characteristic  and  is  to  be  carefully 
differentiated  from  that  of  the  ataxic  and  spastic  paralytic.  It  depends 
upon  the  motor  paralysis,  the  slight  rigidity  or  contracture  and  the 
slight  weakness  and  wasting  of  the  muscles.  In  severe  cases  it  is 
typical.  The  support  of  the  body  is  placed  w^ell  upon  the  sound  limb ; 
the  paralyzed  member,  slightly  rigid  and  even  contractured  in  old  cases, 
is  dragged  forward  in  a  sort  of  a  half-circle  around  the  sound  member 
as  an  axis,  the  pelvis  drawn  up  a  trifle  on  the  affected  side  and  the  foot 
planted  forward  upon  the  entire  sole  without  the  toes  having  once  been 
clearly  lifted  from  off  the  floor.  The  simple  manoeuvre  of  stepping 
sidewise  w^ill  usually  discover  the  hemiplegic  side  in  those  verv  slight 
cases,  as  in  some  instances  of  senile  hemiplegia,  in  which  the  gait  is  not 
very  obviously  altered. 


TtiE  NON-NEURONIC  DISEASES  835 

After  the  first  few  weeks  the  paralysis  assumes  the  spastic  type. 
In  rare  and  unaccountable  cases  it  may  remain  flaccid  throughout. 
From  being  absent  during  the  comatose  stage,  the  reflexes  become 
normal  and  ultimately  exaggerated.  Even  ankle-clonus  may  be  present. 
Sometimes  the  exaggeration  of  the  reflexes  is  bilateral,  though  it  is 
always  more  exaggerated  on  the  paralyzed  than  on  the  well  side.  The 
superficial  reflexes  usually  recover  in  part,  though  they  are  always 
more  or  less  diminished.  The  electrical  reactions  are  normal ;  and 
there  is  no  true  muscular  atrophy,  only  a  slight  wasting  from  non-use. 
An  early  rigidity  appears  in  the  muscles  during  the  reaction  period.  A 
late  rigidity  with  contracture  and  deformity  appears  as  the  accom- 
paniment of  the  secondary  degenerative  sclerosis  in  the  pyramidal 
tracts.  These  late  contractures  affect  the  hand  and  arm  more  than  the 
leg,  are  somewhat  painful  and  remain  permanently.  As  a  result  the 
elbow  is  partially  flexed  and  the  fingers  bent.  I  have  seen  during  the 
development  of  this  late  rigidity  violent  muscular  spasm  or  cramp 
with  most  excruciating  pains.  In  a  few  instances  there  has  been  no 
rigidity  or  contracture,  but  tremor,  post-paralytic  chorea,  athetosis, 
arthropathy  and  even  muscular  atrophy  have  been  observed  on  the 
hemiplegic  side. 

The  sensory  phenomena  of  cerebral  hemorrhage  and  hemiplegia 
are  not  in  any  way  pathognomonic.  H eniiancesthesia  may  occur  with 
the  paralysis  if  the  posterior  part  of  the  internal  capsule  is  injured. 
This,  however,  is  rarely  total.  Usually  it  passes  off  quickly  and  leaves 
only  a  partial  anaesthesia  or  rather  hypsesthesia  in  various  parts  of  the 
affected  side.  Much  more  common  are  the  various  parassthesise,  show- 
ing irritation  of  the  sensory  tracts  or  cortex.  Pain  is  often  com- 
plained of,  especially  of  a  burning  character,  about  the  articulations. 
Numbness  is  the  more  common  form  of  parsesthesia  spoken  of.  The 
special  senses  as  a  rule  escape  all  involvement.  Occasionally,  how- 
ever, hemiopia  on  the  side  of  the  lesion  has  been  noted  and  the  taste, 
smell  and  hearing  have  been  blunted.  According  to  Gowers,  hom- 
onymous hemianopsia  of  the  half-fields  opposite  the  lesion  is  more 
frequent  than  reports  would  seem  to  indicate.  If  the  examiner  sud- 
denly brings  the  finger  before  the  eye  in  the  early  stage  of  the  trouble, 
first  from  one  side  and  then  from  the  other,  it  will  be  noticed  that  the 
eyelids  blink  when  the  finger  comes  from  the  unparalyzed  side,  but 
not  when  it  approaches  from  the  other  side. 

Trophic  manifestations  often  show  themselves  early,  within  the 
first  five  or  six  weeks,  in  severe  cases.  The  joints  become  inflamed 
and  acute  decubitus  develops  on  the  paralyzed  side  of  the  gluteal  re- 
gion. Sloughing  in  the  lower  part  of  the  back,  which  may  come  on 
as  early  as  forty-eight  hours  after  the  stroke,  is  a  very  unfortunate 
event.  It  usually  means  death.  A  flushing  occurs  first,  according  to 
Charcot,  then  a  violet  discoloration,  vesicles,  ulceration  and  finally  an 
eschar.  The  hypostatic  pneumonia  which  sometimes  occurs  is  be- 
lieved by  some  to  be  a  trophic  phenomenon.  The  same  may  be  said 
of  the  gastric  hemorrhages.  Hyperidrosis,  cutaneous  eruptions  and 
increased   erowth  of  hair  have  been   observed  in  rare  instances.      I 


836  THE   XOX-XEUROXIC  DISEASES 

have  often  noted  the  glossy  appearance  and  cool  character  of  the  skin 
in  the  paralyzed  limbs. 

Rare  but  interesting  are  the  ataxic  hciiiiplcgias.  Here  the  hem- 
orrhage has  confined  itself  to  the  area  of  the  sensory  tract  and  the 
ataxia  results  from  the  complete  hemiansesthesia.  The  hemiplegia  in 
such  instances  may  be  absent  entirely  or  only  transient.  Honiataxia, 
of  course,  is  the  true  character  of  the  trouble  and  its  one-sidedness 
readily  distinguishes  it  from  all  other  forms  of  ataxia. 

It  would  be  extraordinary  if  so  profound  a  shock  as  cerebral  hem- 
orrhage induces  did  not  affect  the  mind  somewhat.  The  aphasia,  early 
stupor,  delirium  and  somnolence  are  all  partly  in  the  psychic  sphere. 
Irritability,  emotionalism,  failure  of  memory  are  some  of  the  more 
specific  mental  disturbances  that  occur  in  the  older  victims  of  the  dis- 
ease. Marked  mental  deterioration,  irritative  epilepsy  and  terminal 
insanity  have  been  known  to  follow-  cerebral  hemorrhage,  especially  one 
of  large  degree.  It  is  to  be  remembered  that  mentalization  is  sub- 
served by  language  and  that  when  aphasia  is  of  long  duration  the  want 
of  speech  may  well  react  upon  the  mental  faculties  and  cause  them  to 
deteriorate.  The  mere  realization  of  the  fact  that  the  paralysis  is  per- 
manent and  that  the  apoplectic  danger,  as  shown  by  the  present  attack, 
hangs  like  the  sword  of  Damocles  constantly  over  the  patient's  head, 
has  its  influence  in  depressing  the  mental  forces. 

The  discussion  of  the  symptomatology  of  other  than  cerebral 
forms  of  intracranial  hemorrhage  will  be  taken  up  when  the  diseases 
of  the  meninges,  pons,  medulla,  etc.,  are  considered.  A  word  should 
be  spoken  here,  however,  in  regard  to  ventricular  hemorrhage.  As  a 
primary  condition  it  is  exceedingly  rare.  Usually  the  blood  enters 
the  ventricles  by  extravasation  from  neighboring  parts  of  the  brain  or 
bursts  into  them  suddenly  in  the  course  of  an  ordinary  apoplexy.  The 
symptoms  are  always  under  such  circumstances  serious  and  profound. 
The  coma  deepens,  or  if  it  had  begun  to  clear  up,  it  abruptly  returns 
and  is  more  profound  than  it  w'as  before.  Convulsions  sweep  over 
all  four  extremities,  followed  by  complete  paralysis.  The  muscles  are 
rigid  on  the  hemiplegic  side,  or  in  all  four  members.  The  pulse  is 
retarded,  respiration  is  extremely  embarrassed,  the  temperature  is  de- 
creased and  just  before  death,  which  usually  takes  place  inside  of 
twenty-four  hours,  the  eyes  become  fixed  and  staring,  the  pupils  dilated 
and  the  general  appearance  of  cyanosis  and  asphyxia  occurs. 

Diagnosis. — The  physician  is  rarely  confronted  with  a  more  im- 
portant problem  and  one  that  makes  larger  demands  upon  his  knowl- 
edge and  judgment,  than  when  he  is  called  upon  to  make  a  diagnosis 
in  an  apoplectic  stroke.  The  proper  management  of  the  case  depends 
at  first  almost  entirely  upon  whether  the  stroke  is  due  to  hemorrhage, 
embolism  or  thrombotic  obstruction.  Moreover,  the  coma  and  other 
s3'mptoms  of  the  first  stage  are  simulated  by  a  number  of  other  dis- 
eases that  are  not  apoplectic.  And  finally  there  are  dift'erent  degrees 
among  the  cerebral  hemorrhages  themselves  that  must  be  differen- 
tiated if  possible  in  order  to  form  some  opinion  in  regard  to  the  prob- 
able ultimate  outcome. 

While  all  these  questions  and  distinctions  are  at  times  hard  to 


THE  NON-NEURONIC  DISEASES  837 

settle,  owing  to  the  multiplicity,  variety  and  great  differences  in  the 
individual  symptoms  of  cerebral  hemorrhage,  there  is  a  uniformity  and 
consistency  generally  about  the  clinical  picture  that,  when  studied  in 
toto,  help  very  materially  towards  the  establishment  of  the  diagnosis. 
Coma  and  paralysis  are  the  two  guiding  posts  that  always  point  unerr- 
ingly to  a  serious  intracranial  lesion.  The  approach  of,  the  character 
of  and  the  associated  manifestations  surrounding  the  coma  and  the 
paralysis  are  the  chief  means  by  which  we  must  determine  the  nature 
of  the  lesion  producing  them.  In  hemorrhage  the  onset  is  sudden 
or  with  very  slight  prodromes,  and  the  maximum  is  attained  almost 
immediately.  The  coma  is  usually  deep  and  precedes  the  paralysis. 
The  latter  at  first  seems  to  involve  all  the  limbs,  but  soon  recedes  from 
one  side.  The  face,  arm  and  leg  of  the  hemiplegic  side  are  implicated. 
The  paralysis  is  flaccid  and  complete  from  the  start  and  is  only  rarely 
preceded  by  convulsive  movements.  The  pupils,  contracted  at  first, 
soon  become  dilated,  unequal  and  irresponsive  to  light.  The  flushed 
countenance,  puffing  cheek,  labored  stertorous  breathing,  rapid  pulse, 
early  subnormal  temperature  and  occasional  involuntary  micturition 
and  evacuation  of  the  bowels  are  contributing  signs  to  the  completing 
of  the  clinical  picture  of  cerebral  hemorrhage. 

The  cases  of  cerebral  hemorrhage  that  develop  slowly,  taking  a  day 
or  two  for  the  attainment  of  their  maximum  degree  of  coma  and 
paralysis,  may  be  mistaken  for  thrombosis,  especially  in  the  aged  with 
atheromatous  arteries.  So  common  is  this  error  in  diagnosis  that  I 
am  confident  the  relative  proportion  of  cases  of  hemorrhage  has  been 
greatly  exaggerated  in  the  reports.  A  large  number  of  them  have  been 
cases  of  thrombosis.  Admitting  the  occasional  difficulty  encountered 
in  making  the  differentiation,  a  closer  attention  to  the  course  of  the 
disease  and  the  changes  exhibited  by  the  individual  symptoms  will 
render  such  errors  less  frequent. 

There  is  a  group  of  cases,  usually  seen  for  the  first  time  when 
they  are  comatose,  in  which  the  coma  comes  on  rapidly  rather  than 
abruptly  and  the  paralysis  is  not  as  profound  as  in  many  other  cases. 
Or  the  loss  of  power  develops  in  the  course  of  a  few  hours  and  is 
followed  by  a  gradual  loss  of  consciousness.  These  so-called  ingraves- 
cent cases  cannot  be  distinguished  usually  from  cases  of  embolism  or 
thrombosis  unless  there  are  some  very  suggestive  circumstances  in 
connection  with  the  age  of  the  patient,  his  constitutional  diseases  and 
the  immediate  cause  of  the  stroke.  Even  then  the  diagnosis  falls  short 
of  being  positive. 

The  typical  cases  of  cerebral  hemorrhage  that  come  on  abruptly 
and  are  in  a  state  of  profound  coma  and  paralysis  must  be  differentiat- 
ed from  the  coma  of  ureemia,  alcoholism,  opium  poisoning,  diabetes  and 
syncope.     Epilepsy  and  hysteria  must  be  excluded  also. 

In  urmnic  coma  there  is  no  hemiplegia  and  the  pupils  are  not 
unequal.  The  coma  comes  on  gradually  or  less  suddenly  than  it  does 
in  hemorrhage  and  is  usually  preceded  by  blindness,  convulsions  and 
vomiting.  The  temperature  is  below  normal  always.  A  chemical  and 
microscopic  examination  of  the  urine  and  the  existence  of  albuminuric 
retinitis,  with  the  peculiar  physiognomy   that  accompanies  nephritis, 


838  THE   XOX-XEUROXIC  DISEASES 

would,  of  course,  determine  the  diagnosis.  In  diabetic  coma  the  breath 
may  exhale  the  odor  of  acetone.  Urinalysis  here  will  also  establish  the 
nature  of  the  disease. 

Sczrrc  alcoholism  is  not  infrequently  confounded  with  hem- 
orrhagic apoplexy,  as  the  records  of  some  of  the  police  stations  will 
amply  prove.  The  odor  of  the  breath  cannot  be  taken  as  a  criterion, 
for  the  patient  may  have  felt  the  apoplex}-  coming  on  and  taken  the 
stimulant  to  ward  off  the  sudden  weakness  or  vertigo.  In  alcoholism 
the  coma  is  incomplete,  the  pupils  are  equal,  the  limbs  show  no  ten- 
dency to  a  hemiplegic  condition,  the  temperature  is  not  lowered  and 
there  are  some  manifestations  of  delirium.  The  examination  of  the 
contents  of  the  stomach,  as  the  patient  usually  vomits,  will  strongly 
suggest  the  length  of  time  the  alcohol  has  been  ingested. 

In  opium  poisoning  the  pupils  are  equal  and  strongly  contracted, 
the  respirations  are  slow  and  there  is  no  true  paralysis. 

Epileptic  attacks  are  preceded  by  a  cry.  The  pupils  are  equal 
and  dilated,  the  tongxie  is  serrated,  the  teeth  are  clenched,  and  instead 
of  paralysis  the  muscles  are  in  a  state  of  convulsion.  Consciousness 
returns  rapidly,  to  be  followed  by  headache  and  drowsiness. 

Hysteria  is  so  purely  psychic  that  one  wonders  how  the  mistake 
can  ever  be  made  between  it  and  the  coma  of  cerebral  hemorrhage. 
The  stigmata  of  hysteria,  such  as  the  anaesthesias,  will  always  be  dis- 
covered if  sought  for  in  cases  of  hysterical  hemiplegia. 

Syncope  is  not  characterized  by  complete  coma.  It  depends  upon 
an  impaired  heart  action  and  therefore  leads  one  to  examine  care- 
fully the  pulse,  the  general  hue  of  the  patient  and  the  heart.  Moreover, 
syncope  is  of  short  duration  and  is  not  accompanied  by  any  paralytic 
symptoms. 

In  general  paresis  apoplectiform  seizures  are  not  uncommon.  The 
history  of  preceding  mental  symptoms,  headache,  elevation  of  tem- 
perature and  preservation  of  the  reflexes  are  usually  enough  to  indicate 
the  presence  of  encephalitis. 

Perhaps  the  greatest  difficulty  in  the  dififerential  diagnosis  of 
cerebral  hemorrhage  is  when  an  attempt  is  made  to  distinguish  it 
from  an  embolic  or  thrombotic  apoplexy.  In  some  cases  the  differen- 
tiation is  absolutely  impossible.  The  history  of  the  case,  its  mode  of 
onset  and  its  associated  conditions  are  most  important. 

Cerebral  embolism  occurs  earlier  in  life  than  hemorrhage.  The 
age  of  forty  is  approximately  the  period  before  and  after  which  occur 
respectively  embolism  and  hemorrhage.  Embolism  is  usually  asso- 
ciated with  heart  disease,  rheumatism,  syphilis  or  the  puerperium. 
Prodromes  sometimes,  but  rarely,  precede  the  apoplectic  stroke.  The 
coma  comes  on  gradually,  is  less  deep  than  it  is  in  hemorrhage  and  as 
a  rule  follows  the  appearance  of  the  hemiplegia.  The  pulse  and  heart 
action  in  embolism  are  weak,  in  hemorrhage  they  are  strong  and  vio- 
lent. The  face  is  not  flushed,  the  temperature  is  not  disturbed,  nor  is 
the  coma  so  prolonged  as  in  hemorrhage.  The  paralysis  comes  on  more 
gradually,  is  less  complete,  is  associated  with  convulsive  movements, 
and  is  more  rigid  and  less  widelv  distributed  in  embolic  obstruction 


THE   NON-NEURONIC  DISEASES  839 

than  in  hemorrhagic  apoplexy.  Infarcts  in  remote  organs  and  repeti- 
tions of  the  stroke  indicate  embolus. 

It  is  much  more  difficult  to  differentiate  hemorrhage  from  throm- 
bosis, particularly  as  both  occur  in  old  age  and  are  dependent  upon 
similar  diseased  states  of  the  blood  vessels.  Prodromata,  often  for 
days  and  weeks,  precede  the  coma,  which  is  apt  to  be  slight  in  degree 
and  short  of  duration.  The  succession  of  slight  spells  of  semi-con- 
sciousness, the  irritability,  the  parsesthesise,  the  general  asthenia,  the 
muscular  twitchings  of  thrombosis  I  have  seen  diagnosed  and  treated 
as  hysterical.  In  thrombosis  there  is  psychic  weakness,  hardness  of 
the  arteries,  evidences  of  a  fatty  heart,  and  absence  of  stertorous 
breathings,  flushed  face,  temperature  phenomena  and  convulsive  move- 
ments of  large  amplitude. 

Prognosis. — The  prognosis  of  cerebral  hemorrhage  should  al- 
ways be  guarded,  especially  in  the  comatose  stage  and  until  after  the 
period  of  febrile  reaction.  The  size  of  the  hemorrhage,  its  location  and 
the  duration  of  the  coma  all  determine  the  future  outlook.  If  the  coma 
is  profound  and  prolonged  three  or  four  days,  if  it  is  initiated  with  a 
subnormal  temperature  or  accompanied  by  an  excessive  rise  of  tem- 
perature, if  decubitus  or  pneumonia  appears,  or  if  delirium  develops 
and  continues,  the  outlook  is  bad. 

Ingravescent  apoplexy  with  its  progressive  somnolence  passing 
into  deep  coma  is  usually  fatal. 

Signs  of  nephritis,  Cheyne-Stokes  breathing  and  symptoms  of 
rupture  into  the  ventricles  are  all  bad  indications.  A  history  of  alcohol- 
ism adds  to  the  gravity  of  the  prognosis.  Death  under  these  circuni- 
stances  may  occur  anywhere  from  a  few  hours  to  a  few  days  after  the 
stroke. 

The  larger  number  of  cases  of  cerebral  hemorrhage  usually  re- 
cover, in  part  at  least,  from  their  first  attack.  In  a  few  years,  three 
TO  five,  they  have  another  attack,  from  which  they  die  or  recover  with 
(Ufficulty  and  more  serious  residua.  Rarely  do  they  have  a  third  or 
fourth  stroke. 

A  favorable  prognosis  may  be  held  out  if  the  coma  clears  up  early 
and  at  the  end  of  the  first  week  there  has  been  no  fever  or  only  a  slight 
rise  of  temperature  and  none  of  the  ill  omens  referred  to  above. 

Complete  recovery  is  rare,  though  improvement  may  continue  for 
two  years. 

A  hemiplegia  that  remains  the  same  for  one  month  can  hardly 
le  expected  to  improve  very  much.  After  a  year  no  further  change 
can  be  hoped  for  in  the  great  majority  of  cases.  If  a  return  of  move- 
ment shows  itself  within  a  few  days  after  the  stroke,  and  continues, 
the  outlook  for  recovery  from  the  paralysis  is  particularly  bright. 

Hemiplegic  aphasia  dependent  upon  hemorrhage  usually  disap- 
pears sooner  or  later.  Partial  aphasia,  however,  ma}^  remain  perma- 
nently. Initial  hemianopsia  as  a  rule  disappears  after  a  few  days.  If  it 
does  not  it  may  be  looked  upon  as  permanent. 

The  power  of  walking  is  acquired  at  various  periods  in  different 
cases.  In  some  cases  only  a  few  weeks  or  even  days  intervene  between 
the  stroke  and  the  time  when  the  patient  begins  moving  about.     In  the 


840  THE   XOX-NEURONIC  DISEASES 

majority  of  cases,  however,  walking  is  not  commenced  for  three  or  four 
month.s  after  the  stroke.  The  gait  at  the  end  of  a  year  is  apt  to  be  the 
permanent  one  thereafter. 

Treatment. — As  the  management  of  apoplexy,  and  especially  of 
the  hemiplegia  that  follows  it,  is  in  the  main  the  same  for  all  forms, 
I  will  treat  of  it  here  in  detail  and  merely  refer  to  the  differences  in 
the  treatment  of  embolic  and  thrombotic  apoplexy  in  the  next  section 
headed  cerebral  softening. 

The  dissimilar  modes  of  first  handling  the  patient  demanded  in 
cerebral  hemorrhage  and  embolic  obstruction  enhance  a  hundred- fold 
the  need  of  care  in  diagnosing  the  nature  of  the  lesion.  A  misjudg- 
ment  in  the  arrangement  of  the  position  of  the  patient  may  mean  death 
instead  of  life.  The  administration  of  a  heart  stimulant  in  place  of  a 
sedative  may  bring  the  case  promptly  to  a  fatal  issue.  An  unwise 
attempt  to  evacuate  a  full  stomach  may  provoke  a  renewal  of  the 
hemorrhage.  A  simple  venesection  may  hasten  or  retard  the  end. 
.Ml  tliese  points  must  be  quickly  and  seriously  considered,  usually  in 
the  presence  of  the  patient,  who  will  be  found  surrounded  by  terrified 
and  clamorous  friends. 

In  considering  the  general  treatment  of  apoplexy  most  authors 
begin  by  dividing  the  subject  into  the  prophylactic  treatment  and  the 
management  of  the  attack  and  its  sequelae.  It  had  been  better,  it  seems 
to  me,  if  the  emphasis  had  been  laid  more  upon  the  treatment  of  the 
respective  conditions  of  hemorrhage  and  embolism.  In  the  main 
the  prophylaxis  is  about  the  same  for  both. 

A  quiet  life,  both  physically  and  mentally,  is  a  desideratum.  The 
digestive  and  nutritive  organs  should  be  relieved  of  strain  and  encour- 
aged to  functionate  normally.  The  emunctories  should  all  be  kept 
active  to  rid  the  system  of  deleterious  substances.  Sleep  should  be  se- 
cured. Mental  and  physical  activity  should  be  evenly  balanced.  In  a 
word,  the  threatened  victim  should  be  induced  to  lead  a  life  of  mild 
and  even  tenor,  devoid  of  anxiety  and  brightened  by  as  much  happi- 
ness as  possible.  Beyond  this  little  can  be  offered  in  the  w^ay  of  advice 
against  an  attack  of  hemorrhage  or  embolism. 

It  is  quite  otherwise  in  regard  to  the  attack  itself.  Now  the  advice 
becomes  of  definite  and  distinct  importance.  The  differential  diagnosis^ 
must  be  made  as  sharply  as  possible.  The  suggestions  to  the  nurse 
and  attendants  must  be  precise  and  not  open  to  the  least  misconstruc- 
tion. The  patient  when  first  seen  will  be  almost  invariably  found  lying 
flat  on  his  back.  Position  is  an  important  factor,  and  it  behooves  one 
to  decide  quickly  how  to  place  the  patient  to  the  best  advantage. 
Gravity  plays  a  role,  though  a  slight  one,  in  the  force  of  the  circula- 
tion ;  hence  it  must  be  remembered  in  connection  with  the  nature  of 
the  lesion.  If  the  case  is  one  of  hemorrhage,  a  half-reclining  position 
on  one  or  the  other  side  of  the  body  is  the  best.  Heidenhain  recom- 
mends that  the  patient  be  put  in  a  sitting-erect  position  and  maintained 
in  such  an  attitude  as  long  as  possible.  I  have  seen  amelioration  of 
the  symptoms  by  this  simple  manoeuvre.  Often  the  friends  standing 
about  will  strenuously  object,  but  a  compromise  may  be  made  by  prop- 
ping the  patient  against  the  overturned  back  of  a  chair  in  a  half- 


THE  NON-NEURONIC  DISEASES  84I 

reclining  position.  While  he  is  in  this  attitude  cold  in  the  form  of 
cracked  ice  should  be  applied  to  the  head  to  cauSe  as  far  as  possible 
contraction  of  the  cerebral  vessels,  and  heat  to  the  lower  extremities 
to  dilate  the  blood  vessels  there  and  so  lessen  the  blood-pressure  in  the 
brain.  The  latter  may  be  further  accomplished  by  the  cautious  ad- 
ministration of  a  cardiac  sedative,  such  as  tincture  of  aconite  or  vera- 
trum. 

If  the  case  is  one  of  embolic  obstruction  the  reverse  of  all  this 
should  be  done.  Now  we  desire  to  increase  the  intracranial  blood- 
pressure  ;  for  the  embolism  being  already  there  and  beyond  the  hope 
of  immediate  removal,  it  is  our  object  to  check  its  progress  and  fur- 
ther development  by  suddenly  making  it  stationary.  To  do  this  the 
patient's  head  should  be  placed  as  low  as  possible.  The  cold  and  heat 
may  be  applied  as  before,  but  instead  of  a  cardiac  sedative  a  stimulant 
now  acts  more  favorably,  such  as  alcohol,  ammonia,  or  even  small 
doses  of  digitalis  and  ether. 

The  importance  of  attending  at  once  to  the  decubitus  of  the  pa- 
tient is  brought  out  by  the  fact  that  undoubtedly  some  fatalities  occur 
frorfi  suffocation.  Kind  friends,  not  knowing  what  to  do,  put  the 
patient  on  his  back,  with  head  low,  and  administer  brandy,  milk  or 
whisky.  Very  often  the  tongue  is  partially  paralyzed,  as  well  as  the 
pliarynx,  while  the  sensitiveness  of  the  buccal  mucous  membrane  is 
lost.  vSaliva  and  fluids  collect,  obstruct  and  even  enter  the  air-passages, 
setting  up  inhalation-pneumonia.  The  obvious  thing  to  do  is  of  course 
to  "aise  the  head,  place  the  patient  on  the  side,  carefully  pull  forward 
the  tongue,  and  swab  out  the  mouth  with  a  dry  rag  or  bit  of  linen 
moistened  with  some  aromatic,  antiseptic  mouth-wash. 

As  the  respiratory  power  is  usually  diminished,  it  is  important  that 
the  patient  should  have  all  the  fresh  air  possible.  Crowding  about  his 
bed  should  be  forbidden,  and  the  windows  even  in  cold  weather  should 
be  more  or  less  open.  It  may  even  be  necessary  to  perform  artificial 
respiration,  this  being  done  with  as  little  disturbance  of  the  patient  as 
possible,  and  only  until  the  respiratory  centers  have  sufficiently  recov- 
ered from  their  shock  to  resume  their  normal  functions.  All  con- 
striction about  the  neck  by  tight  clothing  must  be  removed,  so  that  the 
return  of  circulation  may  not  be  obstructed.  To  increase  the  blood- 
pressure  within  the  cranium  in  embolism,  it  may  be  well  at  times  to 
a-[)ply  the  Esmarch  elastic  bandage  to  the  lower  extremities.  It  would 
be  unwise  to  do  this  as  a  routine  measure,  but  its  worth  in  some  cases 
cannot  be  doubted. 

To  determine  the  blood  away  from  the  head  we  have  two  rapii 
and  powerful  methods — namely,  bleeding  and  hydragogue  purgatior. 
The  old-time  practice  of  placing  two  or  three  drops  of  croton  oil  on  the 
back  of  the  patient's  tongue  is  a  good  one.  A  brisk  enema  may  be 
employed  in  some  cases,  but  usually  it  is  too  slow  in  action.  The  same 
may  be  said  of  elaterium.  Cerebral  congestion  is  certainly  modified 
by  quick  action  upon  the  circulatory  and  glandular  apparatus  of  the 
bowel,  as  can  be  clearly  demonstrated;  hence  it  is  a  rational  con- 
clusion to  hold  that  the  same  means  will  be  effective  in  lessening  the 
intracranial  blood-pressure  in  hemorrhage. 


842  THE  NON-NEURONIC  DISEASES 

In  regard  to  venesection,  or  the  abstraction  of  ten  or  a  dozen 
ounces  of  blood,  there  is  a  wide  divergence  of  opinion.  At  one  time  it 
was  a  routine  practice  and  consequently  abused.  On  the  other  hand, 
there  are  those  who  boast  that  they  never  bleed  a  patient.  Of  the 
two  extremes  the  latter  is  the  preferable  one.  The  abstraction  of  a 
few  ounces  of  blood  is  almost  immediately  followed  by  a  partial  return 
to  consciousness,  and  hence  the  one-time  popularity  of  the  treatment. 
It  should  be  remembered,  however,  that  the  heart  action  in  apoplexy 
is  usually  weakened.  Therefore,  to  still  more  weaken  it  by  depriving  it 
of  its  natural  stimulus,  the  blood,  is  hardly  a  commendable  procedure. 
Only  in  sthenic  cases  with  flushed  countenance,  full  pulsating  vessels, 
and  a  vigorous  general  physique  is  venesection  to  be  thought  of.  The 
thinning  of  the  blood  diminishes  its  tendency  to  coagulation  at  the  seat 
of  hemorrhage  and  lessens  its  stimulating  power  upon  the  medullary 
cardiac  center  and  heart  muscle.  In  most  cases  these  disadvantages 
would  so  far  outweigh  the  possible  little  benefit  due  to  the  niechanical 
diminution  of  the  intracranial  blood-pressure  that  I  am  generally  op- 
posed to  the  operation.  In  the  few  cases  in  which  I  have  abstracted 
blood,  it  seemed  to  me  that  the  slight  benefit  and  partial  restoration  to 
consciousness  were  so  temporary  as  to  be  without  any  special  value. 
In  one  case  I  fear  it  hastened  the  end,  though  both  the  attendant  and 
myself  anticipated  the  best  of  results. 

All  such  slow  means  of  withdrawing  blood  from  the  head  as 
leeches  to  the  temples,  mustard  to  the  nape  of  the  neck,  blisters,  etc., 
may  be  tried  in  some  cases,  perhaps  most  cases ;  for,  fortunately,  even 
if  they  are  slow,  they  are  not  open  to  such  objections  as  is  venesection. 
If  they  irritate  the  patient  they  had  better  be  desisted  from,  for  the 
patient's  distress  will  tend  to  a  return  or  extension  of  the  hemorrhage. 

Diuretics  are  judicious,  and  in  this  connection  it  is  well  to  mention 
that  catheterization  will  sooner  or  later  be  required  in  almost  every 
case.  The  bladder  is  usually  paralyzed  to  a  certain  extent  and  fails 
to  void  its  contents.  Unless  the  catheter  is  promptly  and  systematically 
used  the  patient  will  experience  distress,  if  he  does  not  acquire  a 
cystitis. 

The  skin  should  be  attended  to,  and  a  gentle  rubbing  of  the  surface 
of  the  body  with  alcohol  and  tepid  water  cannot  fail  to  be  of  some 
benefit.  The  enormous  capillary  circulation  in  the  deeper  layers  of  the 
skin  may  be  made  to  retain  a  large  amount  of  blood  by  the  application 
of  warmth  to  the  body  surface.  Moreover,  the  cleansing  of  the  skin 
with  warm  water  awakens  the  activity  of  the  glandular  apparatus,  and 
this  will  aid  in  determining  the  flow  of  blood  away  from  the  head. 

It  will  thus  be  seen  that  very  active  treatment  immediately  after 
an  apoplectic  shock  is  uncalled  for.  Beyond  careful  nursing,  quietude, 
arranging  of  the  patient's  position,  attending  to  the  respiration,  nutri- 
tion and  excretions,  the  physician  can  give  but  little  advice.  If  the 
shock  is  so  severe  that  death  is  inevitable,  little  that  art  or  science  can 
do  will  be  of  any  value  one  way  or  the  other.  The  end  will  come  in  a 
few  days  or  hours,  and  though  the  occasional  twitching  of  the  muscles 
of  the  extremities  as  a  result  of  the  local  irritation  of  the  clot  may 
awaken  false  hopes  of  a  return  to  consciousness,  the  physician  will 


THE   XON-NEUROXIC  DISEASES  84 J 

serve  his  interests  best  by  carefully  guarding  the  family  against  any 
fallacious  anticipations.  If,  however,  consciousness  partially  or  com- 
pletely returns,  and  the  patient  is  a  hemiplegia  zvith  or  zvithout  aphasia, 
the  physician  can  do  a  great  deal,  not  only  for  the  victim's  comfort, 
but  even  to  ameliorate  to  a  large  extent  the  distress  caused  by  the 
A^arious  sequelae.  In  fact,  this  is  the  stage  of  apoplexy  in  which  medical 
science  can  play  its  best  hand.  The  storm  has  passed ;  it  now  remains 
to  restore  order  as  far  as  possible  out  of  the  wreck,  and  in  doing  this 
the  attendant  can  sometimes  do  wonders.  In  the  first  place,  every 
precaution  spoken  of  under  the  head  of  prophylaxis  should  be  adopted 
to  prevent  a  return  of  the  shock.  x\bsolute  quiet,  mental  and  physical, 
with  the  head  elevated ;  light,  nutritious,  non-nitrogenous  diet ;  gentle 
sponging  of  the  surface  of  the  body ;  abundance  of  fresh  air ;  and  all 
those  agencies  calculated  to  cheer,  invigorate  and  nourish  the  patient, 
so  far  as  he  is  capable  of  being  so  acted  upon,  should  be  carefully 
thought  of. 

While  the  clot  is  undergoing  organization  and  surrounding  itself 
"with  a  capsule,  the  paralysed  muscles  will  become  somewhat  atrophied. 
To  preserve  the  muscles  in  the  hope  of  their  resuming  their  function 
if  the  nervous  centers  should  regain  part  of  their  power,  faradism, 
massage  and  gentle  passive  movements  are  to  be  instituted.  Just  how 
soon  this  is  to  be  done  is  the  source  of  a  difference  of  opinion.  In  my 
own  experience  I  have  found  it  advantageous  to  begin  very  early — 
gently,  of  course,  at  first — not  later  than  the  first  or  second  week  after 
the  shock  and  subsidence  of  all  signs  of  irritation  or  possible  inflam- 
mation. Passive  movements  and  the  passage  through  the  muscles  of  a 
current  of  faradic  electricity,  just  sufficiently  strong  to  produce  easy, 
Tegular  contractions,  should  be  made  systematically  for  a  few  minutes 
each  day.  I  am  fond  of  using  olive  or  cocoanut  oil  when  giving  the 
massage,  as  it  softens  the  skin  and,  I  believe,  favors  to  a  slight  extent 
the  nutrition  of  the  underlying  tissues.  At  no  time  should  anything 
cold  be  placed  against  the  body,  and  at  all  times  the  patient  should  be 
clad  with  warm,  non-irritating  garments.  Later  on  it  is  a  good  thing 
to  encourage  the  patient  to  attempt  voluntary  movement.  Of  course, 
this  will  be  impossible  in  many  instances,  but  he  should  move  the  well 
side,  and  the  attendant  may  assist  him  by  raising  at  the  same  time  the 
paralyzed  limb.  Ofttimes  the  patient  thinks  he  is  doing  this  of  his 
own  will,  and  the  hopefulness  which  it  inspires  cannot  bdt  be  of  benefit : 
nay,  more,  such  simple  manceuvres  have  kept  the'  cortical  memory  or 
representative  centers  alive,  so  that  when  the  motor  areas  had  partially 
recovered  their  function  the  patient  was  better  able  to  attempt  and 
even  succeed  in  performing  voluntary  movement  than  he  otherwise 
would  have  been.  Re-education  of  paralyzed,  or  rather  partially 
paralyzed,  muscles  is  an  important  part  of  the  physician's  duty.  JNIany 
a  hemiplegic  would  have  been  less  hemiplegic  if  the  memories  of  mus- 
cular movement  had  been  preseived  by  the  early  practice  of  passive 
movement  in  conjunction  with  attempted  voluntary  movement. 

\\'hat  I  have  just  said  applies  Hkewise  to  the  aphasia  following  the 
shock.  The  speech  center  should  be  encouraged  to  functionate,  or  at 
least  an  attempt  made  early  in  the  trouble  to  awaken  the  activity  of 


844  THE   NON-NEURON]  C  DISEASES 

the  corresponding-  speech  center  of  the  opposite  side.  These  centers 
are  memory  or  representative  centers  for  speech,  and  hence  if  a  patient 
is  utterly  neglected  it  will  happen  that  when  the  center  recovers  from 
the  shock,  the  power  of  speech  will  be  much  less  than  it  otherwise 
would  have  been.  Hence,  as  soon  as  consciousness  is  sufficiently  re- 
stored, I  have  the  nurse  for  a  few  moments  each  day  teach,  as  she 
would  a  child,  the  names  of  persons  and  things,  and  if  possible  get  the 
patient  to  repeat  them  after  her.  It  is  astonishing  in  a  certain  per- 
centage of  cases  how  strikingly  and  rapidly  the  aphasic  symptom  may 
in  part  be  recovered  from  by  this  prompt  and  regular  re-education  of 
the  memory  centers  for  speech.  In  cerebral  as  well  as  muscular  physi- 
ology it  is  an  axiom  that  exercise  increases  nutrition  and  function. 
Many  an  aphasic  hemiplegic  would  undoubtedly  have  been  less  of  an 
aphasic  and  less  of  a  hemiplegic  by  the  systematic  exercise  of  his  cere- 
bral structures  as  soon  after  the  shock  as  possible,  and  when  all  signs- 
of  inflammation  and  irritation  had  subsided. 

In  all  traumatic  cases,  and  in  all  cases  in  which  the  symptoms  in- 
dicate a  superficial  location  of  the  clot,  trephining  for  the  removal  of 
the  latter  is  to  be  taken  into  serious  consideration.  I  recall  the  case 
of  a  boy  of  some  five  years  of  age  who  fell  over  a  balustrade  and  sus- 
tained a  severe  concussion  of  the  head,  with  the  formation  of  an  intra- 
cranial clot  with  all  its  accompanying  signs  of  unconsciousness,  local- 
ization and  stertor.  The  spreading  of  the  clot  immediately  after  the 
fall  could  be  clearly  observed  by  the  spreading  and  deepening  of  the 
muscular  paralysis.  Trephining  was  immediately  performed,  with  a 
partial  restoration  to  consciousness  and  a  slight  return  of  the  muscu- 
lar power.  .The  action  of  the  muscles  was  a  striking  phenomenon.  At 
first  they  were  violently  contracted,  probably  because  of  the  irritative 
action  of  the  clot ;  then  they  became  paralyzed  completely,  with  a. 
more  or  less  set  rigidity.  After  trephining  they  relaxed  completely,, 
and  remained  so,  or  were  very  feebly  moved  as  a  result  of  subcon- 
scious volition.  Death  occurred  in  a  few  hours,  however,  from  ex- 
haustion and  shock.  The  removal  of  a  clot  deep  in  the  centrum  ovale 
is  a  hazardous  and  difficult  operation.  It  is  attempted,  however,  but 
with  little  genuine  success.  The  paralysis  in  such  a  case  is  not  re- 
lieved, but  a  source  of  infection  and  irritation  is  removed  and  makes- 
the  operation  at  least  one  to  be  thoughtfully  considered. 

I  have  very  little  faith  in  the  so-called  sorbefacient  powers  of  such 
remedies  as  the  iodide  of  potash,  gold,  arsenic,  etc.  As  alteratives, 
they  may  indeed  someliow  modify  the  clot  or  the  results  of  its  presence 
in  the  cerebral  tissues,  but  I  am  inclmed  to  think  that  much  of  their 
effect  is  due  to  some  kind  of  stimulant  tonic  power.  At  all  events,  their 
administration  does  seem  to  be  of  some  benefit  in  some  cases,  and  they 
are  therefore  to  be  commended. 


THE   XON-XEUROXIC  DISEASES  84^ 

EXCEPHALO.AIALACIA. 
EMBOLISM  AND  THROMBOSIS. 

Acute  cerebral  softening,  or  encephalomalacia,  is  a  local  ansemic 
necrobiosis  caused  by  the  sudden  occlusion  of  an  artery,  and  is  char- 
acterized by  an  apoplectic  stroke  and  hemiplegia.  The  immediate  cause 
of  the  obstruction  to  the  circulation  is  an  embolus  or  a  thrombus.  The 
origin  of  the  latter  is  an  abnormal  condition  of  the  blood  or  vascular 
walls. 

Etiology. — The  etiology  of  the  circulator}-  disease  determines 
practically  the  etiology  of  encephalom.alacia.  Embolism  generally  oc- 
curs in  the  young  and  middle-aged,  before  the  fortieth  year.  Throm- 
bosis is  a  complication  of  advanced  years.  Syphilitic  thrombosis,  how- 
■ever,  occurs  in  early  adult  life.  Women  are  said  to  suffer  more  from 
embolism  than  men,  but  statistics  differ  on  this  point. 

The  predisposing  causes  of  both  embolism  and  thrombosis  are 
many  and  of  the  highest  degree  of  importance.  They  are  so  clearlv 
bound  up  with  the  pathology  and  pathogenesis  of  cerebral  softening, 
that  it  will  be  well  to  discuss  all  together. 

Given  the  predisposing  causes,  certain  exciting  influences  such  as 
fright  and  other  sudden  mental  shock,  unwonted  ph^^sical  exercise, 
abnormal  physiological  strains  of  all  sorts,  parturition,  sudden  chilling 
of  the  skin,  lowered  heart  action,  etc.,  may  provoke  an  apoplectic  at- 
tack. 

Pathology  and  Pathogenesis. — Eighty-nine  per  cent,  of  the 
cases  of  embolism  are  associated  with  heart  disease.  Vegetations  from 
acute  or  chronic  endocarditis  and  segments  from  ulcerative  processes 
within  the  heart  are  the  source  of  the  emboli.  Heart  clots  in  the 
auricular  appendix  and  during  the  puerperium  have  produced  them. 
They  may  spring  from  a  disintegrating  thrombus  elsewhere.  Atheroma 
or  aneurism  of  the  aorta,  as  well  as  ulcerative  bronchitis,  disease  in 
and  about  the  pulmonary  veins,  and  gangrene  of  the  lung, 
may  all  be  responsible  for  them.  A  history  of  rheumatism 
with  valvular  disease  and  cardiac  weakness  is  present  in  the 
great  majority  of  the  cases  of  embolism.  Changes  in  the  condition 
of  the  blood  itself  wrought  by  such  influences  as  the  acute  infectious 
fevers,  pulmonary  tuberculosis,  puerperal  sepsis  and  even  anfemia  have 
been  credited  with  the  formation  of  emboli.  It  is  more  likely,  however, 
that  an  endocarditic  condition  is  set  up  under  these  conditions,  which, 
together  with  the  disturbed  heart  action,  is  the  source  of  the  clots. 
Such  deteriorated  blood  states  are  more  prone  to  originate  thrombi. 
These,  however,  may  send  oft'  secondary  embolic  particles,  a  view 
which  is  supported  somewhat  by  the  fact  that  in  these  infectious  states 
the  obstructions  in  the  brain  are  usually  minute  and  multiple. 

After  reaching  the  brain  an  embolus  usually  lodges  at  the  bifurca- 
tion of  some  vessel,  or  if  small  enough  may  pass  on  into  an  arteriole 
and  completely  occlude  it.  The  middle  cerebral  artery  and  its  end 
branches  are  the  favorites.    The  left  side  is  mostly  affected  because  the 


846  THE   NON-NEURONIC  DISEASES 

blood  current  is  most  direct  from  the  heart  on  that  side.  Other  arteries 
may  rarely  be  the  seat  of  the  obstruction.  Emboli  have  gotten  caught 
in  the  internal  carotid,  vertebral  deep  cerebral  and  posterior  cerebral 
aiteries. 

Once  lodged,  the  embolus  becomes  more  or  less  closely  attached 
to  the  vascular  wall,  at  times  calcified  and  the  center  of  a  secondary 
local  thrombus.  It  may  thus  continue  to  grow  and  extend  into  the- 
neighboring  vessels.  Sometimes  it  begins  ta  break  up  and  send  off 
other  emboli  before  necrobiosis  has  been  instituted  by  the  first. 

The  thrombotic  process  is  quite  different  from  all  this.  Here 
syphilitic  arteritis,  senile  atheroma,  weakened  heart  action  and  various 
blood  dyscrasije  constitute  the  great  predisposing  causes.  Alcohol, 
lead,  gout,  chlorosis,  leukaemia  and  even  heredity  are  obviously  impor- 
tant elements  in  the  causation  of  thrombosis  in  this  manner.  Multiple 
thrombi  have  been  seen  after  extensive  burns  upon  the  skin  and  carbon 
monoxide  poisoning.  They  may  result  secondarily,  as  I  have  already 
stated,  from  a  fixed  embolus.  Oppenheim  affirms  that  in  his  experi- 
ence atheroma  has  been  incited  by  certain  diseases  of  the  nervous  sys- 
tem and  by  continued  emotional  excitement  in  which  there  was  a  per- 
manent disturbance  in  the  functions  of  the  vascular  apparatus. 

The  most  common  location  of  a  thrombus  is  the  middle  cerebral 
and  basilar  arteries,  though  it  may  start  up  anywhere.  In  a  general 
way  the  base  of  the  brain  and  the  larger  vessels  are  its  favorite  lo- 
calities. 

The  complete  occlusion  of  a  vessel  by  an  embolus  or  thrombus 
produces  an  intense  local  anmnia  and  if  there  is  no  anastomosis  with 
other  vessels,  softening  and  destruction  of  tissue  in  the  affected  area. 
These  softened  areas  may  be  found  anvwhere  in  the  brain,  most  com- 
monly in  the  cortex  and  centrum  ovale,  where  the  blood  vessels  are  of 
the  terminal  varietv.  The  necrobiosis  usually  begins  about  a  day  and 
a  half  after  the  occlusion  of  the  vessel,  though  swelling  and  other 
changes  probably  occur  immediately. 

Red,  yellow  and  white  encephalomalacia  are  usually  referred  to  by 
the  pathologists.  They  are  m.erely  different  stages  of  the  necrobiotic 
process,  the  color  being  dependent  upon  the  blood.  Red  softening  is 
the  first  stage  and  is  most  marked  in  cortical  foci.  As  the  coloring 
matter  of  the  blood  changes  in  the  affected  area  a  yelloivish  hue  is 
given  to  it.  This  is  seen  only  after  several  weeks.  Finally  the  yellow 
tinge  passes  into  a  white  or  bluish-white  and  the  focus  contains  the 
debris  of  degenerated  nerve  cells  and  fibres.  The  presence  of  the 
mveline  drops,  parenchymatous  detritus  and  granular  cells  aids  in 
distinguishing  this  condition  from  mere  post-mortem  maceration. 
Absorption  ultimately  takes  place,  a  cyst  is  formed,  contracts  and  leaves 
a  permanent  cicatrix.  Inflammation,  suppuration  and  sclerosis  may  all 
be  observed  in  the  aft'ected  and  adjoining  areas.  The  size  of  the 
softened  focus  may  be  from  that  of  a  pinhead  to  an  entire  hemisphere. 
It  may  be  large  and  single  or  small  and  multiple. 

It  is  unnecessary  to  describe  here  the  contributory  pathological 
findings  in  encephalomalacia,  such  as  the  diseases  of  the  heart,  blood 
vessels  and  other  organs. 


THE  NON-NEURONIC  DISEASES  847 

Symptoms. — The  onset  of  embolism  is  usually  sudden  and  without 
premonitory  indications.  In  rare  cases  there  may  be  the  slightest  sort 
of  pargesthesia  immediately  before  the  occlusion,  especially  if  the 
embolus  should  catch  at  a  bifurcation.  If  the  obstructed  artery  is 
particularly  small  there  may  be  no  disturbance  of  the  consciousness. 
Usually,  however,  after  some  local  or  general  convulsive  twitchings, 
hemiplegia  appears  and  then  temporary  loss  of  consciousness.  The 
coma  is  lighter  and  of  shorter  duration  than  it  is  in  hemorrhage.  The 
temperature  does  not  alter  at  first,  but  in  a  few  days  it  rises  somewhat. 
In  septic  embolism  it  may  attain  a  very  high  degree  and  be  preceded 
by  distinct  chills.  A  unilateral  epiletiform  seizure,  or  even  a  condition 
resembling  status  epilepticus,  may  take  the  place  of  the  coma.  In 
sonie  cases  merely  drowsiness  with  slight  delirium  occurs.  Vomiting, 
flushed  countenance,  stertorous  breathuig  and  other  symptoms  of  hem- 
orrhage are  wanting.  The  pulse  is  feeble  as  a  rule,  the  countenance 
slightly  paler  than  normal  and  the  skin  cool. 

Thrombosis  is  always  preceded  by  prodromes.  These  are  so  in- 
sidious, varied  and  prolonged  sometimes  that  mistakes  in  diagnosis  are 
easily  made.  In  syphilitic  cases  they  consist  of  headache,  queer  feel- 
ings about  the  body,  temporary  attacks  of  double  vision,  cranial  nerve 
palsies  and  sudden  spells  of  weakness.  In  other  cases  hysteroid  mani- 
festations may  be  observed  ;  vertigo,  extreme  emotionalism  and  irrita- 
bility, numbness  of  the  hands  and  feet,  temporary  aphasia,  transient 
hemiplegic  attacks  and  periods  of  drowsiness  and  stupor.  Loss  of 
memory,  incoherence  of  speech,  slight  dysarthria,  temporary  attacks 
of  disturbed  respiration  and  heart  action  add  to  the  confusion.  Swal- 
lowing may  be  troublesome  at  times,  a  slight  cough  may  appear  and 
other  temporary  symptoms  may  indicate  bulbar  difficulty.  When  the 
attack  begins  in  thrombosis  the  loss  of  consciousness  is  gradual.  If 
the  vessels  involved  are  small,  or  it  is  due  to  syphilis,  there  may  be  no 
disturbance  of  the  mind  whatever.  The  hemiplegia  is  usually  slow 
in  developing  and  precedes  somewhat  the  development  of  the  coma. 
Neither  the  paralysis  nor  the  loss  of  consciousness  is  as  deep  as  it  is 
in  hemorrhage,  nor  as  abrupt  and  limited  as  it  is  in  embolism.  The 
hemiplegia  is  variable  and  rarely  complete.  The  temperature  may  fall 
slightly  in  the  beginning  just  as  it  does  in  hemorrhage.  As  the  basal 
arteries,  such  as  the  basilar,  vertebral  and  posterior  cerebral,  are  more 
liable  to  be  the  seat  of  thrombosis  than  of  hemorrhage,  basal  and 
bulbar  manifestations  are  to  be  expected  more  in  the  former. 

The  hemiplegia  of  both  embolism  and  thrombosis  tends  toward 
rapid  and  early  improvement,  unless  a  very  large  vessel  has  been  ob- 
structed. It  may  be  preceded  for  some  days  by  a  hemiparesis,  but  as 
a  rule  it  appears  pretty  much  in  the  same  way  that  it  appears  in 
hemorrhage.     If  it  is  right-sided,  aphasia  accompanies  it. 

The  conditions  after  the  subsidence  of  the  acute  stage  are  the  same 
in  softening  as  they  are  in  hemorrhage.  Occasionally,  however,  in 
cortical  softening  the  limitation  of  the  area  affected  gives  rise  to 
limited  paralyses,  monoplegias,  aphasia  alone  or  monoplegias  with 
hemianopsia.  Hemianaesthesia  may  appear  with  the  hemiplegia  or 
exist  alone. 


848  THE  XOX-NEUROKIC  DISEASES 

The  location  of  the  softened  spot  cannot  always  be  determined 
from  the  clinical  picture,  for  the  lesion  may  be  a  multiple  one.  In  many 
cases,  however,  the  vessel  occluded  and  the  area  involved  can  be  more 
than  suspected  from  the  peculiar  character  and  grouping  of  the  symp- 
toms. One  needs  only  to  recall  the  functions  of  the  particular  part 
of  the  cortex  supplied  by  the  affected  artery. 

Bulbar  and  pontile  symptoms  occur  when  the  vertebrals  or  basilar 
artery  is  obstructed.  In  the  case  of  the  former  the  symptoms  are 
those  of  acute  "bulbar  paralysis,  as  detailed  elsewhere.  In  the  latter 
the  paralysis  is  apt  to  be  bilateral,  associated  with  rigidity  or  spasm, 
and  accompanied  by  a  rapid  rise  of  temperature. 

The  results  of  obstruction  in  the  internal  carotid  are  very  variable 
on  account  of  the  anastomoses  in  the  circle  of  Willis.  If  these  are 
abundant,  the  vessel  may  be  ligated  and  no  paralysis  will  follow ;  if  the 
vessels  are  too  narrow  or  wanting,  the  softening  may  be  very  extensive 
with  hemiplegia,  permanent  coma  and  early  death.  In  such  a  case 
the  clot  usually  extends  into  the  branching  arteries.  The  inclusion  of 
the  arteria  centralis  retinae  in  this  same  lesion  provokes  of  course  most 
serious  visual  disturbances. 

Of  all  the  arteries  the  middle  cerebral  is  the  one  most  commonly 
alTected.  The  internal  capsule  is  softened  and  a  permanent  hemiplegia 
is  established,  with  temporary  or  permanent  hemiansesthesia.  Aphasia 
occurs  with  disease  of  the  left  artery.  If  one  of  the  branches  of  the 
artery  is  obstructed,  the  s}-mptoms  will  follow  the  localization  of  the 
encephalomalacia  in  the  particular  convolutions  supplied  by  those  re- 
spective branches.  Hence  various  monoplegias,  hemiplegia  and  motor 
aphasia  will  develop.  Facio-lmgual  monoplegia  follows  obliteration  of 
the  first  branch,  and  aphasia  also,  if  it  is  on  the  left  side.  The  second 
branch  when  occluded  causes  a  facio-lingual  paralysis."  The  third  and 
fourth  branches  supply  the  lower  part  of  the  parietal  lobes,  including 
the  supra-marginal  and  angular  gyri.  Their  damage  results  in  alexia, 
in  hemianopsia  and  word-deafness.  When  the  fifth  branch  is  plugged 
w^ord-deafness  is  the  main  symptom. 

It  will  be  noted  that  our  modern  knowledge  of  cerebral  localiza- 
tions, coupled  with  the  knowledge  of  the  minute  circulation  of  the 
brain,  underlies  our  appreciation  of  these  various  groups  of  symptoms. 

The  anterior  cerebral  arteries  supply  the  anterior  parts  of  the  brain. 
Their  obstruction  is  compensated  for  in  part  by  the  middle  cerebrals. 
No  symptoms  therefore  usually  occur,  though  it  has  been  thought  that 
mental  inefficiency  as  well  as  monoplegia  of  the  leg  have  been  caused 
by  it. 

Diagnosis. — The  most  important,  and  ofttimes  the  most  difficult, 
differential  diagnosis  to  make  is  between  hemorrhage  and  acute  soft- 
ening. The  subject  is  discussed  under  the  head  of  cerebral  hem- 
orrhage, but  it  will  probably  be  w'ell  to  enumerate  here  some  of  the 
more  significant  differential  signs.  In  acute  softening  early  and  late 
period  of  life  point  respectively  to  embolism  and  thrombosis.  Hem- 
orrhage occurs  more  particularly  in  the  latter  half  of  adult  life  and  at 
the  beginning  of  old  age,  from  forty  to  sixty  approximately.  In  acute 
softening  there  is  a  history  of  syphilis,  rheumatism  with  recurrent 


THE  XON-XEUROXIC  DISEASES  849 

endocarditis,  infection  or  an  atheromatous  condition  of  the  arteries  ; 
in  hemorrhage  heredity  and  vascular  disease  are  present  somewhat! 
Abrupt  onset  without  premonitory  indications,  sudden  deep  coma,  gen- 
eral paralysis  that  shows  a  tendency  to  recede  and  become  more  re- 
stricted in  its  distribution,  unequal  pupils,  conjugate  deviation  of  the 
head  and  eyes,  flushed  face,  full  bounding  pulse  and  the  temperature 
phenomenon  indicate  hemorrhage ;  whereas  in  acute  encephalomalacia 
prodromes  are  frequent,  much  more  so  in  thrombosis  than  in  embolism, 
the  paralysis  and  loss  of  consciousness  approach  more  gradually,  the 
former  slightly  preceding  the  latter,  the  limbs  are  convulsed,  the'heart 
is  weak,  the  muscles  are  not  completely  relaxed,  and  the  temperature 
phenomenon  of  hemorrhage  is  absent.  Aphasia  is  common  in  embol- 
ism, as  the  lesion  usually  affects  the  left  side;  and  mental  changes 
characterize  thrombosis  on  account  of  the  prolonged  disturbance  of 
the  nutrition  of  the  brain. 

Prognosis. — The  prognosis  ni  regard  to  life  is  generally  favor- 
able in  softening  and  as  compared  with  that  of  hemorrhage  during  the 
stage  of  coma  the  hope  of  recovery  may  be  expressed  with  a  greater 
degree  of  positiveness.  However,  it  is  an  unfavorable  sign  if  the 
coma  is  deep,  the  heart  action  bad  and  the  patient  does  not  come  to 
for  several  days. 

The  outlook  in  carotid  and  basilar  thrombosis  is  bad.  Recovery 
practically  never  takes  place,  though  the  end  may  be  long  deferred, 
the  patient  continuing  sometimes  for  months  and  even  years,  experi- 
encing remissions  and  relapses  in  thrombosis  particularly.  I  have  seen 
several  of  these  cases  variously  diagnosed  and  treated  by  different 
practitioners  during  a  period  of  many  months,  in  one  case  over  a  year. 

Recurrence  is  less  prone  to  appear  in  embolism  than  in  thrombosis. 
Most  of  the  hemiplegics  that  continue  to  live  many  }ears  without  a 
relapse  owe  their  paralysis  to  a  small  area  of  softening. 

In  regard  to  the  future  outlook  for  the  hemiplegia,  it  is  about  the 
same  in  softening  as  it  is  in  hemorrhage.  If  after  the  first  month 
there  is  no  change,  the  patient  had  better  be  informed  of  the  perma- 
nency of  the  condition.  Speech  disturbances  are  apt  to  be  a  little  more 
fixed  here  than  in  hemorrhage  after  a  certain  period  has  been  passed, 
and  yet  in  the  latter  the  initial  aphasia  usually  lasts  a  trifle  longer. 

In  arriving  at  the  prognosis  of  encephalomalacia  the  extent  of  the 
lesion  and  the  location  of  the  obstruction  exercise  great  v/eight. 

Treatment. — The  difl^erential  treatment  of  the  comatose  stage 
of  acute  softening,  and  the  general  management  of  the  sequelae,  are  dis- 
cussed in  detail  under  the  head  of  cerebral  hemorrhage.  I  desire  here 
inerely  to  reiterate  the  injunction  to  do  as  little  as  possible,  in  some 
cases  practically  nothing,  until  it  is  decided  whether  the  case  is  one  of 
softening  or  hemorrhage.  If  it  is  the  former,  the  patient  had  better 
be  placed  horizontal  or  even  with  the  foot  of  the  bed  slightlv  elevated, 
As  the  clot  cannot  be  removed,  it  is  desirable  to  urge  it  on  to  a  smaller 
vessel  if  possible  and  to  fix  it  there  as  soon  as  possible.  Its  furthoi 
enlargement  is  to  be  prevented  by  every  means  in  our  power.  The 
indications  for  the  accomplishment  of  these  ends  are  to  favor  the 
flow  of  the  blood  towards  the  head  bv  gravitv  and  stimulation  of  the 


850  THE   NON-NEURONIC  DISEASES 

heart  aiul  by  avoiding  all  measures  that  have  a  tendency  to  deplete  the 
b'ood.  Venesection  must  be  rigidly  avoided.  The  bowels  must  not 
be  acted  upon  with  cathartics  too  soon.  The  patient  must  be  kept 
at  absolute  rest  with  his  head  low.  Alcohol,  digitalis,  strophanthus, 
strvchnia  and  nitroglycerin  are  available  for  stimulating  the  circula- 
tion. With  these  exceptions,  the  treatment  of  apoplexy  from  arterial 
obstruction  differs  in  nowise  from  that  of  apoplexy  from  hemorrhage. 

A  history  of  syphilis  calls  for  the  prompt  administration  of  mer- 
cury and  the  iodides.  These  had  better  be  continued  for  a  long  time 
with  the  heart  stimulants  and  general  tonics. 

The  management  of  the  hemiplegia,  aphasia  and  other  symp- 
tomatic treatment  are  discussed  elsewhere. 

THROMBOSIS     OF     THE     INTRACRANIAL     VEINS     AND 

SINUSES. 

Thrombi  are  liable  to  form  in  any  of  the  intracranial  veins  and 
sinuses.  They  are  of  serious  import  both  on  accoimt  of  the  effects 
they  themselves  produce,  and  on  account  of  the  effects  produced  by  the 
malady  of  which  they  are  a  collateral  result. 

Etiology. — Etiologically,  thrombi  must  be  divided  into  the  pri- 
mary and  secondary.  A  primary  thrombus  is  one  that  forms  merely 
on  account  of  the  inherent  state  of  the  blood  or  the  circulation.  A 
secondary  thrombus  is  the  outgrowth  of  some  serious  disease,  usually 
septic,  in  the  neighborhood. 

Primary  thromboses  are  called  "marantic,"  because  they  usually 
occur  in  adynamic  states.  Children  and  the  aged  are  usually  affected, 
though,  of  course,  all  ages  are  subject  to  marantic  conditions  or  states 
of  marasmus.  In  exhausting  diarrhoeas,  such  as  infants  particularly 
suffer  from,  wasting  pulmonary  affections,  prolonged  fevers  and  long- 
continued  suppurative  processes,  even  acute  specific  maladies,  the 
blood  is  so  altered  and  the  heart  is  so  weakened  that  coagulation  readily 
supervenes  in  these  veins,  where  the  circulation  at  best  is  not  an  active 
one.  The  anatomical  structure  of  a  sinus  precludes  any  great  elas- 
ticity in  its  walls ;  hence  when  the  blood  is  thinned  and  diminished  in 
amount  in  these  low  states,  the  sinus  does  not  contract  and  equalize 
the  circulation.  This  fosters  stasis  and  coagulation.  Anaemia  less 
frequently  than  chlorosis  provokes  a  primary  thrombosis.  Severe  hem- 
orrhages have  been  followed  by  it.  It  occurs  in  adults  sometimes  after 
a  long  cachexia,  such  as  cancer  and  phthisis.  The  puerperal  state 
must  at  times  be  charged  with  it. 

The  superior  longitudinal  sinus  seems  to  be  the  favorite  site  for 
the  formation  of  a  primary  thrombus.  After  this  come  the  lateral  and 
cavernous  sinuses.  There  are  certain  mechanical  features  about  the 
circulation  that  go  far  towards  explaining  this  selective  action  on  the 
part  of  the  clot.  The  collateral  veins  that  enter  the  longitudinal  sinus 
do  so  at  an  angle  and  in  a  direction  the  reverse  of  that  of  the  blood 
current  in  it.  The  sinus  and  venous  currents  thus  m.eet  in  opposing 
directions.  The  latter  also  have  to  ascend  to  reach  the  main  flow  in 
the  sinus  besides  themselves  receiving  blood  from  ascending  arteries. 


THE  NON-NEURONIC  DISEASES  85 1 

The  irregularity  of  the  inner  wall  of  the  vessels  has  some  effect  also,, 
as  is  shown  by  the  fact  that  the  clot  is  attached,  as  it  were,  to  one  side 
while  the  blood  goes  flowing  along  in  the  channel  beside  it. 

Secondary  thrombosis  is  usually  the  product  of  a  phlebitis  in  the 
sinus  wall  or  of  the  veins  entering  it.  This  phlebitis  is  most  commonly 
originated  by  caries  of  the  bone  or  internal  ear  disease.  It  is  the 
result  of  a  septic  process  generally  of  infectious'  origin.  Nearly  every 
sinus  is  the  recipient  of  veins  from  the  exterior  of  the  skull.  The 
transverse  sinus  receives  tlius  through  the  mastoid  foramen  a  vein 
which  brings  in  blood  from  the  occipital  and  posterior  auricular  veins 
on  the  outside  of  the  head ;  while  the  longitudinal  sinus  receives  a 
communication  through  the  parietal  foramen  from  the  external  veins 
of  the  skull.    Other  sinuses  are  similarly  supplied. 

Injuries  to  the  bone  with  inflammation  of  the  diploe,  tubercular 
meningitis,  erysipelas,  carbuncle  of  the  face  or  neck,  malignant  ulcera- 
tion, orbital  phlegmon,  panophthalmitis  and  suppurating  eczema  of  the 
scalp  are  all  sources  of  the  infection.  A  general  septicaemia  is  to  blame 
for  it  sometimes.  Compression  of  the  sinus  has  been  followed  by  a 
secondary  thrombosis. 

Of  course,  these  secondary  thrombi  always  occur  m  the  sinus  that 
is  nearest  to  the  primary  seat  of  infection.  The  ear  is  probably  the 
most  common  seat  and  hence  these  thrombi  are  most  frequently  seen 
in  the  superior  petrosal  or  lateral  sinus.  Unlike  the  primary  thrombi, 
they  are  rather  infrequent  in  the  superior  longitudinal  sinus. 

Pathology  and  Pathogenesis. — All  or  part  of  a  sinus  may  be 
filled  with  the  clot.  In  rare  instances  every  sinus  has  been  the  seat 
of  the  thrombotic  formation.  The  clot  is  dark  red,  soft  and  friable 
if  recent,  but  is  lighter  in  color,  harder,  more  friable,  granular  and 
laminated  if  an  old  one.  Recent  clots  are  not  quite  as  adherent  to  the 
sinus  wall  as  are  the  older  ones.  Secondary  thrombi  are  usually  asso- 
ciated with  phlebitis,  are  puriform  and  softened.  The  veins  are  not, 
as  a  rule,  inflamed  in  the  primary  or  marantic  thrombi.  It  is  said  that 
Heubner  recovered  microorganisms  from  what  seemed  to  be  primary 
thrombi.  In  secondary  thrombi  abscesses  are  observed  in  the  vessel 
walls,  and  masses  of  pus  are  discovered  in  even  remote  veins,  such  as 
the  subclavian  and  superior  vena  cava.  Meningitis  is  common  under 
these  conditions,  naturally. 

Behind  the  thrombus  there  is,  of  course,  congestion,  oedema.  The 
contributing  vessels  are  engorged  and  swollen.  The  capillaries  are 
often  ruptured  in  the  gray  substance  of  the  brain  and  there  are  in- 
numerable, minute  hemorrhagic  foci. 

A  sinus  thrombus  may  be  compensated  for  by  the  blood  passing- 
around  by  another  channel.  This  is  not  possible  in  venous  thrombosis- 
The  veins  not  encasing  the  clot  are  tortuous  and  dilated. 

Softening  occurs  in  the  cerebral  tissues  as  a  result  of  the  cedema: 
and  hem.orrhage.  It  may  be  very  extensive  or  minute  or  in  innumer- 
able scattered  or  mulberry-like  spots.  Meningeal  hemorrhage  takes, 
place  occasionally,  but  rarely. 

If  recovery  should  happily  take  place,  the  damage  is  hardly  as 
great  as  that  which  is  left  after     arterial     obstruction.      Secondary 


852  THE   XOX-XEUROXIC  DISEASES 

abscesses  have  been  found  in  the  hnigs  and  remoter  parts  from  a  soft- 
ened, scattered  intracranial  thrombus.  Gowers  says  that  in  about  half 
of  the  cases  of  secondary  thrombosis  these  secondary  remote  septic 
abscesses  are  found. 

Symptoms. — These  are  not  very  distinctive.  They  are  very  apt 
to  be  masked  by  the  symptoms  of  the  disease  out  of  which  the  throm- 
bus originated.  In  primarv  thrombosis,  for  instance,  the  adynamia, 
the  anaemia,  the  heart  weakness,  the  chlorosis  are  so  prominent  that  one 
loses  sight  of  the  symptoms  caused  by  the  sinus  obstruction.  The  ear 
disease,  the  meningitis,  the  septic  manifestations  generall}"  quite  over- 
ride the  signs  of  the  secondary  thrombus  that  may  be  present. 

The  presence  of  an  obstruction  to  the  venous  flow  in  the  brain 
would  be  expected  to  produce  two  sets  of  symptoms — namely,  those 
of  a  local  character  depending  upon  the  location  of  the  clot  and  the 
part  of  the  brain  implicated,  and  those  dependent  upon  the  disturbed 
circulation  outside  of  the  head.  Neither  of  these,  however,  are  at  all 
characteristic,  and  the  latter,  which  are  the  most  so,  are  at  the  same 
time  the  rarest.  A  clot  in  the  sinus  produces  obvious  enough  mani- 
festations in  the  external  cranial  and  facial  veins  that  happen  to  pass 
through  and  connect  with  that  sinus  ;  but  unfortunately  the  phenomena 
are  not  often  to  be  seen. 

Superior  Longitudinal  Sinus. — Thrombosis  of  this  sinus  may  be 
accompanied  by  an  oedematous  condition  in  the  cranium  and  a  dilated, 
twisted  and  tortuous  state  of  the  veins  lying  over  the  frontal,  parietal 
and  temporal  bones.  \'enous  epistaxis  may  occtir  from  the  vessels  of 
the  nose  that  connect  with  it  in  front.  In  children,  who  have  been 
afflicted  with  exhausting  diarrhoea,  the  fontanelles  are  usually  de- 
pressed. When  this  thrombus  appears,  however,  the  fontanelles  bulge 
and  become  very  tense  from  the  associated  cedema  and  congestion. 

Among  the  cerebral  complications  are  to  be  noted  symptoms  simi- 
lar to  those  of  increased  intracranial  pressure,  meningitis  and  soften- 
ing. There  is  apathy,  stupor,  somnolence,  even  coma.  Severe  head- 
ache is  indicated,  with  vomiting  and  convidsions.  Delirium  is  some- 
times present.  The  convulsions  may  be  local  or  general.  Rigidity  of 
the  neck  and  back,  as  in  opisthotonos,  more  or  less  obtains.  Tremor, 
incoordination  and  contracture,  strabismus  and  paralysis  of  the  limbs 
are  possible  symptoms.  The  paralysis  may  be  unilateral  if  the  clot 
extends  into  the  veins  covering  one  hemisphere.  Even  monoplegic 
phenomena  have  been  rarely  seen.  Aphasia  is  almost  unknown. 
Hemiansesthesia  has  been  but  infrequently  observed. 

The  pulse  and  respiration  are  variable.  They  may  be  normal  or 
subnormal.  They  are  usually  elevated  near  death,  which  in  most 
patients  occurs  in  coma  in  a  few  days  or  a  week  or  two.  The  tempera- 
ture as  a  rule  is  normal,  though  it  has  risen  in  leaps  at  times,  even  as 
high  as  108  degrees  F. 

These  symptoms  are  so  irregular  and  indefinite  that  it  is  clear  a 
diagnosis  can  only  be  made  upon  the  etiolog}-  and  signs  of  congestion. 
Often  no  diagnosis  can  be  made,  for  a  similar  clinical  picture  can 
occasionally  be  presented  by  infantile  hydrocephaloid  disease,  chlorosis, 
menini;i.tis,  encephalitis  and  cerebral  hemorrhage. 


THE   NON-NEURONIC  DISEASES  853 

Cavernous  Sinus. — Here  the  eyelids  and  temples  are  apt  to  be 
oedeniatous,  and  the  veins  in  and  aboiit  the  orbit  to  be  tortuous  and 
dilated.  The  eyeball  rnay  be  protruded  and  the  optic  papilla  cedematous. 
It  is  said  that  even  choked  disc  has  been  observed.  The  retinal  veins 
have  certainly  been  congested.  Amblyopia  and  amaurosis  have  result- 
ed in  some  cases,  even  with  a  normal  appearance  of  the  eye  ground. 
Neuralgic  pains  have  been  felt  in  the  fifth  nerve  and  headache  is 
common.  The  nerves  that  run  to  the  orbit  in  the  wall  of  the  sinus,  such 
as  the  third,  fourth  and  sixth  nerves,  are  liable  to  be  involved.  Neuro- 
paralytic manifestations  may  be  not  unexpected. 

Petrosal  Sinus. — There  are  no  known  symptoms  of  thrombosis  in 
either  of  the  petrosal  sinuses. 

Lateral  or  Transverse  Sinus. — There  is  here  apt  to  be  oedema 
behind  and  over  the  mastoid  process.  Gerhardt's  observation  is  open 
to  question — namely,  that  the  external  jugular  vein  on  the  affected 
side  is  less  full  of  blood  than  it  is  on  the  unaffected  side,  because  on 
the  affected  side  of  the  head  the  blood  that  should  flow  into  the  external 
jugular  flows  largely  on  account  of  the  presence  of  the  clot  now  into 
the  internal  jugular.  There  are  no  distinctive  cerebral  symptoms,  but 
there  have  been  observed  disorders  of  the  ninth,  tenth,  eleventh  and 
twelfth  cranial  nerves. 

In  secondary^  phlebitic  thrombosis  there  is  not  nuich  direct  dam- 
age done  to  the  brain.  The  meningitis  that  is  present,  however,  may 
provoke  marked  cerebral  manifestations  and  the  septic  source  of  the 
whole  trouble  may  lead  to  a  cerebral  abscess.  The  mere  occlusion, 
however,  does  not  produce  these  or  other  distinctive  cerebral  phenom- 
ena. Sometimes  the  clot  itself  is  the  seat  of  a  violent  purulent  process. 
It  softens  and  breaks  down  and  lights  up  a  virulent  form  of  septicaemia, 
with  the  establishment  of  secondary  distant  foci  in  the  lungs  and  else- 
where, these  being  the  first  indications  of  the  presence  of  the  clot. 
These  secondary  septic  symptoms  are  of  the  usual  character  and  need 
no  special  description  here. 

Among  the  cerebral  symptoms  that  now  begin  to  appear  are  to  be 
noted  apathy,  dullness,  stupor,  headache,  motor  and,  sensory  irritative 
meningitic  phenomena,  such  as  unequal  paralysis,  muscular  twitchings, 
rigidity  and  disordered  sensation.  These  secondary  thrombi  last  from 
a  few  days  to  a  couple  of  weeks  and  the  sufferer  dies  in  coma.  Recov- 
ery is  so  rare  as  hardly  ever  to  be  counted  upon.  Primary  clots  offer 
a  -better  prognosis,  sometimes  being  absorbed  entirely  or  leaving  per- 
manent cerebral  damage. 

Prognosis. — This  is  very  serious  in  all  cases.  Secondary  phlebitic 
thrombosis  is  practically  a  fatal  disease.  Occasionally  in  children  the 
symptoms  of  a  primary,  marantic  clot  disappear.  In  adults  this  is  much 
rarer.  If  the  generaf  signs  pass  away,  there  may  nevertheless  remain 
some  local  permanent  damage  and  disorder.  Operative  treatment  has 
improved  somewhat  the  prognosis  of  the  secondary  thrombi.  The 
secondary  results,  such  as  the  leptomeningitis,  cerebral  abscess,  septic 
foci  in  the  lungs,  have  their  own  prognosis,  which,  of  course,  deter- 
mines that  of  the  thrombosis. 

Treatment. — The  treatment  of   sinus  thrombosis   almost   limits 


§54  THE   XOX-XEUROXIC  DISEASES 

itself  to  the  treatment  of  the  cause.  In  the  primary  form  the  vigor  and 
general  health  must  be  restored  as  rapidly  as  possible.  The  circulation 
should  be  stimulated  and  tonics  administered.  Never  should  blood- 
letting be  practiced.  The  recumbent  attitude  with  the  head  slightly 
elevated  should  be  maintained  and  flexion  of  the  neck  must  be  care- 
fully avoided. 

In  the  secondary  form  all  accessible  foci  of  pus  should  be  sur- 
gically drained.  The  statistics  of  some  surgeons  are  remarkably  favor- 
able. According  to  Henschen.  of  145  cases,  fifty-eight  per  cent,  were 
cured.  The  reader  is  referred  to  works  upon  surgery  for  further 
details.  When  septicemia  is  general,  tincture  of  the  perchloride  of 
iron,  quinine  and  the  salicylates  should  be  persistently  administered. 

INFANTILE  HEMIPLEGIA. 

The  cerebral  palsies  of  cliikihood  constitute  a  group  of  cases  that 
has  provoked  hitherto  a  great  deal  of  discussion  and  much  unnecessary 
refinement  of  classification.  As  the  name  indicates,  and  as  will  appear 
in  the  study  of  their  pathology  and  pathogenesis,  they  are  all  due  pri- 
marily to  some  defect  or  lesion  in  the  brain.  They  are  all  heiiiiplegic 
in  character  and  distribution.  If  the  lesion  extends  to  bilateral  parts  of 
the  brain,  the  hemiplegia  is  bilateral  or  double,  and  the  disease  is  known 
as  cerebral  diplegia.  No  distinction  of  any  practical  value  can  be 
made  between  unilateral  and  bilateral  hemiplegia  in  childhood  except 
upon  an  etiological  and  pathological  basis.  As  no  such  basis  is  yet 
known,  we  must  perforce  continue  to  recognize  them  both  as  mani- 
festations of  the  same  general  trouble. 

Under  the  name  of  Little's  disease,  cerebral  paraplegia,  con  genital 
or  juvenile  spastic  paraparesis,  congenital  spastic  I'igidity  of  the  limbs, 
some  writers  have  endeavored  to  establish  a  separate  affection,  though 
they  admit  that  it  is  cerebral  in  origin,  in  the  vast  majority  of  cases  at 
least,  and  that  the  paralysis  has  all  the  characteristics  of  a  true  henn- 
plegia.  The  term  paraplegia,  which  has  become  so  fixed  as  a  defini- 
tion of  spinal  paralysis,  is  extremely  inappi-opriate.  The  limitation  of 
the  palsy  more  particularly  to  the  lower  limbs,  the  absence  of  certain 
mental  manifestations,  and  the  prominence  of  the  lesion  in  the  pyra- 
midal tracts  do  not  in  the  least  withdraw  Little's  disease  from  the 
double  hemiplegias  of  childhood.  On  the  other  hand,  the  etiology, 
pathogenesis  and  symptomatology  show  ver}-  conclusively  that  it  is 
primarily  cerebral  in  origin  with  secondary  changes  in  the  cord  char- 
acteristic of  all  hemiplegias. 

All  of  the  cerebral  palsies  of  childhood  now  under  consideration, 
including  Little's  type,  are  due  to  a  degenerative  change  in  the  upper 
motor  or  cortico-spinal  tract.  The  unilateral  or  bilateral  distribution  of 
this  degeneration  is  a  mere  matter  of  etiology.  By  all  the  more  recent 
pathologists  it  is  believed  that  cortical  disease  of  some  sort  is  to  be 
charged  with  the  beginning  of  the  degeneration.  The  separation  of 
these  palsies  into  different  types  therefore  merely  on  account  of  the 
distribution  of  the  paralysis,  their  relationship  to  the  act  of  parturition, 
or  the  prominence  of  the  lesion  in  the  pyramidal  tracts  is  unnecessary, 


THE  NON-NEUROiS-IC  DISEASES  855 

unwarranted  and  confusing.  The  only  way  to  dispose  of  them,  until 
we  have  a  better  foundation  for  differentiation  than  we  have  to-day  in 
their  etiology  and  pathology,  is  to  group  them  all  together  in  a  single 
class  and  to  discuss  them  under  the  head  of  diseases  of  the  brain  or  of 
the  upper  motor  segment. 

Etiology. — The  cerebral  palsies  of  childhood  arc  accidental  and 
are  therefore  not  influenced  by  such  etiological  factors  as  heredity, 
age,  sex,  nationality,  climate,  etc.  Their  causes  are  numerous;  for 
the  sake  of  convenience,  therefore,  we  divide  them  into  the  prenatal, 
natal  and  postnatal,  remembering  all  the  while  that  the  same  immediate 
cause,  ars,  for  example,  cerebral  hemorrhage  or  embolism,  may  be  the 
same  in  all  three  periods. 

In  about  one-third  of  these  palsies  the  cause  is  prenatal,  and  we 
denominate  the  disease  congenital.  The  damage  to  the  brain  is  ac- 
complished during  intrauterine  life  and  the  disease  is  merely  congenital 
and  not  in  the  least  hereditary,  as  I  have  seen  it  stated.  Intrauterine 
traumata,  injuries  to  the  mother  during  pregnancy,  psychic  shocks, 
any  accident  in  fact  that  may  cause  an  inflammation  to  the  motor  zone 
of  the  fetal  brain,  are  among  the  more  common  prenatal  causes. 
Hemorrhage  and  embolism  are  the  lesions  in  the  majority  of  these 
cases.  Hereditary  syphilis  has  been  credited  with  the  disease,  though 
this  is  open  to  doubt.  The  evidences  of  a  meningo-encephalitis,  which 
Striimpell  believed  to  be  the  underlying  condition  in  the  diplegic  cases, 
are  not  forthcoming,  though  it  is  still  held  that  syphilis  and  other  toxic 
influences  are  at  work  in  some  cases.  Simple  agenesis,  or  lack  of  brain 
development,  ah  initio,  without  apparent  cause,  traumatic  or  toxic,  may 
account  for  a  few  cases. 

The  cases  due  to  injur}^  during  birth  are  more  numerous.  Among 
these  natal  causes  should  be  remembered  slow  and  tedious  parturition, 
compression  of  the  head  by  the  mother's  birth  passage  or  by  the  for- 
ceps, retention  of  the  head  high  up  before  delivery,  precipitate  labor, 
etc.  Most  of  these  accidents  occur  in  first  labors  and  many  of  them 
are  associated  with  asphyxia  and  foot  presentations.  The  possible 
existence  of  a  prenatal  cause  should  always  make  one  hesitate  before 
positively  attributing  the  accident  to  one  of  these  obstetrical  causes. 
The  most  skillful  use  of  the  forceps  will  not  save  an  obstetrician's  rep- 
utation if  the  child  is  paralyzed,  though  from  an  almost  positivelv  es- 
tablished prenatal  accident.  The  laity  have  unfortunately  acquired  the 
notion  that  all  these  forms  of  paralysis  are  due  to  the  use  of  the 
forceps,  and  it  behooves  us  to  re-educate  them.  In  these  cases  the 
lesion  is  usually  thrombosis,  embolism,  meningeal  or  intracerebral 
hemorrhage.  They  are  less  frequently  diplegic  in  character  than  are 
the  prenatal  cases,  and  they  are  more  distinctively  hemiplegic. 

The  postnatal  cases  may  be  hemorrhagic  and  due  to  traumata,  but 
they  are  more  commonly  due  to  disease,  tunior  and  general  constitu- 
tional influences.  It  is  these  cases  that  Striimpell  believed  especially  to 
be  dependent  upon  a  polioencephalitis,  an  afl^ection  analogous  to  and  in 
the  same  general  category  as  poliomyelitis.  Infection  certainly  plays 
here  a  large  role ;  measles  and  scarlet  fever  with  nephritis  and  endo- 
carditis especially  being  frequent  among  its  antecedents,     it  has  b^en 


856  THE   NON-NEURONIC  DISEASES 

attributed  also  to  pneumonia,  pertussis,  variola  and  even  vaccination. 
Vascular  disease  and  probably  embolism  are  the  immediate  causes  of 
the  paralytic  condition.  Cranial  injuries  and  mental  shock  in  pro- 
voking hemorrhage  are  undoubtedly  among  the  later  postnatal  causes. 
In  one  case  the  child  was  thought  to  be  dead  immediately  after  birth 
and  allowed  to  lie  a  long  time  exposed  upon  a  marble  slab.  It  is 
doubtful,  however,  whether  the  disease  is  ever  produced  in  this  way, 
especially  in  the  absence  of  infection  or  trauma. 

Pathology  and  Pathogenesis. — The  pathological  findings  in  the 
cerebral  palsies  of  infants  are  numerous  and  varied.  In  one  thing  only 
are  they  uniform,  and  that  is  in  their  involvement  of  the  cortex  and 
related  subcortical  and  spinal  structures.  The  varied  etiology  of  the 
trouble  causes  the  varied  pathology.  The  relationship  of  the  clinical 
picture  to  the  morbid  anatomy  is  not  always  as  distinct  as  could  be 
desired,  but  the  connection  between  the  primary  cortical  damage  and 
the  secondary  spinal  degeneration  is  definitely  recognized.  Post- 
mortem testimony  affirms  very  clearly  that  the  pathogenesis  of  all  this 
class  of  paralysis  involves  a  simple  agenesis,  or  failure  of  brain  develop- 
ment, a  general  diffuse  sclerosis  of  the  cortex  following,  perhaps,  a 
meningo-encephalitis  or  a  very  doubtful  polioencephalitis,  a  hemorrhage 
or  an  encephalomalacia  from  embolism  or  thrombosis.  These  condi- 
tions do  not  differ  per  sc  from  the  same  conditions  in  the  adult ;  but 
as  they  occur  in  the  young  and  undeveloped  brain,  their  ultimate  re- 
sults are  not  the  same.  An  inflammation,  sclerosis  or  a  compressing 
clot  that  prevents  the  growth  of  the  brain  will,  of  course,  produce  a 
different  pathological  and  clinical  exhibition  from  that  produced  by  the 
same  influences  in  a  fully  grown  brain.  The  same  is  to  be  said  of  the 
secondary  degenerations  in  the  underlying  related  tracts.  The  most 
obvious  of'  the  congenital  changes  thus  brought  about  is  the  condition 
known  as  porencephaly.  In  all  of  these  conditions  the  motor  area  of 
the  cortex  is  almost  constantly  involved.  In  rare  instances  it  may  be 
the  only  area  implicated.  In  the  larger  number  of  cases  other  parts  of 
the  brain  are  also  affected,  though,  it  may  be,  not  so  obtrusively  as  the 
motor  areas.  The  general  process  is  a  more  or  less  diffuse  one,  with 
the  initial  focus  usually  in  or  near  the  motor  elements,  but  occasionally 
away  from  them.  Thus  porencephaly  as  well  as  other  changes  have 
been  found  in  the  occipital  lobe  and  cerebellum,  with  corresponding 
congenital  clinical  manifestations.  On  account  of  the  porencephaly, 
late  sclerosis  with  induration  and  atrophy  of  the  hemispheres,  it  is 
often  quite  impossible  to  make  a  satisfactory  guess  as  to  the  exact 
nature  of  the  original  lesion  or  disorder. 

Many  cases  are  believed  to  be  due  to  simple  failure  of  development, 
cerebral  agenesis,  without  any  other  discoverable  cause  or  pathogenetic 
factor.  The  nervous  elements  in  the  cortex  exhibit  microscopic  changes 
that  suggest  mere  defective  development.  Such  cases  have  been 
studied  especially  by  Sachs  and  may  in  part  explain  such  anomalous 
observations  as  that  of  Oppenheim,  wherein  a  mother  and  a  daughter 
were  afflicted  with  the  same  type  of  paralysis. 

A  general,  diffuse  sclerotic  condition  of  the  cortex  is  found  more 
frequently  than  that  of  simple  agenesis.     This  is  probably  due  to  a 


THE   NON-NEUROXIC  DISEASES  857 

low  grade  of  chronic  inflammation,  whicli  may  have  been  chronic  from 
the  beginning  or  have  succeeded  a  meningo-encephahtis.  If  the  in- 
flammation is  more  or  less  localized,  it  may  have  diffused  itself  from 
a  focus  started  by  a  hemorrhage  or  other  trauma ;  or  if  it  is  so 
widely  spread  out  as  to  involve  the  greater  part  of  the  cortex  it  is 
probably  toxic  or  infectious  in  origin.  The  few  cases  that  are  attribut- 
ed to  syphilis,  and  the  many  that  seem  to  follow  the  infectious  fevers, 
may  thus  be  explained.  A  whole  hemisphere  may  be  affected  thus,  and 
on  account  of  the  atrophy  may  be  rendered  much  smaller  than  it  nor- 
mall}^  should  be.  This  is  sometimes  called  lobar  sclerosis.  Excrescences 
in  the  brain  substance,  hypertrophic  sclerosis  and  hydrocephalus  are 
accompaniments  sometimes  of  this  condition.  The  effort  of  Striimpell 
to  align  these  cases,  in  part  at  least,  with  infantile  spinal  palsy  by  at- 
tributing them  to  a  pure  polioencephalitis,  has  not  been  very  successful ; 
largely  because  no  evidences  of  such  inflammation,  apart  from  men- 
ingo-encephalitis,  have  been  found  post  mortem.  The  hypothesis,  how- 
ever, is  not  unworthy  of  further  investigation. 

By  all  odds  the  great  majority  of  these  cases,  even  of  the  diplegic 
type,  are  due  to  hemorrhage,  emholism  or  thrombosis.  The  relative 
f requeue V  of  these  respectively  cannot  be  definitely  determined.  In 
traumatic  cases,  whether  intra-  or  extra-uterine,  intra-cerebral  hem- 
orrhage certainly  accounts  for  the  hemiplegia,  while  meningeal  hem- 
orrhage explains  the  bilateral  or  diplegic  paralyses.  Infective  and  toxic 
states,  with  the  associated  vascular  disease,  are  the  general  causes 
underlying  most  of  the  cases  of  embolism  and  thrombosis.  Areas  of 
focal  softening,  dried-up  cysts  and  spots  of  cicatricial  atrophy  are  the 
evidences  usually  presented. 

When  the  nutrition  of  a  part  of  the  brain  is  shut  off  by  direct 
damage  or  by  arterial  obstruction,  it  ceases  to  grow,  a  large  cavity 
is  formed,  which  may  extend  into  the  ventricle,  funnel-shaped  and  the 
condition  of  porencephaly  established.  This  is  usually  prenatal  in 
origin,  though  it  may  start  after  birth.  It  is  said  to  occur  in  about  one- 
fourth  of  the  cases.     It  may  be  observed  in  one  or  both  hemispheres. 

A  curious  condition  that  has, been  found  in  the  brains  of  some  of 
these  diplegics  is  that  known  as  microgyria.  It  is  a  developmental 
anomaly  clearly  and  reveals  a  great  increase  in  the  number  of  gyri 
and  intervening  sm.all  sulci.  The  whole  gray  cortex  seems  to  be  fold- 
ed in  and  out  much  as  it  is  in  the  vermis  cerebelli.  Otto  has  illustrated 
it  well. 

The  secondary  changes  in  the  projection  tracts  from  the  defective 
cortex  are  again  slightly  different  from  what  they  are  in  the  adult 
cases.  The  development  is  checked  and  not  fully  developed  elements 
merely  destroyed.  Some  have  thought  that  this  developmental  inhibi- 
tion might  be  primary  in  the  cord  and  so  account  for  the  cases  of 
supposed  primary  congenital  spastic  paraplegia.  This  is  very  doubtful, 
however.  Developmental  degeneration  in  neuraxones  without  primary 
changes  of  any  sort  in  the  related  cell  bodies  would  upset  all  our  mod- 
ern ideas  in  regard  to  neurone  histopathology. 

Symptoms. — In  most  of  the  cases  of  infantile  cerebral  palsy  the 
disease  does  not  attract  attention  until  the  paralysis  is  quite  noticeable. 


858  THE   NOX-XEUROXIC  DISEASES 

Only  in  the  postnatal  cases  can  the  initial  phenomena  be  observed,  and 
even  in  these  cases  they  are  frequently  overlooked  or  misinterpreted. 
According  to  the  nature  of  the  case,  they  consist  of  a  unilateral  or 
general  convulsion,  followed  by  a  hemiplegia,  or  a  febrile  outbreak 
with  vomiting,  delirium,  stupor,  followed  by  a  more  or  less  diplcgic 
form  of  paralysis.  Instead  of  one  or  two  general  or  unilateral  con- 
vulsions, a  series  of  spasms  may  appear  for  several  days  or  weeks,  and 
ukimately  pass  into  a  state  of  bilateral  or  unilateral  hemiplegia.  The 
convulsions  may  occur  at  or  immediately  after  birth,  but  the  paralysis 
mav  not  be  noticed  for  weeks  or  months  later.  This  is  not  so  much 
due  to  the  fact  that  the  paralytic  is  far  removed  from  the  convulsive 
stage  as  that  the  former  is  not  made  obvious  until  the  period  has  ar- 
rived at  which  the  finer  movements  of  the  limbs,  which  suffer  the 
most,  would  normal!}"  begin  to  announce  themselves.  Therefore  most 
of  the  cases  of  cerebral  palsy  in  children  occur  in  the  period  between 
six  months  and  three  years  of  age.  The  infantile  peculiarities  of  these 
hemiplegias  are  due  obviously  to  the  fact  that  they  occur  in  the 
preeminently  developmental  period  of  life. 

The  two  prominent  features  that  stand  out  in  the  clinical  picture  of 
these  palsies  are  the  eharacteristic  paralysis  of  the  extremities  and  cer- 
tain other  symptoms  that  are  even  more  distinctively  of  cerebral 
origin,  such  as  epilepsy,  strabismus,  speech  troubles  and  psychical  dis- 
turbances. 

The  paralysis  in  the  limbs,  as  I  have  said,  follows  soon  after  the 
convulsive  stage.  It  is  distinctly  a  hemiplegia  or  unilateral  symptom. 
It  usually  involves  the  lower  extremities  more  than  the  upper.  In  some 
cases  its  onset  is  the  same  as  it  is  in  the  hemiplegia  of  adults.  The 
entire  body  is  convulsed  and  paralyzed  during  a  brief  comatose  stage. 
Gradually,  however,  one  side  of  the  body  recovers  leaving  the  face, 
arm  and  leg  of  the  opposite  side  limp  or  immovable.  More  frequently 
spasmodic  movements  occur  in  the  face,  eyes,  neck,  arm  or  leg.  As 
these  quiet  down,  some  slight  return  of  movement  appears  in  the  face, 
then  the  arm  and  even  the  leg.  The  face  as  a  rule  quickly  regains  its 
normal  appearance  and  activity ;  the  arm  continues  to  improve  until 
in  some  cases  it  may  appear  to  be  quite  natural  again ;  the  leg.  how- 
ever, usually  recovers  only  in  part  and  is  nearly  always  permanently 
affected.  When  the  arm  continues  to  be  paralyzed  the  leg  as  a  rule 
is  still  more  so.  When  the  age  arrives  for  the  child  to  attempt  walk- 
ing, the  paralysis  of  the  limbs  becomes  extremely  obvious  and  often  it 
is  not  until  this  time  that  the  parents  fully  realize  that  their  child  is 
seriously  affected.  The  attempted  steps  taken  by  the  little  one  are 
seen  to  be  awkward,  difficult,  stiff  and  jerky.  In  the  course  of  time 
the  gait  assuines  a  characteristic  manner.  The  strong  adduction  of 
the  legs,  their  irregular,  stiff",  spasmodic  movements  and  their  want 
of  equilibrium  in  the  activit}'  of  the  antagonistic  sets  of  muscles,  cause 
the  typical  cross-legged  progression  and  attitude  shown  in  the  accom- 
panying photographs.  The  knees  rub  against  each  other,  the  joints 
are  slightly  flexed,  and  the  foot  is  so  extended  that  it  rests  entirely  on 
the  balls  of  the  toes.  Rigidity,  motor  weakness  and  marked  exagger- 
ation of  the  knee-jerks  can  all  be  observed.       There  are  no  sensorv 


THE   NON-NEURONIC  DISEASES 


859 


O 


2 


86o  THE   XOX-NEUROXIC  DISEASES 

symptoms,  no  muscular  atrophy,  or  very  little,  no  electrical  alterations. 
of  importance  ;  simply  a  spastic,  motor  paralysis  with  contracture  in 
certain  groups  of  muscles  resulting  in  a  characteristic  gait  and  attitude. 

The  arms  may  or  may  not  be  affected  in  company  with  the  legs.. 
When  they  are.  their  movements  and  attitude  are  typical.  As  they  are- 
less  involved  as  a  rule  than  the  legs,  their  movements  are  not  so  rigid 
and  weak  as  they  are  choreic  and  athctoid  or  vermicular  and  waxy-like. 
The  joints  are  somewhat  flexed  and  the  muscles  contractured.  Ad- 
duction, flexion  and  exaggerated  tendon  reflexes  are  characteristic 
phenomena. 

I  have  described  the  above  symptoms  as  being  hemiplegic  in  order 
to  impress  the  fact  that  they  are  unilateral  in  origin.  As  a  matter  of 
fact  they  are  bilateral  in  distribution,  and  being  more  frequent  and  more 
marked  in  the  lower  than  in  the  upper  extremities,  the  entire  clinical 
picture  so  closely  resembles  a  spinal  paraplegia  that  it  aft'ords  some 
slight  ground  for  the  suspicion  that  there  may  be  a  primary  spastic, 
paraplegia  in  infants  comparable  to  the  adult  primary  spastic  para- 
plegia of  Erb.  Until  the  existence  of  spinal  spastic  paraplegia  is  better- 
established  than  it  is  to-day,  it  seems  to  me  preferable  to  apply  to  these 
cases  the  name  diplegia,  or  double  hemiplegia,  and  not  the  misleading 
term  paraplegia. 

In  the  cases  that  are  distinctively  unilateral  the  same  general  de- 
scription of  the  paralysis  applies,  except  that  here  the  arm  is  more 
affected  than  the  leg.  The  face  usually  manifests  irritative  rather  than 
paralvtic  symptoms.  The  tongue  is  temporarily  involved.  The  leg' 
recovers  earlier  and  more  than  the  arm.  In  a  word,  the  clinical  pic- 
ture is  identical  with  that  of  cerebral  hemorrhage,  embolism  and  throm- 
bosis in  adults.  The  motor  weakness,  the  rigidity,  the  flexions,  the 
contractures  and  the  exaggerated  reflexes  differ  in  nowise  from  the 
adult  forms,  only  as  they  interfere  with,  the  further  development  of  the 
parts.  Deformity,  shortening,  diminution  in  size  and  muscular  wasting" 
from  non-use  are  the  inevitable  results.  All  degrees  of  the  trouble  may 
be  observed,  from  a  scarcely  perceptible  rigidity  up  to  an  extreme 
paralysis.  The  tendon  reflexes  are  always  increased  and  the  muscular 
tone  heightened.  Occasionally  an  ankle  clonus  may  be  evoked.  The 
arm  may  be  paralyzed  and  the  leg  merely  spastic.  In  fact,  great  varia- 
bility occurs  in  the  grouping  of  the  symptoms  of  infantile  hemiplegia.. 

A  curious  and  noteworthy  phenom.enon  in  these  early  hemiplegias 
is  the  associated  movements.  AMien  a  movement  is  performed  on  the 
well  side,  a  lesser  but  corresponding  movement  is  automatically  per- 
formed on  the  paralyzed  side. 

*  Much  more  common  in  childhood  hemiplegia  are  the  symptoms  of 
cerebral  irritation.  They  consist  chiefly  of  choreiform,  athetoid  and 
trembling  movements.  Involuntary,  irregular,  incoordinated  jactita- 
tions occur  in  the  limb  and  resemble  exactly  a  true  chorea  except  irr 
being  so  localized.  They  have  been  more  or  less  present  in  every  case 
that  I  have  examined.  The  frequency  and  distribution  of  these  post- 
hemiplegic choreas  throw  considerable  light  upon  the  probable  patho- 
genesis of  all  forms  of  chorea.  The  athetoid  movements  often  observed 
in  these  cases  consist  of  slow,  deliberate,  wormv,  wax-like  flexion  and 


THE  NON-NEURONIC  DISEASES  86l 

-extension,  especially  of  the  fingers  and  hand.  They  give  to  the  move- 
ments and  attitude  an  appearance  of  excessive  afifectation.  Athetosis 
may  occur  in  the  leg  as  well  as  in  the  arm.  One  limb  may  even  be 
choreic  and  another  athetoid.  In  some  exceptional  cases  an  intentional 
tremor,  such  as  is  observed  in  disseminated  sclerosis,  may  be  detected. 

The  cranial  nerves  may  be  implicated,  causing  strabismus,  speech 
disturbances,  difficult  deglutition  and  other  signs  of  bulbar  disease. 
The  motor  character  of  all  these  manifestations  is  so  overwhelming  that 
one  is  prone  to  regard  the  lesion  as  solely  one  of  the  motor  area  of  the 
cortex.  It  would  upset,  or  at  least  greatly  confuse,  the  accepted  patho- 
genesis of  these  cases  if  no  sensory  symptoms  were  ever  to  have  been 
found.  As  it  is  now  believed  that  the  sensory  elements  of  the  cortex 
are  largely  intermingled  with  the  motor  elements,  one  would  think  that 
sensory  symptoms  ought  to  be  more  frequently  met  with.  Two  ex- 
planations are  possible  to  account  for  their  absence  in  the  report  of 
cases.  In  the  first  place,  it  is  extremely  difficult  to  examine  sensation 
satisfactorily  in  children  so  young  as  these  are  and  to  get  reliable  re- 
sponses ;  and  in  the  second  place,  the  lesion  in  a  large  number  of  cases, 
perhaps  the  largest  number,  involves  more  particularly  the  motor 
part  of  the  internal  capsule,  and  only  temporarily  and  indirectly  affects 
the  sensory  part.  Nevertheless  in  a  few  carefully  examined  cases 
hypaesthesia,  Wernicke's  mental  tactile  ansesthesia,  hemianopsia  and 
aphasia  have  been  noted. 

In  all  of  the  cases  of  infantile  hemiplegia,  whether  unilateral  or 
bilateral,  prenatal  or  postnatal,  cerebral  symptoms  of  an  irritative  and 
developmental  character  sooner  or  later  announce  themselves.  Some 
•of  these  have  alread}^  been  referred  to,  as,  for  instance,  the  cranial 
nerve  disturbances,  the  aphasia,  the  hemianopsia,  and  the  choreic  and 
athetoid  exhibitions.  Most  important,  however,  are  the  epileptic  at- 
tacks and  the  mental  deterioration.  Epilepsy  and  imheciUty  are  so  fre- 
quent that  when  found  in  conjunction  with  the  paralysis  become  almost 
pathognomonic. 

Nearly  two-thirds  of  the  cases  are  subject  to  epileptic  attacks. 
Spratling  finds  that  the  most  potent,  immediate  and  single  cause  of 
epilepsy  is  the  cerebral  palsies  of  early  life.  The  attacks  may  come  on 
soon  after  the  convulsive  stage  or  years  after.  Usually  the  paralysis 
lias  existed  a  year  or  two  before  the  fits  began.  I  have  seen  a  case  in 
which  the  convulsion  was  entirely  epileptiform  and  in  which  the  fits 
soon  ceased  in  spite  of  the  high  degree  of  hemiplegia.  The  fit  may  be 
of  the  Jacksonian  or  partial  type,  but  more  commonly  it  is  generalized 
as  in  ordinary  genuine  epilepsy.  Unilateral  epileptiform  convulsions 
and  spasms,  without  loss  of  consciousness,  are  not  uncommon.  The 
fit  is  rarely  as  protean  as  it  is  in  ordinary  epilepsy,  though  one  may 
not  be  surprised  to  see  the  severest  kind  of  fits  with  the  cry,  the  tongue- 
biting,  the  unconsciousness  and  the  convulsions  of  the  idiopathic  dis- 
ease. Even  status  epilepticus,  followed  by  early  death,  may  occur.  I 
lately  saw  a  case  in  which  the  hemiplegia  had  left  only  the  merest  trace 
in  the  hand,  but  the  epilepsy  was  formidable. 

So  severe  a  lesion  as  usually  causes  these  infantile  palsies  could 
bardly  be  expected  to  leave  the  mental  faculties  intact.     The  mental 


862  TLiK   XON-XEUKONIC  DISEASES 

iccakiicss,  iijibccility  and  even  idiocy  are  usually  the  direct  result  of  the 
damage  done  to  the  growing  brain.  On  the  other  hand,  care  must  be 
taken  to  discover,  if  possible,  if  the  mental  deterioration  may  not  be  a 
secondary  result  of  the  epilepsy,  of  loss  of  hearing,  or  absence  of  lan- 
guage from  mere  aphasia.  In  many  cases  the  general  intelligence  is 
not  much  affected,  but  upon  close  examination  it  will  be  noted  that 
there  is  some  degree  of  irritability  of  temper,  exalted  emotionalism 
and  other  symptoms  that  are  hy steroid  in  character.  It  is  important 
always  to  note  the  degree  of  mental  impairment,  for  the  prognosis  and 
possible  improvement  of  the  paralytic  symptoms  depend  in  large  meas- 
ure upon  the  degree  of  mentality  in  the  case.  Moreover  in  those  cases 
in  which  the  psychic  disturbances  are  the  least  the  paralyses  that  have 
remained  somewhat  stationary  occasionally  undergo  a  slight  change  for 
the  better  after  puberty. 

Cranial  malformations,  facial  asvmmetry,  prognathism,  defective 
teeth  and  other  stigmata  of  degeneration  are  found  in  a  certain  per- 
centage of  these  early  hemiplegics.  The  skull  may  be  microcephalic  or 
macrocephalic,  flattened  on  the  side  of  the  lesion  or  otherwise  altered 
with  depressions,  fissures,  etc.  It  is  well  to  carefully  distinguish  always 
true  stigmata  of  degenerac}-  from  the  mere  changes  wrought  in  the 
bones  and  other  tissues  by  such  influences  as  pressure,  disturbed  local 
nutrition  and  delayed  development. 

Diagnosis. — The  diagnosis  of  a  case  of  cerebral  palsy  of  child- 
hood is  not  particularly  difficult  if  the  history  of  the  case  is  well 
studied  and  the  hemiplegic  character  of  the  paralysis,  with  the  possible 
existence  of  cerebral  symptoms,  are  taken  well  into  consideration.  As 
distinguished  from  a  spinal  palsy,  these  cases  involve  larger  groups  of 
muscles,  have  exaggerated  reflexes,  show  no  true  muscular  atrophy  or 
electrical  reaction  of  degeneration  and  are  accompanied  by  cranial 
symptoms,  epilepsy  and  mental  disorders. 

The  real  differential  diagnosis  in  these  cases  involves  more  par- 
ticularly the  distinction  between  the  unilateral  hemiplegias,  the  diple- 
gias and  the  spastic  paralysis  of  Little's  type.  It  must  be  remembered 
that  they  are  all  cerebral  in  origin  and  therefore  are  all  hemiplegic.  In 
regard  to  the  character  of  the  paralysis,  it  is  the  same  in  all  of  them.  ; 
being  merely  tmilateral  in  some  cases,  bilateral  in  others.  This  indi- 
cates involvement  of  one  or  both  hemispheres  with  such  lesions  as 
hemorrhage,  embolism,  thrombosis,  meningo-encephalitis,  encephalitis 
or  simple  agenesis.  The  pathological  diagnosis  is  not  always  easy, 
because  the  same  pathogenetic  factors  may  underlie  very  different 
sets  of  symptoms.  In  general,  however,  it  may  be  said  that  prenatal 
cases  produce  largely  the  Little's  type  of  the  disease  in  which  a  diple- 
gia of  the  lower  limbs,  with  but  little  involvement  of  the  arms  and 
scarcely  any  of  the  mental  faculties,  constitutes  the  salient  feature  in 
the  clinical  picture,  all  depending  upon  simple  cerebral  agenesis,  hem- 
orrhage, chiefly  meningeal,  or  meningo-encephalitis.  The  natal  cases 
or  true  birth  palsies  are  in  most  instances  due  to  meningeal  hemorrhage. 
They  are  diplegic  and  involve  the  arms  and  the  mental  faculties  rather 
more  frequently  than  the  preceding  group  of  cases.  In  the  postnatal 
cases  and  those  following  the  infectious   fevers  hemorrhage,   chiefly 


THE  NON-NEURONIC  DISEASES  863 

intracerebral,  embolism  and  thrombosis  are  the  more  common  causes 
of  the  paralysis.  These  cases  are  usually  unilateral.  They  exhibit  the 
pre-hemiplegic  and  post-hemiplegic  choreic  phenomena,  and  athetosis 
rather  more  frequently  than  the  cases  that  are  more  distinctly  diplegic. 
While  epilepsy  and  mental  deterioration  are  present  in  these  cases,  the 
imbecility  and  idiocy  are  rare  as  compared  with  the  diplegic  cases.  As 
the  paralysis  in  all  of  these  cases  may  occasionally  be  slight  and  the 
epilepsy,  chorea  or  psychic  disturbance  be  very  prominent,  confusion  is 
likely  to  arise  in  the  differential  diagnosis  between  these  accompani- 
ments of  congenital  spastic  palsy  and  ordinary  epilepsy,  chorea  and 
insanity.  A  careful  regard  for  the  anamnesis,  the  character  and 
distribution  of  the  special  symptoms  and  the  results  of  treatment  will 
make  clear  the  real  nature  of  the  case  in  hand. 

Prognosis.^ — The  cerebral  palsies  of  childhood  are  chronic  and 
incurable.  Nervous  elements  that  have  been  profoundly  damiaged  or 
prevented  from  growing  cannot  be  restored  by  human  agencies.  The 
course  of  the  disease,  the  time  and  cause  of  death  and  other  factors 
in  its  prognosis  are  determined  largely  by  the  appearance  and  course 
of  particular  symptoms.  Hemorrhagic  and  acute  encephalitic  cases 
usually  recede  somewhat  and  some  improvement  in  the  resulting 
paralysis  may  be  hoped  for  up  to  the  end  of  the  first  year.  After  that 
it  remains  stationary,  except  in  a  few  of  the  diplegic  cases  in  which 
the  mind  continues  intact,  in  whom  some  improvement  may  be  looked 
for  after  puberty.  Diplegic  cases  as  a  rule  are  more  stationary  than 
the  simple  hemiplegic.  If,  however,  epilepsy  and  imbecility  develop, 
the  prognosis  becomes  bad  and  the  asylum  is  usually  their  final  refuge. 
The  absence  of  mental  disorder  secures  a  better  prognosis  for  the 
paralysis.  The  diplegia  of  Little's  type  therefore  can  often  be  mark- 
edly improved,  as  cerebral  disturbances  other  than  the  double  hemi- 
plegia are  relatively  infrequent. 

Chorea,  athetosis  and  contractures  are  unfavorable  symptoms. 
They  usually  remain  in  spite  of  all  kinds  of  treatment.  Epilepsy  may 
come  on  late  or  early.  It  may  pass  at  any  time  into  status  epilepticus 
and  destroy  the  patient.  The  presence  of  true  stigmata  of  degeneracy 
renders  the  prognosis  unfavorable.  Aphasia  usually  disappears,  though 
dysarthria  may  continue  permanently.  Some  hemiplegics  reach  an  old 
age,  others  succumb  about  the  time  of  the  change  of  life  or  pass  into 
actual  insanity. 

Treatment. — The  treatment  of  the  onset  must  be  in  accordance 
with  the  pathological  diagnosis.  Hemorrhage,  embolism,  thrombosis, 
encephalitis  have  their  own  particular  lines  of  treatment.  In  febrile 
cases  ice  bags,  antipyretics,  cathartics,  etc.,  are  all  in  order.  The 
treatment  should  be  carried  out  on  general  principles.  Rarely,  how- 
ever, is  the  practitioner  called  upon  to  treat  the  early  onset  of  the 
trouble.  As  a  rule  he  is  consulted  only  when  the  paralysis  has  been 
some  time  in  existence. 

Mechanical  and  pedagogic  treatment  is  about  all  that  can  be  in- 
stituted. There  is  no  medicine  with  which  to  combat  the  changes  in 
the  central  nervous  system.  Tonics  are  all  that  can  be  thought  of  in 
the  way  of  medicinal  agents.     Daily  massage,  electricity  and  passive 


864  THE   NON-NEURONIC  DISEASES 

movements  may  be  employed  for  the  paralysis.  Epilepsy  is  to  be 
treated  as  usual  with  the  careful  administration  of  the  bromides.  This 
symptom,  like  the  chorea  and  athetosis,  is  not  very  amenable  to  me- 
dicinal management.  Contractures  should  be  overcome  by  .stretching, 
forcible  replacement,  splints,  tenotomy  and  other  well-known  orthor- 
paedic  and  surgical  procedures. 

Education,  discipline,  gymnastics  and  systematized  exercises  can 
sometimes  accomplish  very  gratifying  results  in  cases  in  which  the 
intelligence  is  preserved.  I  would  warn  against  over-exercise  in  car- 
rying out  this  line  of  treatment.  Exhaustion  must  be  guarded  against. 
With  this  single  proviso,  it  may  be  truthfully  said  that  these  patients 
cannot  be  encouraged  too  much  to  use  and  use  systematically  as  well 
as  they  can  their  paralyzed  limbs. 

Trephining  and  craniectomy  as  suggested  by  Lannelongue  have 
been  tried  in  some  of  these  cases ;  clots  have  been  removed  and  cysts 
have  been  evacuated.  The  ultimate  results  have  not  been  sufficiently 
favorable  in  a  large  enough  number  to  pronounce  definitely  upon  the 
utility  of  these  surgical  measures.     Further  experimentation  is  needed. 

ENCEPHALITIS. 

By  the  term  oicephalitis  is  meant  an  inflammation  of  any  part 
of  the  encephalic  mass,  particularly  the  gray  substance.  The  inflam- 
matory process  may  be  acute  or  chronic,  diffuse  or  focal,  suppurative  or 
non-suppurative,  simple,  toxic,  exudative  and  hemorrhagic.  It  may  be 
primary  and  limited  to  the  gray  substance,  or  it  may  be  secondary  and 
associated  with  a  meningitis  or  other  inflammatory  process.  There  are 
many  forms  of  encephalitis,  therefore,  some  of  which  will  now  be  dis- 
cussed, while  others  will  be  considered  in  other  chapters. 

Chronic  meningo-cncephalitis,  or  dementia  paralytica,  is  of  suffi- 
cient dignity  to  have  a  chapter  by  itself.  The  encephalitis  sometimes 
found  in  connection  with  chorea  insaniens,  acute  mania,  delirium 
tremens,  the  maniacal  form  of  exophthalmic  goitre  and  hydrophobia, 
will  be  noticed  when  these  diseases  are  discussed.  The  spastic  paralysis 
of  childhood  is  in  some  instances  doubtless  due  to  a  foetal  meningo- 
encephalitis, while  the  hemiplegia  of  children  has  been  thought  by 
Striimpell,  though  not  by  others,  to  be  the  result  of  a  polio-encephalitis, 
a  sort  of  homologue  of  poliomyelitis.  Indeed,  after  infectious  diseases 
there  sometimes  is  found  a  diffuse  encephalitis,  which  constitutes  a 
part  of  a  disseminated  my'elo-encephalitis.  Disseminated  encephalitis 
is  the  name  sometimes  given  to  the  cerebral  form  of  multiple  sclerosis. 
Syphilitic  encephalitis  will  be  noticed  vmder  the  head  of  syphilis  of  the 
nervous  system.  When  treating  of  the  ocular  palsies  and  of  diseases  of 
the  medulla  oblongata  respectively,  mention  will  be  made  of  superior 
and  inferior  hemorrhagic  polio-encephalitis. 

It  will  be  observed  that  these  forms  of  encephalitis  are  either  parts 
of  a  larger  inflammatory  process,  or  are  so  focalized  as  to  be  dis- 
cussed to  a  better  advantage  elsewhere. 

In  this  section  two  of  the  principal  forms  of  the  disease  only  will 
be  treated  of  in  detail — namely,  the  acute  non-purulent  hemorrhagic 


THE  NON-NEURONIC  DISEASES  865 

encephalitis  and  the  acute  and  chronic  purulent  encephalitis,  or  cerebral 
abscess. 

ACUTE   HEMORRHAGIC   ENCEPHALITIS. 

This  is  a  scattered,  focal,  non-suppurative  inflammation  of  the 
Brain,  characterized  especially  b)^  spots  of  intense  congestion  with 
capillary  hemorrhages. 

Etiology. — Though  many  causes  have  been  credited  with  this 
disease,  it  is  now  pretty  well  established  that  some  form  of  infection 
is  the  cause  in  the  vast  majority  of  cases.  Influenza  seems  particu- 
larly blameworthy,  many  cases  always  occurring  during  an  epidemic. 
It  has  followed  measles,  scarlet  fever,  pneumonia,  erysipelas,  pertussis, 
mumps  and  diphtheria.  It  has  been  seen  in  the  victims  of  an  ulcerative 
endocarditis.  According  to  Osier,  the  most  typical  encephalitis  ac- 
companies the  meningitis  of  cerebro-spinal  fever.  Dana  adds  typhoid 
and  typhus  to  the  causative  infections  and  says  that  it  may  occur  in 
connection  with  the  puerperal  state.  It  is  an  open  question  whether 
it  can  result  from  acute  alcoholism  without  coincident  infection.  Sun- 
stroke, Dana  believes,  has  produced  it,  while  some  observations  would 
seem  to  indicate  that  it  may  follow  simple  traumata.  It  is  not  im- 
probable that  the  traumatic  encephalitis  may  be  difi^erent  from  the 
infectious,  so  little  is  known  about  it.  It  is  a  common  observation, 
however,  that  a  simple  contusion  or  local  shock  often  serves  to  estab- 
lish a  nidus  for  the  bacteria  or  other  microorganisms  of  a  latent  infec- 
tion to  begin  their  work  in. 

Pathology  and  Pathogenesis. — -The  disease  process  is  seen  post 
mortem  as  an  acute  inflammation  of  the  exudative  and  hemorrhagic 
type.  The  capillaries  are  engorged ;  the  tissues  are  hyperaemic,  swol- 
len and  moist ;  the  vascular  sheaths  are  distended  with  fluid ;  there  is 
an  infiltration  of  leucocytes ;  and  in  the  older  cases  there  are  granu- 
lated cells  and  proliferated  gliomatous  cells.  There  is  irritation  and 
■degeneration  of  the  nervous  elements.  All  of  which  are  seen  to  be 
limited  to  more  or  less  circumscribed  areas  scattered  about  in  the  cere- 
bral cortex,  central  ganglia,  centrum  semiovale  and  cerebellum.  Some- 
times these  extend  into  the  medulla  and  pons,  giving  rise  to  the 
form  of  the  disease  known  as  acute  bulbar  myelitis  and  acute  inferior 
polioencephalitis.  The  process  may  even  reach  as  far  dovm  as  the 
cord,-  thus  involving  the  whole  cerebro-spinal  axis  and  giving  rise  to 
the  disease  known  as  disseminated  myelo-encephalitis.  According  to 
Oppenheim,  a  combination  of  encephalitis  with  acute  anterior  polio- 
myelitis has  been  observed,  and  it  was  Striimpell's  idea  that  the  acute 
encephalitis,  which  he  believed  to  be  the  cause  of  infantile  cerebral 
paralysis,  was  in  some  way  related  by  analogy  with  inflammation  of  the 
anterior  cornua  in  infantile  spinal  paralysis.  Many  observers  have 
noted  a  sinus  thrombosis  with  this  encephalitis,  while  in  severe  cases 
Oppenheim  has  found  a  marked  ventricular  exudate,  meningeal  hyper- 
semia,  etc.  When  the  process  is  a  mild  one  with  recovery,  minute 
sclerotic  foci  may  be  left  in  the  brain.  In  the  severer  cases  an  extensive 
softening  may  occur  and  larger  hemorrhages,  even  terminating  in  a 
massive  apoplexy,  as  once  seen  by  Dana. 


866  THE  NON-NEURONIC  DISEASES 

Symptoms. — This  disease  is  most  frequently  observed  in  girls  and 
children  of  tender  years.  They  rarely  complain  of  any  premonitions, 
for  the  headache,  the  malaise,  the  mental  apathy  may  be  the  result  of 
the  infection  rather  than  of  the  encephalitis.  The  latter  usually  an- 
nounces itself  abruptly  by  a  chill,  a  sudden  rise  of  temperature  and  a 
stuporous,  seinicoiiscious  condition  that  closely  simulates  an  apoplectic 
attack.  Unlike  apoplexy,  however,  the  pupil's  react  to  light,  the  re- 
flexes remain  unaffected  and  the  coma  is  not  so  deep.  The  pulse  be- 
comes quick  and  feeble  and  the  respirations  are  rapid.  Unlike  menin- 
gitis, there  is  no  stiffness  of  the  back  of  the  neck  and  no  signs  of  a 
generalized  cortical  irritation.  In  many  cases  the  coma  rapidly  deep- 
ens and  in  twenty-four  or  forty-eight  hours  the  patient  is  dead. 

Sometimes  the  disease  runs  a  milder  and  more  protracted  course 
of  several  weeks,  with  remissions  and  exacerbations.  In  such  cases 
there  mav  be  a  temporary  clearing  up  of  the  mental  stupor,  but  there 
will  be  left  a  monoplegia  or  a  hemiplegia.  Aphasia  is  not  unlikely  to 
occur  and  even  cortical  epilepsy  and  hemianopsia.  In  some  cases 
optic  neuritis  was  seen.  The  location  and  nature  of  the  lesions  are 
various  and  hence  there  is  no  strict  uniformity  in  the  clinical  picture. 

Di.-\GNOSis. — ^Meningitis  is  the  disease  with  which  hemorrhagic 
encephalitis  is  most  frequently  confounded.  Sometimes  it  is  absolutely 
impossible  to  make  a  diff'erential  diagnosis.  In  encephalitis,  however, 
the  absence  of  the  irritative  signs,  like  the  muscular  rigidity  of  the 
back  of  the  neck,  the  normal  pupillary  reaction,  the  absence  of  Kernig's 
sign,  the  absence  of  cutaneous  hypergesthesia,  involuntary  cry  with  the 
presence  of  paralytic  manifestations,  epileptiform  attacks  and  a  history 
of  infection,  wnll  give  much  assistance.  The  differentiation  of  a  tuber- 
culous meningitis  might  be  made  by  lumbar  puncture  and  the  discovery 
of  a  tuberculous  process  in  the  lungs  or  bowels. 

Prognosis. — The  prognosis  is  grave,  but  not  necessarily  bad.  Re- 
covery occasionally  occurs  with  a  convalescence  lasting  for  weeks, 
months  and  sometimes  years.  Rarely  does  recovery  take  place  devoid 
of  all  permanent  defect.  A  hemiplegia,  multiple  sclerosis  or  mental 
deterioration  may  be  the  after-clap. 

Treatment. — Rest,  both  mental  and  physical,  absolute  rest,  is  the 
best  that  can  be  done  in  the  way  of  treatment.  In  the  beginning  active 
purgation  with  calomel,  croton  oil  and  stimulation  of  the  kidneys  are 
indicated.  Cold  compresses  and  an  ice-bag  to  the  head,  venesection, 
leeches  all  constitute  good  routine  measures.  The  feet  may  be  kept  in 
hot  water.  Stupor  with  a  high  fever  would  indicate  the  need  of 
aconite.  Strychnia  might  be  used  in  asthenic  cases.  In  all  classes  of 
cases  the  nourishment  should  be  kept  well  up  and  the  excessive  pain 
should  be  controlled  with  morphine.  Chloral  and  the  bromides  may 
be  used  to  combat  sleeplessness  and  irritability.  Oppenheim  says  that 
in  one  case  that  recovered  calomel  ni  large  doses — even  to  the  point  of 
producing  stomatitis — was  used.  There  is  nothing  to  be  said  particu- 
larly of  the  after-treatment  and  the  management  of  the  convalescence. 
It  is  about  the  same  as  it  would  be  in  a  case  of  ordinary  cerebral  hem- 
orrhage. 


THE   NOiM-NEURONIC  DISEASES  867 

ACUTE  SUPPURATIVE  ENCEPHALITIS. 
(CEREBRAL  ABSCESS.) 

Idiopathic  brain  abscess  is  practically  unknown,  though  at  rare 
intervals  a  case  is  observed  in  which  no  cause  can  be  found  for  the 
suppurative  process.  It  is  probable  that  in  such  cases  a  direct  cause 
was  present  sometime,  but  so  long  ago  or  so  unobtrusive  was  it  that  it 
had  been  quite  forgotten.  Cerebral  abscess  is  then  the  result  of  an 
acute  suppurative  encephalitis,  focal  or  diffuse,  produced  by  microor- 
ganisms introduced  into  the  brain  from  without. 

Etiology. — Acute  suppurative  encephalitis  is  always  the  result  of 
bacteria  that  have  gained  entrance  into  the  brain  substance  in  three 
general  ways.  It  is  etiologically  due,  therefore,  to  direct  injury  of  the 
head,  to  extension  of  a  suppurative  process  in  the  tissues  hnmediately 
surrounding  the  brain,  or  to  a  metastatic  transference  of  the  bacteria 
by  the  blood  from  some  remote  center  of  suppuration  in  the  body. 

It  is  estimated  that  about  30  per  cent,  of  the  brain  abscesses  are 
due  to  traumatism.  A  fracture  or  puncture  of  the  skull  is  the  usual 
form  of  the  injury.  In  some  cases  a  foreign  body  has  passed  into  the 
brain ;  in  others  a  mere  contusion  of  the  scalp  has  been  sufficient  to 
give  entrance  to  the  germs.  The  majority  of  the  traumatic  cases  have 
been  complicated  fractures  in  the  frontal  and  parietal  parts  of  the 
head.  Operations  within  the  nasal  and  orbital  cavities  have  been  re- 
sponsible in  a  few  instances.  Bone  fracture  is  not  absolutely  necessary 
for  the  admission  of  the  germs,  since  infected  emboli  and  implication 
of  the  lymphatics  are  fully  adequate.  It  is  clear  how  some  of  these 
slighter  traumatic  causes  may  readily  be  overlooked  when  it  is  remem- 
bered that  sometimiCS  the  cerebral  symptoms  do  not  announce  them- 
selves until  many  years,  ten,  twenty  and  thirty  even,  after  the  injury. 

Somewhat  more  than  a  third  of  the  cases  are  due  to  extension  of 
the  suppurative  process  or  the  transmission  of  the  microorganisms  from 
chronic  otitis  media  and  disease  of  the  mastoid  cells.  Of  these  ear  cases, 
it  is  found  that  about  85  per  cent,  are  due  to  chronic  suppuration,  and 
the  remaining  15  per  cent,  to  acute  suppuration  in  the  ear.  The  number 
of  cases  due  to  mastoid  disease  is  less  than  those  due  to  otitis  media. 
Most  of  these  ear  troubles  follow  the  infectious  fevers  of  childhood. 
They  sometimes  continue  many  years,  undergo  remissions,  or  even 
disappear  entirely  long  before  the  evidences  of  brain  trouble  declare 
themselves.  In  a  considerable  number  of  cases  I  have  been  struck  with 
the  statement  of  the  patient  that  many  years  before  she  had  had  a 
running  from  her  ears  for  a  time,  but  her  physician  had  succeeded  in 
stopping  the  discharge.  Sometimes  there  is  perforation  of  the  tympanic 
membrane  in  these  cases  and  even  caries  of  the  petrous  bone,  with 
periodical  attacks  of  otorrhoea.  In  rare  instances  the  suppurative 
process  has  extended  from  the  nasal  or  orbital  cavity;  or  there  has. 
been  caries  of  the  neighboring  bones,  such  as  the  ethmoid,  sphenoid^ 
superior  maxilla. 

The  distant  sources  of  infection  are  numerous  and  varied.     In 


868  THE   XOX-.\EL"KOXIC  DISEASES 

some  way  by  nictastasis  the  germs  are  carried  to  the  brain  from  the 
most  remote  parts  of  the  body.  Even  a  purulent  osteitis  or  arthritis 
may  in  rare  instances  be  the  origin  of  the  brain  abscess.  It  is  stated 
that  about  one-fifth  of  the  cases  are  due  to  pyemic  emboli  ^om  the 
thoracic  cavity.  Bronchiectasis,  empyema,  pulmonary  gangrene  or 
abscess,  purulent  pericarditis,  ulcerative  endocarditis,  have  been  fol- 
lowed by  brain  abscess.  The  latter  has  been  attributed  to  abscesses  in 
the  abdominal  viscera,  to  actinomycosis  and  to  simple  thrush.  Tubercle 
bacilli  and  pneumococci  have  been  recovered  from  it.  In  these  cases 
the  abscesses  are  apt  to  be  small  and  multiple. 

Cerebral  abscess  occurs  more  frequently  in  males  than  in  females, 
and  oftenest  between  the  ages  of  ten  and  thirty. 

Pathologv  axd  Pathogexesis. — Abscesses  may  occur  in  all  parts 
of  the  brain  and  are  usually  associated  with  signs  of  traumatism,  ear 
trouble  or  remote  suppurative  foci.  They  may  be  outside  of  the  dura 
{extradural) ,  inside  of  the  dura  {subdural) ,  in  the  cortex  or  in  the  cen- 
trum semiovale.  Multiple  abscesses,  as  many  as  a  hundred  having  been 
counted  in  one  case,  may  be  no  larger  than  a  pea;  simple  abscesses 
may  attain  the  size  of  an  orange,  or  even  occupy  one  whole  hemi- 
sphere. Cerebral  abscesses  are  usualh  single ;  cerebellar  are  more  apt 
to  be  multiple.  As  a  rule  the  abscess  lies  just  beneath  the  seat  of 
injury;  occasionally,  however,  it  is  found  on  the  opposite  side,  the 
result  of  the  contre-coup.  Traumatic  abscesses  are  largely  extradural 
and  are  accompanied  by  meningitis.  They  are  more  frequent  in  the 
frontal  and  parietal  lobes,  as  the  front  of  the  head  is  most  exposed  to 
blows.  Otitic  cerebral  abscesses  are  found  usually  in  and  just  beneath 
the  gray  cortex  of  the  temporo-sphenoidal  lobe  on  the  same  side  as 
the  affected  ear.  Abscesses  due  to  mastoid  disease  are  generally  located 
in  the  cerebellum.  In  the  pons  and  medulla  they  are  rarly  seen. 
Chronic  abscesses  are  round  in  shape  and  encapsulated  within  a  fibrous 
wall,  which  takes  about  four  weeks  to  form. 

There  is  nothing  unique  about  the  formation  process  of  these 
abscesses.  The  usual  pyogenic  microorganisms  are  found  within  them, 
especially  the  streptococcus  pyogenes,  the  staphylococcus  pyogenes 
aureus,  albus  and  citreus.  They  undergo  the  usual  transformation  of 
red  and  yellow  softening,  with  crowding  of  the  leucocytes,  infiltration 
of  inflammatory  exudate,  destruction  of  nerve  cells  and  processes,  ap- 
pearance of  granular  corpuscles,  etc. 

Symptoms. — ^The  symptoms  of  brain  abscess  arrange  themselves 
into  three  groups — namely,  those  of  a  general  character  due  to  the 
presence  of  a  septic  process,  those  due  to  intracranial  pressure  from 
the  presence  of  the  abscess,  and  those  that  depend  upon  the  particular 
location  of  the  abscess  within  or  upon  the  encephalic  mass. 

In  the  histor}-  of  every  cerebral  abscess,  especially  if  it  is  clonic, 
practically  all  of  these  three  groups  of  symptoms  have  been  more 
or  less  in  evidence  sometime  or  other.  They  may  not  all  be  present 
simultaneously,  and  the  last  or  localization  group  is  the  one  most  fre- 
quently absent.  Moreover,  they  do  not  all  exist  with  the  same  degree 
of  prominence.  In  one  case  the  septic  symptoms  may  be  the  most 
prominent,   as   is  often   the   case   in   the  pysemic  metastatic   multiple 


THE  NON-NEURONIC  DISEASES  869 

abscesses;  in  another  case  the  pressure  symptoms  may  be  the  only 
markedly  noticeable  ones ;  in  a  third  case  there  may  be  distinct  local- 
ization symptoms,  but  the  septic  and  pressure  signs  may  be  so  slight 
or  evanescent  that  one  hesitates  to  diagnose  the  neoplasm  as  an  abscess. 
It  is  calculated  that  in  about  8  or  lo  per  cent,  of  cases  the  symptoms 
are  so  slight  that  they  are  overlooked  entirely  and  the  abscess  is  not 
discovered  until  after  death. 

With  all  this  variability  and  uncertainty  about  its  symptomatology, 
a  brain  abscess  can  pretty  nearly  always  be  strongly  suspected,  if  not 
absolutely  diagnosed,  if  the  history  and  physical  examination  are  gone 
into  minutely  and  conscientiously.  This  applies  with  special  force  to 
the  early  diagnosis  of  the  trouble  and  is  of  paramount  importance 
because  the  earlier  the  diagnosis  is  made  the  brighter  is  the  hope  from 
surgical  intervention. 

Strictly  speaking,  there  are  no  prodromes,  but  what  are  sometimes 
called  prodromes  are  early  symptoms  in  one  case  or  even  late  symptoms 
in  a  mild  or  latent  abscess.  A  slight  headache,  a  feeling  of  malaise,  oc- 
casional chilliness,  attacks  of  cardiac  palpitation,  sudden  and  unac- 
countable slight  elevations  of  temperature,  certain  fugitive  vasomotor 
manifestations,  occasional  attacks  of  insomnia,  an  annoying  degree  of 
slight  mental  hebetude  with  a  feeling  of  depression  and  anxiety — in  a 
word,  all  the  signs  of  a  mild  form  of  toxccmic  neurasthenia — may  con- 
tinue for  months  and  years  before  more  definite  indications  declare 
themselves.  I  saw  a  case  that  misled,  by  reason  of  the  indefiniteness  of 
its  clinical  manifestations,  many  diagnosticians  for  seventeen  years, 
during  which  period  the  patient  had  been  a  number  of  times  suspected 
of  being  insane,  being  sent  each  time  to  an  asylum  and  discharged  as 
cured  after  several  weeks.  When  I  saw  her  the  clinical  picture  was 
clear  enough  to  warrant  a  positive  diagnosis  of  abscess,  from  which 
the  patient  finally  died  in  coma  several  days  later. 

It  is  difficult  to  say  usually  how  much  of  these  early  symptoms  are 
due  to  the  sepsis,  especially  if  there  are  other  septic  foci  elsewhere  in 
the  body,  and  how  much  to  the  cerebral  neoplasm  alone  and  its  non- 
septic  disturbances.  The  headache,  for  instance,  in  these  circumstances 
cannot  always  be  assigned  to  the  toxic  disturbance  or  the  pressure. 
Such  a  group  of  manifestations,  neurasthenic  and  phrenasthenic  in 
character,  if  associated  with  a  history  of  head  injury,  abscess  foci  else- 
where and  especially  ear  trouble,  should  always  put  the  physician  on 
his  guard  and  awaken  a  lively  suspicion  of  a  possible  cerebral  abscess. 

It  is  in  the  acute  abscesses,  following  wounds  about  the  head,  and 
in  the  exacerbations  of  the  chronic  abscesses  from  the  other  causes, 
that  the  constitutional  septic  symptoms  m_ake  themselves  particularly 
obvious.  They  are  the  same  as  symptoms  that  occur  in  all  septic 
poisoning — namely,  chills,  variable  temperature,  anorexia,  coated 
tongue,  constipation,  headache,  dullness  of  mind,  general  feeling  of 
malaise  and  emaciation.  A  general  cachectic  condition  with  icteric 
discoloration  of  the  skin,  loss  of  appetite,  irritability,  restlessness  and 
mental  confusion  sometimes  obtain.  The  fever  is  very  irregular  and 
slight.  In  some  cases  it  is  entirely  absent.  In  no  case  does  it  ever 
last  very  long.     Subnormal   temperature  is   so   frequent  as  to  be  a 


870  THE   NON-NEURONIC  DISEASES 

highly  suggestive  s}'mptoni.  The  pulse  ma}'  be  rapid  and  unsteady ; 
often  it  is  very  slow,  beating  only  40  or  30  to  the  minute.  With  dis- 
turbance of  the  pulse  and  sudden  elevation  of  the  temperature  the 
headache  increases  in  severity.  The  respiration  is  sometimes  irregular 
and  slow. 

The  pressure  symptoms  of  brain  abscess  are  much  the  same  as 
those  of  any  form  of  intracranial  growth.  They  are  headache,  mus- 
cular tivitching  and  rigidity,  local  and  generalized  convulsions,  epilepti- 
form phenomena,  paralysis,  vertigo,  vomiting  and  mental  stupor.  Con- 
traction and  dilatation  of  the  pupils,  disturbed  vision,  optic  neuritis, 
tinnitus  aurium  and  other  symptoms  dependent  upon  the  cranial  nerves 
sometimes  occur.  The  subnormal  temperature,  retarded  pulse-beat 
and  respiration  and  certain  vasomotor  disturbances  are  in  part  due  to 
the  intracranial  pressure. 

Of  all  these  pressure  symptoms  the  headache  is  probably  the  most 
reliable.  It  is  generally  constant  and  severe  and  definitely  localized 
by  the  patient.  He  usually  points  to  a  particular  spot  on  the  head, 
not  un frequently  behind  the  ear  or  in  the  occipital  region,  percussion 
upon  which  causes  him  to  wince.  Sudden  jars  and  disturbances  of 
the  heart  action,  as  well  as  the  onset  of  a  febrile  exacerbation,  cause 
the  headache  to  become  almost  intolerable.  The  same  result  follows  a 
sudden  flash  of  light  or  a  sudden  noise.  Though  more  or  less  constant, 
the  pain  is  often  worse  at  night,  causing  insomnia.  Partly  on  account 
of  this  constant  pain  and  partly  on  account  of  the  pressure  and  general 
septic  condition,  the  patient  becomes  extremely  melancholy,  depressed, 
apathetic  and  stupid.  Occasionally  marked  delirium  occurs  and  passes 
into  coma,  which  in  turn  terminates  in  death.  Sometimes  the  headache 
diminishes  and  I  have  known  it  to  vanish  entirely  after  a  time  without 
any  disappearance,  however,  of  the  other  suspicious  signs  of  abscess. 
Not  always  do  these  headaches  indicate  the  location  of  the  abscess. 
It  may  occur  that  the  headache  is  frontal,  while  the  localization  symp- 
toms point  to  an  occipital  abscess.  A  characteristic  of  them  having 
some  diagnostic  value  is  that  they  are  usually  unrelieved  by  medica- 
tion. 

Vertigo  and  vomiting  are  frequent  symptoms,  the  latter  especially 
so  in  cerebellar  abscess. 

Round  about  the  abscess  minute  hemorrhages  occur.  These  being 
more  marked  in  the  early  stage  of  the  process,  they,  with  the  abscess 
itself,  give  rise  to  irritative  symptoms,  followed  sooner  or  later  by 
paralysis.  Hence  in  cortical  abscesses  there  are  epileptic  phenomena, 
focal  and  generalized,  with  monoplegic  symptoms.  In  this  irritative 
stage  it  is  hard  to  determine  at  times  whether  the  symptoms  are  due 
solely  to  the  abscess  or  to  a  meningitis.  Not  un  frequently  such 
abscesses  are  accompanied  by  a  local  meningitis,  and  then  the  symp- 
toms will  be  of  a  combined  character.  It  is  in  the  traumatic  abscesses 
that  the  meningitis  mostly  occurs  and  the  irritative  symptoms  are  the 
more  prominent. 

Among  the  pressure  symptoms  the  optic  neuritis,  when  present,  is 
a  most  valuable  one.  It  is  of  the  so-called  choked  disc  variety,  Knies' 
obstructive  optic  neuritis.     It  is  never  so  marked  nor   is  it  so  con- 


THE  NON-NEUKONIC  DISEASES  87 1 

stant  as  it  is  in  cerebral  tumor.  It  is  believed  that  ocular  symptoms, 
including  the  motor  and  pupillary,  are  to  be  found  in  about  half  of 
the  cases.  Witherspoon  asserts  that  cerebellar  abscess  gives  rise  to 
optic  neuritis  in  from  75  to  So  per  cent,  of  cases,  whereas  cerebral 
abscess  is  responsible  for  it  in  only  about  30  or  40  per  cent. 

The  fo'cal  symptoms  are  of  much  consequence,  though  unfortu- 
nately they  are  often  too  indefinite.  Abscesses  lying  in  the  so-called 
latent  parts  of  the  brain  cannot,  of  course,  be  localized  by  any  focal 
signs.  Traumatic  abscesses  of  the  frontal  lobes  are  usually  devoid  of 
localizing  symptoms  unless  they  are  large  or  situated  in  the  posterior 
part  of  the  lobe,  especially  on  the  left  side.  By  encroaching  upon  the 
precentral  convolution,  the  base  or  near  the  posterior  part  of  the  third 
frontal,  they  may  cause,  along  with  psychic  confusion  and  other  mental 
disturbances,  Jacksonian  symptoms,  aphasia,  parosmia  and  ataxia. 
Hemiplegia  or  monoplegia  may  occur  with  abscesses  located  in  and 
about  the  cortical  Rolandic  region.  The  metastatic  embolic  abscesses 
from  septic  foci  in  the  thorax  are  apt  to  form  in  the  area  sup- 
plied by  the  Sylvian  artery  and  give  corresponding  focal 
signs.  The  otitic  abscesses  are  usually  single  and  form  in  the  tem- 
poro-sphenoidal  lobe.  The  hearing  consequently  is  affected.  There 
is  mind-deafness,  auditory  aphasia,  and  possibly  by  pressure  amnestic 
aphasia  and  oculomotor  paralysis,  the  frequency  of  which  in  this  form 
of  abscess  has  been  pointed  out  by  Wernicke.  These  abscesses  when 
deep  affect  the  underlying  motor,  sensory  and  optic  conducting  tracts. 
Hence  there  may  be  opposite-sided  hemiparesis  with  rigidity  or  con- 
tracture. Or  there  may  be  hemianzesthesia  and  hemianopsia.  In  a  case 
observed  by  Jansen  and  Oppenheim  there  were  from  a  right-sided 
temporal  lobe  abscess  left  hemiparesis,  hemihypassthesia,  hemianopsia 
bilateralis  sinistra  and  conjugate  deviation  of  the  head  and  eyes  to- 
ward the  right.  Ptosis  from  paralysis  of  the  third  nerve  and  internal 
strabismus  from  the  sixth  are  rather  common  in  temporal  lobe 
abscesses. 

Blindness  may  occur  when  the  abscess  is  in  the  occipital  lobes, 
while  hemianopsia  occasionally  accompanies  abscesses  of  the  occipital 
lobe  and  of  the  lower  part  of  the  parietal  lobe. 

Cerebellar  abscesses  are  usually  due  to  mastoid  disease  and  de- 
clare their  presence  by  such  localizing  symptoms  as  ataxia,  suboccipital 
headache,  vomiting,  cervical  rigidity  and  rarely  by  bilateral  amaurosis 
and  pressure  on  the  adjoining  cranial  nerves  and  their  nuclei.  Ac- 
cording to  Macewen,  the  knee-jerks  were  absent  in  some  cases  of 
cerebellar  abscess. 

Abscess  of  the  pons  and  medulla  oblongata  is  very  rare,  yet  when 
present  has  the  typical  bulbar  symptoms  to  complete  its  clinical  picture. 

Occasionally  an  abscess  bursts  into  the  ventricles,  giving  all  the 
symptoms  of  a  profound  apoplectic  stroke ;  namely,  convulsions,  fol- 
lowed by  paralysis,  deep  coma,  etc.,  all  quickly  terminating  in  death. 

Diagnosis. — In  spite  of  the  fact  that  cerebral  abscesses  are  so 
often  latent  and  therefore  cannot  be  diagnosed  at  all,  and  even  when 
they  have  symptoms  these  are  so  often  indefinite  and  variable,  the  gen- 
eral clinical  picture  is  sufficiently  unique  and  characteristic  to  enable 


v^ 


THE   XOX-XEUROXIC  DISEASES 


one  in  a  large  majority  of  cases  to  form  a  diagnosis,  or  at  least  a 
strong  suspicion,  especially  when  there  has  been  a  history  of  trauma- 
tism, local  infection  in  the  ear  or  septic  processes  elsewhere  about  the 
body.  It  is  upon  the  history  of  the  case,  with  the  present  symptomatol- 
ogy viewed  en  masse,  rather  than  in  detail,  that  the  strongest  diagnosis 
of  cerebral  abscess  is  made.  It  is  the  tout  ensemble  of  the  picture  that 
here  indicates  the  nature  of  the  trouble,  and  not  this  or  that  particular 
symptom  or  small  group  of  symptoms. 

There  are  quite  a  number  of  diseases  with  which  brain  abscess 
might  be  readily  confused.  This  is  because  of  the  multiplicity  of  its 
symptoms,  all  depending  upon  so  many  different  factors.  From 
meningitis,  particularly  external  purulent  pachymeningitis  or  extra- 
dural abscess,  it  is  distinguished  by  the  greater  degree  of  intracranial 
pressure,  the  more  definite  localization  of  symptoms  and  the  absence 
of  the  characteristic  irritative  signs  like  the  cervical  rigidity,  pupillary 
contraction  and  Kernig's  symptom.  In  diffuse  purulent  meningitis, 
differentiation  is  often  extremely  difficult.  The  irregular  and  low 
fever,  the  slow  pulse,  the  localization  signs  and  the  absence  of  most 
of  the  irritative  symptoms  of  meningitis,  such  as  the  hyperaesthesia,  the 
muscular  rigidity,  the  twitchings,  the  spinal  symptoms  and  the  mental 
restlessness  are  enough  to  make  in  typical  cases  a  differential  diagnosis 
easy.     Lumbar  puncture  will  assist  in  some  cases. 

Other  forms  of  meningitis  that  must  be  eliminated  in  the  diagnosis 
are  a  localized  meningo-encephalitis  and  serous  meningitis  and  tubercu- 
lar meningitis.  In  typical  cases  the  differentiation  is  not  difffcult  when 
one  recalls  that  abscess  produces  only  temporary  or  transient  irritative 
symptoms,  that  its  febrile  characteristics  are  quite  unlike  those  of 
meningitis,  and  that  it  has,  like  tumor,  certain  more  or  less  definite 
intracranial  localization  symptoms.  In  the  combined  cases  it  is  diffi- 
cult, but  if  the  case  is  a  combined  one  we  can  neglect  the  meningitis 
and  diagnose  the  abscess,  or  in  other  words,  a  differential  diagnosis  is 
not  imperatively  called  for.  The  distinction  between  brain  abscess 
and  the  traumatic  neuroses,  especialh'  when  the  former  is  due  to  a 
traumatism,  must  be  carefully  made.  A  careful  consideration  of  the 
symptomatolog}'  of  the  traumatic  neuroses,  hysteria  and  neurasthenia, 
and  its  unlikeness  to  that  of  abscess,  with  its  distinct  organic  and  septic 
symptoms,  ought,  it  seems  to  me,  to  make  a  differentiation  here  a 
matter  of  no  very  great  difficulty. 

Tumor  of  the  brain  has  many  symptoms  in  common  with  those 
of  abscess.  In  tumor,  however,  the  headache  and  optic  neuritis  are 
more  constant  and  pronounced,  the  development  of  the  disease  is  slow- 
er, there  is  absence  of  fever  and  septic  symptoms  and  altogether  more 
of  a  uniformity,  steadiness  and  chronicity  about  the  clinical  picture. 

Prognosis. — Brain  abscesses  are  both  acute  and  chronic.  Both 
forms  are  sooner  or  later  fatal  if  not  interfered  with  surgically.  It 
is  a  rare  thing  indeed  for  an  intracranial  collection  of  pus  to  break 
into  the  nasal,  orbital  or  buccal  cavity ;  still  more  rarely  does  it  open 
out  directly  on  the  head.  A  spontaneous  cure  by  this  or  any  other 
means  is  not  to  be  looked  for.  These  cases  are  as  fatal  ultimately 
as  anv. 


THE  NOX-XEURONIC  DISEASES  8/3 

Cerebral  abscess  often  runs  a  long  course,  with  occasional  remis- 
sions and  changes  in  its  symptomatology.  When  single  and  encap- 
sulated it  may  remain  in  a  semi-quiescent  state  many  years.  Then  it 
suddenly  bursts  into  the  neighboring  ventricle  or  through  the  mem- 
branes and  brings  on  alarming  symptoms,  with  delirium,  coma  and 
death  in  a  few  hours.  I  have  seen  death  follow  a  semicomatose  condi- 
tion lasting  several  days.  This  coma  is  a  certain  indication  of  an  early 
demise. 

Without  interference,  therefore,  the  prognosis  of  cerebral  abscess 
is  bad.  With  surgical  intervention  a  little  more  than  half  the  traumatic 
cases,  and  a  little  less  than  half  the  otitic  cases,  are  saved  and  cured. 
Of  course,  the  resulting  scar  tissue  and  damaged  cerebral  cells  will 
in  all  probability  leave  some  focal  symptoms  of  a  permanent  character. 
Occasionally  an  abscess  unfortunately  recurs  after  a  successful  opera- 
tion. The  most  favorable  location  for  an  operable  abscess  is  the  tem- 
poral lobe;  the  cerebellum  is  somewhat  less  favorable. 

Treatmext. — The  treatment  cf  brain  abscess  resolves  itself  into 
prophylaxis  and  surgical  evacuation.  In  the  antiseptic  management  of 
fresh  wounds  about  the  head  much  can  be  done  to  ward  ofif  intracranial 
infection.  This  is  an  added  argument  in  favor  of  the  maintenance  of 
rigid  asepsis  in  all  operations  in  the  nose  and  mouth,  about  the  eye  and 
ear.  Forcible  injections  and  irrigations',  especially  in  the  ear,  must  not 
be  resorted  to.  Pus  when  present  must  be  drained  off,  and  under  no 
circumstance  must  a  running  from  the  ear  be  checked  by  closure  of 
the  opening.  I  repeat  that  the  mere  cessation  of  an  otorrhoea  has 
seemed  to  me  in  a  number  of  cases  to  have  been  too  fondly  assumed  as  a 
cure  of  the  ear  disease. 

When  an  abscess  of  the  brain  is  finally  diagnosed,  and  its  location 
is  favorable  for  operation,  there  should  be  no  further  temporizing,  but 
immediate  evacuation  with  drainage  should  be  insisted  on.  There 
is  no  other  treatment  for  an  abscess.  I  cannot  see  the  wisdom  of 
Oppenheim's  suggestion  to  first  try  if  removal  of  the  pus  in  the  ear  or 
in  the  extradural  region  will  relieve  the  cerebral  symptoms  in  cases 
where  the  diagnosis  of  uncomplicated  otitic  cerebral  abscess  can  be 
definitely  made.  As  a  preliminary  micasure  these  operations  will  be 
done  anyhow,  and  if  the  cerebral  symptoms  are  thereby  relieved  in  part, 
it  is  no  proof  that  a  cerebral  abscess  does  not  exist.  Therefore  instead 
of  recommending  a  measure  that  might  readily  be  interpreted  into 
meaning  a  delay,  it  seems  to  me  the  better  part  of  wisdom  to  advise  that 
every  case  of  otitic  cerebral  abscess,  where  a  diagnosis  can  be  definitely 
made  and  where  the  location  of  the  abscess  is  favorable  for  operation, 
should  be  operated  at  once  or  as  early  as  possible.  In  view  of  their 
almost  certain  fatality  without  operative  measures,  I  do  not  feel  that 
external  purulent  pachym.eningitis,  circumscribed  purulent  meningitis, 
diffuse  purulent  meningitis,  sinus  thrombosis  or  even  beginning  pyjemia 
should  be  looked  upon  as  contra-indications  to  operative  interference. 
The  patient's  life  is  never  safe  so  long  as  there  is  a  nidus  of  pus  within 
his  cranium ;  it  is  safe  in  a  large  proportion  of  cases  w^hen  that  nidus 
of  pus  is  opened  and  drained. 

Some  operators  report  recovery  by  surgical  interference  in  the 


874  THE  NOX-XEUROXIC  DISEASES 

cases  of  metastatic  multiple  abscess.  Such  cases,  however,  must  nec- 
essarily be  very  rare.  Moreover,  so  often  is  the  original  source  of  in- 
fection incurable  that  it  would  seem  to  be  an  almost  useless  task  to 
attempt  to  cure,  under  such  hopeless  conditions,  the  trouble  in  the 
brain. 

ACUTE  DELIRIUM.    BELL'S  MANIA. 

So  varied  are  the  opinions  in  regard  to  the  nature  of  this  brain 
disease  that  many  names  have  been  applied  to  it.  The  one  that  I  have 
here  selected  is  the  one  most  commonly  used.  In  the  form,  described  by 
Bell,  and  most  of  the  authors  who  have  followed  him,  there  are  no 
constant,  distinctive  post-mortem  findings.  Ford,  Wood  and  others 
believe  that  it  is  a  type  of  inflammation  and  should  therefore  be  classi- 
fied as  a  meningo-enccphalitis,  or  a  periencephalitis.  I  am  inclined  to 
classify  it  with  the  brain  inflammations  in  spite  of  the  fact  that  the 
microscopical  findings  are  negative. 

The  symptoms  are  those  of  a  profound  intoxication,  autochthonous 
or  otherwise,  and  in  a  few  cases  which  have  been  carefully  examined 
signs  of  a  diffuse  inflammation  have  been  discovered.  The  poison, 
either  by  reason  of  its  extreme  virulence  or  the  peculiar  susceptibility 
of  the  patient,  so  overwhelms  the  brain  cells  in  some  cases  that  death 
ensues  before  histological  changes  have  had  time  to  take  place.  In  other 
cases  by  reason  of  the  weaker  character  of  the  poison,  the  longer  con- 
tinuance of  its  action  or  the  greater  power  of  resistance  on  the  part 
of  the  patient,  histological  changes  of  a  diffuse,  inflammatory  character 
are  able  to  develop  and  so  are  revealed  post  mortem.  Therefore,  as  in 
the  analogous  instance  of  Landry's  paralysis,  it  seems  to  me  that  in 
Bell's  delirium  we  are  witnessing  merely  an  early  stage  of  a  high  de- 
gree of  intoxication,  which,  if  granted  time  to  pass  into  a  later  stage, 
without  the  sudden  intervention  of  death,  would  frankly  declare  itself 
as  a  form  of  toxic,  diffuse  encephalitis.  This  will  be  more  clearly 
brought  out  in  the  further  discussion  of  the  disease. 

Etiology. — Most  authors  find  that  women  are  much  more  subject 
to  the  trouble  than  men,  and  that  it  occurs  most  frequently  between 
the  ages  of  twenty-five  and  forty-five.  It  occurred  in  a  girl  of  eleven 
years  of  age  in  a  case  of  Morel,  quoted  by  Maudsley.  Heredity  does 
not  seem  to  play  a  very  prominent  role.  Emotional  strain,  distress, 
anxiety,  worry,  mental  shock  are  more  important  as  causative  factors. 
Schule  has  attributed  it  to  severe  physical  pain.  Sunstroke,  injury 
to  the  skull  and  the  climacteric  have  been  mentioned  in  its  etiology; 
to  these  must  be  added  alcoholism,  of  course.  More  significant  than 
any  of  these  causes  are  those  that  involve  infection.  It  has  followed 
typhus  and  typhoid  fever,  epidemic  influenza,  erysipelas  and  some  skin 
affections.  It  has  accompanied  exhaustive  dysentery,  puerperal  sepsis 
and  epileptic  attacks.  Wood,  Hurd,  Berkeley,  Dercum,  Briand,  Rohe 
and  others  consider  a  toxjemia  or  infection  to  be  the  primary  cause,  if 
not  the  essential  cause  in  all  cases. 

Pathology  and  Pathogenesis. — Some  authors,  as.  for  example, 
Pritchard.  affirm  patholog}-  shows  that  under  the  name  Bell's  disease 
we  have  heretofore  been  describing  two  fundamentally  different,  though 


THE  NON-NEURONIC  DISEASES  875 

symptomatically  similar,  conditions  of  disease;    the  one  organic,  with 
a  variable  but  always  demonstrable  pathology,  essentially  inflammatory, 
due  to  toxines,  infection  or  trauma,  the  lesion  varying  from  a  gross 
menin go-encephalitis    to    limited    lepto-meningitis    or    arachnitis,    the 
other  non-organic,  or  at  least  with  findings  indicating  simply  nutritional 
or  dynamic  changes  without  adequate  or  other  than  conjectural  ex- 
planation either  as  to  their  etiological  nature  or  pathological  signifi- 
cance and  interpretation.     Most  authorities  would  assume  that   this 
second,  non-organic  class  was  due  to  an  intoxication.     If  this  be  so, 
there  is  no  difficulty  in  recognizing  both  classes  of  cases  as  but  two 
types  of  the  same  disease,  for  they  agree  in  everything     except     the 
pathological  findings,  and  in  respect  to  this  discrepancy  the  case  is  the 
same,  as  we  have  seen  in  Landry's  paralysis  and  certain  inflammatory 
conditions  of  the  cord.     The  so-called  non-organic  cases  are  but  the 
earlier  stages  of  an  overwhelming  intoxication,  which,  given  more  time, 
less  virulence  or  other  conditions,  would  go  on  to  provoke  distinct 
gross   signs  of  a   diffuse  inflammation.     Granting  the   frequent  con- 
founding of  other  forms  of  inflammation,  such  as  traumatic  meningitis 
and  encephalitis,  with  this  disease,  the  findings  are  yet  sufficiently  sug- 
gestive  of   an    incipient   inflammation    in   the   later    stages    of   Bell's 
delirium.     There  is  congestion  of  the  vessels  of  the  meninges  and  of 
the  cortex  and  engorgement  of  the  veins.     In  two  cases  examined  by 
Osier  there  were  perivascular  exudation  and  leucocytes  in  the  lymph 
sheaths  and  periganglia   spaces.     In  Pritchard's  case  the  pia  mater 
was  markedly  cedematous  and  the  blood  vessels  injected.     The  capil- 
laries of  the  cortex  showed  marked  distention,  but  no  petechial  herti- 
orrhages  were  observed.     The  choroid  plexus  of  the  ventricles  was 
cedematous.     The  cells  were  practically  unchanged.     Osier  urges  that 
a  careful  examination  in  fatal  cases  be  always  made  of  the  lungs  and 
ilium.     In  the  majority  of  cases  he  says  there  is  engorgement  of  the 
bases  of  the  lungs  and  even  deglutition  pneumonia.     I  found  this  in  a 
recent  case  of  my  own.    Though  the  nature  of  the  disease  is  thus  not 
positively  demonstrated,  the  findings  point  strongly  to  a  condition  of 
acute,  severe  infection. 

Symptomatology. — The  symptoms  of  this  disease  are  almost  en- 
tirely mental,  which  doubtless  accounts  for  some  of  its  names,  as  well 
as  for  the  fact  that  it  has  been  so  long  regarded  as  a  pure  psychosis. 
There  are,  in  almost  every  case  when  closely  studied,  seen  to  be  symp- 
toms that  point  to  organic  lesions  and  disturbances  in  the  brain  cortex. 
The  abruptness  of  onset,  the  rapid  advancement,  the  extreme  violence, 
the  utter  incoordination  and  unsystematized  character  of  them,  their 
frequent  remission,  and  their  ultimate  subsidence  in  death  or  dementia 
.  are  the  striking  traits  about  the  mental  manifestations. 

The  patient  will  be  resting  quietly  when  all  of  a  sudden  there  will 
be  a  terrific  outburst  of  wild  delirium  and  intense  frenzy.  This  is  hys- 
tero-maniacal  in  general  character  and  is  associated  with  hallucina- 
tions, great  violence  and  motility,  destructiveness  and  incoherence. 
Chattering  and  talking  is  incessant.  The  speech  is  absolutely  uncon- 
trolled so  that  obscene,  boastful,  lascivious  ideas  are  voluminously 
poured  forth.    Laughing  and  screaming,  alternating  with  wild  singing, 


876  THE  XOX-XEUROXIC  DISEASES 

occur,  all  without  the  slightest  trace  of  intelligence.  The  patient  has 
been  compared  in  this  state  to  a  maddened  animal.  The  muscular 
movements  are  intense  and  constant  until  exhaustion  puts  an  end  ta- 
them.  A'asomotor  disturbances  are  obvious.  Sleep  is  impossible. 
Auarsthcsia  and  analgesia  are  apt  to  be  complete.  Food  is  obstinately- 
refused.  On  account  of  all  this  the  patient  soon  becomes  utterly  pros* 
trated  and  remains  quiet  with  a  more  or  less  complete  return  to  normal 
consciousness.  In  a  short  time,  however,  another  exacerbation  comes 
on  and  the  noisy,  terrific  scene  is  repeated.  These  remissions  are  a. 
striking  feature  of  the  disease.  They  are  transient  and  become  shorter 
and  less  frequent  as  the  disease  progresses.  In  them  the  patient  may 
seem  to  have  recovered  complete  health  and  for  this  reason  they  oftea 
give  rise  to  false  hopes.  Pritchard  sa}s  that  delusions  occur,  especially 
in  connection  with  the  visual  sense,  and  that  strange  and  familiar  per- 
sonalities arise.  Shameless  masturbation  is  practiced  and  attendants, 
of  the  opposite  sex  are  openly  solicited.  Sometimes  in  the  speech  there 
is  observed  a  certain  connected  sequence  and  almost  coherence,  but  the 
usual,  absolutely  unsysteniatized  character  of  the  ideas  helps  to  dis- 
tinguish this  trouble  from  a  typical  mania.  Proper  notions  in  regard 
to  time,  place  and  surrounding  conditions  are  as  a  rule  completely  lost.. 

Death  almost  always  occurs  in  this  disease  and  in  the  acute  cases  in 
about  a  week;  when  partial  recovery  takes  place  the  delirium  is  suc- 
ceeded b}-  dementia,  which  remains  more  or  less  permanently. 

Such  is  the  mental  picture  of  these  cases,  but  none  of  them  are 
ever  absolutely  devoid  of  constitutional  and  somatic  symptoms.  The 
temperature  usually  rises  rapidly,  especially  during  the  frenzy,  and 
may  attain  to  105  degrees  F.  The  pulse  is  variable,  though  it  is  alway^s 
more  or  less  disturbed.  Both  the  temperature  and  the  pulse  as  a  rule 
remain  above  the  normal.  Convulsions  and  epileptiform  manifesta- 
tions sometinies  occur,  as  well  as  strabismus  and  various  paralyses. 
Even  more  suggestive  are  the  not  unfrequent  trophic  manifestations,, 
such  as  alopecia,  degenerative  atrophy,  petechia;  and  other  lesions  of 
the  skin  and  bones.  Even  bullae  and  pustules,  with  sores  from  abrasions 
and  injuries,  are  frequently  seen  on  the  skin.  The  tongue  is  dry  and 
apt  to  be  coated.  Sometimes  the  sphincters  are  relaxed,  causing  in- 
continence of  urine  and  faeces.  Just  before  death  the  bodily  emaciation 
is  apt  to  be  extreme. 

Obviously  we  have  here  two  fairly  well  marked  sets  of  symptoms, 
the  mental  and  the  somatic.  The  latter  are  not  known  to  be  the  direct 
results  of  the  former  under  any  other  circumstances,  though  the  for- 
mer are  frequently  caused  by  the  latter.  Therefore  it  would  seem  to 
be  a  fair  conclusion  to  draw  that  a  profound  toxic  condition  underlies 
the  disease  and  is  the  cause  of  both  sets  of  symptoms. 

DiAGXosis. — T3'pical  cases  of  Bell's  mania  do  not  give  much 
trouble  in  diagnosis.  The  febrile  condition,  the  zvild  delirium  with  re- 
missions, the  hallucinations,  the  extreme  motility,  the  rapid  course^ 
intense  emaciation  and  somatic  symptoms  are  characteristic.  In  sim~ 
pie  mania  there  are  no  somatic  symptoms,  very  little  febrile  disturbance, 
if  any,  and  the  ideas  are  more  systematized  and  coherent.  In  delirium 
tremens  there  is  a  clear  historv  of  alcoholism,  much  gastric  disturbance^ 


THE  NON-NEURONIC  DISEASES  877 

.peculiar  visual  hallucinations  and  a  general  and  marked  asthenia.  A 
meningitis  is  accompanied  by  more  or  less  nuchal  rigidity  and  opistho- 
tonos, pupillary  symptoms,  motor  spasm  and  paresis,  vomiting,  con- 
tinuous high  fever,  absence  of  complete  remissions,  Kernig's  sign  and 
the  tdche  €erebrale.  The  delirmm  of  typhoid  fever  or  pneumonia  can 
be  determined  by  other  symptoms  present  than  those  of  the  brain. 
With  post-epileptic  mania  there  has  been  a  previous  history  of  epileptic 
attacks  and  the  fatality  is  much  more  swift. 

Prognosis. — This  is  decidedly  bad.  Spitzka  says  that  recovery 
never  occurs,  which  is  the  opinion  of  most  authors.  This  prognosis  of 
•course  applies  to  the  typical  cases  of  the  fulminant  type,  cases  in  which 
the  brain  is  overwhelmed  with  the  virulent  intoxication  and  leaves  no 
changes  of  an  anatomical  character  discoverable  post  mortem.  There 
are  authors,  however,  who  do  not  consider  the  prognosis  so  absolutely 
bad.  It  is  evident  that  they  are  including  in  their  statistics  the  non- 
typical,  less  virulent  cases  which  recover,  or  which  die  at  a  much  later 
period  and  reveal  signs  of  a -diffuse  inflammatory  process.  In  the 
words  of  Pritchard,  "the  prognosis  in  the  non-organic  cases  is  sta- 
tistically worse  than  in  the  organic."  How  analogous  is  all  this  to  the 
history  of  Landry's  paralysis  ! 

Treatment. — The  treatment  is  not  satisfactory.  The  indications 
are  to  support  the  patient's  strength,  eliminate  the  toxin  and  quiet  the 
nervous  excitement. 

To  remove  the  cause  as  expeditiously  as  possible  is  the  first  obliga- 
tion imposed  upon  the  attendant.  Free  diuresis,  purgation  and  dia- 
phoresis should  be  instituted.  Osier  says  he  has  been  criticised  for 
recommending  venesection,  but  yet  he  repeats  the  recommendation.  It 
seems  to  me  commendable  in  robust,  sthenic  cases.  Such  vascular 
agents  as  ergot,  quinine,  etc.,  have  been  tried  and  found  wanting.  The 
slowness  of  their  action  would  seem  to  suggest  their  uselessness  in  this 
disease.  After  the  venesection  in  plethoric  cases,  the  transfusion  of 
blood  or  saline  solution  would  be  a  proper  proceeding.  To  quiet  the 
nervous  system  the  straight  jacket,  with  complete  isolation  and  forced 
feeding,  has  been  proposed.  Some  cases  may  be  quieted  with  the  cold 
bath  or  the  cold  pack.  Morphia,  hyoscine,  chloroform,  the  bromides, 
trional,  all  in  heroic  doses,  may  be  experimented  with,  but  will  fre- 
quently give  negative  results.  Serum  therapy  is  suggested  by  the 
probable  etiology  and  pathology  of  the  disease. 

CEREBRAL  SYPHILIS. 

Syphilis  exerts  its  baleful  influence  upon  the  nervous  system  direct- 
ly and  indire€tly.  The  bacillus  and  its  toxins  by  their  continued  action 
produce  lesions  within  the  nervous  apparatus  (organic  syphilis  of  the 
nervous  system)  or  disturb  the  physio-chemical  and  consequent  func- 
tional characteristics  of  the  nervous  elements  (functional  syphilis  of 
the  nervous  system).  On  the  other  hand,  they  somehow  so  affect 
certain  parts  of  the  nervous  tissue  that  long  after  they  have  ceased  to 
be  active  this  tissue  undergoes  a  steady,  progressive  and  character- 
istically degenerative  change.    The  former  are  the  true  syphilitic  dis- 


8/8  THE   NON-NEURON  IC  DISEASES 

eases  of  the  nervous  system,  the  latter  are  the  so-called  parasyphilific 
diseases.  It  is  but  fair  to  say  that  there  is  some  doubt  as  to  the  ex- 
istence of  the  functional  group  of  syphilitic  diseases.  Some  think  that 
they  are  but  the  early  manifestations  of  what  later  on  will  unmask  itself 
as  true,  organic  syphilitic  trouble,  the  functional  symptoms  being  due 
to  irritation  from  the  organic  lesions,  or  as  true  parasyphilitic  disease, 
the  functional  symptoms  here  being  caused  by  the  early  disturbance 
in  the  nutrition  of  the  cellular  elements  prior  to  their  degeneration.  If 
that  be  so,  a  view  which  I  am  inclined  to  accept,  then  there  are,  strictly 
speaking,  no  functional  diseases  of  the  nervous  system  of  syphilitic 
origin.  There  are  only  the  organic  diseases,  or  true  syphilis,  and  the 
parasyphilitic  diseases.  The  epilepsies,  chorea,  neurasthenia,  hysteria 
and  hystero-neurasthenia,  noted  by  Fournier  and  others,  are  but  early 
manifestations  of  either  the  syphilitic  or  parasyphilitic  troubles. 

Organic  syphilitic  disease  is  an  affection  of  the  entire  nervous 
system.  In  other  words,  the  majority  of  the  cases  of  organic  syphilitic 
disease  reveal  symptoms  sooner  or  later  that  show"  implication  of  the 
brain,  spinal  cord  and  peripheral  nerves.  Pure  brain  syphilis  or  pure 
spinal  syphilis  is  comparatively  rare.  Nevertheless  in  about  two-thirds 
of  the  cases  or  more,  the  predominant  symptoms  are  so  markedly 
intracranial  or  intraspinal  or  neural,  that  for  the  sake  of  practical 
convenience  we  speak  of  brain  syphilis,  spinal  syphilis  and  nerve 
syphilis.    Under  the  present  heading  I  will  discuss  only  brain  syphilis. 

Paradoxical  as  it  may  sound,  it  is  none  the  less  true  that  organic 
syphilitic  disease  of  the  nervous  apparatus  is,  strictly  speaking,  not  a 
nervous  disease  at  all.  It  is  a  disease  of  the  blood  vessels  and  the 
nervous  elements  suffer  because  of  their  close  proximity  to  these  dis- 
eased organs  and  because  of  their  dependence  upon  them  for  their 
nutrition.  The  process  in  the  blood  vessels  is  that  of  an  inflammation, 
a  speciHe  arteritis.  It  may  remain  confined  to  the  walls  of  the  blood 
vessels  and  the  nervous  elements  may  suffer  from  the  ischsemia  caused 
by  the  narrowing  of  the  inflamed  vessels,  their  complete  occlusion,  or 
from  the  presence  of  a  thrombus  or  embolus  within  them.  If  the  inflam- 
mation produces,  as  it  usually  does,  a  more  or  less  profuse  specific 
exudation,  then  a  gummatous  condition  and  multiple  gummatous 
tumors  develop.  The  commonest  distribution  of  this  gummatous  vas- 
cular inflammation  is  in  the  membranes  of  the  base  and  vertex  ;  under- 
lying the  frequent  gummatous  meningitis.  Syphilitic  disease  of  the 
coats  of  the  blood  vessels,  eventuating  in  gummatous  meningitis  on  the 
one  hand  and  in  obstructive  and  other  circulatory  disturbances  within 
the  brain  substance  on  the  other  hand,  is  practically  the  basic  patho- 
logical process  underlying  all  forms  of  organic  cerebral  syphilis.  There 
are  variations  upon  these  two  general  forms  of  pathological  findings. 
There  may  be  combinations  of  the  two;  one  or  the  other  may  be  pre- 
dominant ;  secondary  complications  may  occur ;  and  finally  the  gum- 
matous condition  may  be  dift'use  and  membranous-like.  Or  it  may  simu- 
late single  or  multiple  tumors.  Whatever  the  variation  be,  in  its  last 
analysis  it  will  be  seen  to  originate  primarily  in  a  specific  inflammation 
of  the  blood  vessels.    This  fact  is  a  most  important  one  to  bear  in  mind, 


THE   XOX-XEUROXIC  DISEASES  879 

for  it  explains  the  great  multiplicity,  variability  and  instability  of  the 
individual  symptoms  of  brain  syphilis. 

Etiology. — Syphilis,  whether  it  be  the  germ,  as  in  all  probability 
it  is  a  true  germ  disease,  or  the  toxin  elaborated  by  the  germ,  is  the 
cause  of  the  vascular  disease  constituting  the  basic  lesion  of  brain 
syphilis.  This  sounds  like  a  truism,  but  the  necessity  for  repeating  it 
is  provoked  by  those  cases  in  which  an  honest  denial  of  specific  infec- 
tion is  made.  Many  times  the  early  somatic  signs  of  syphilis  are  so 
slight  and  evanescent  that  they  are  completely  overlooked  and  forgot- 
ten. At  other  times  they  disappear  so  rapidly  during  a  brief  course  of 
mercurialization,  and  remain  away  so  completely  after  the  medication 
has  been  stopped,  that  a  false  notion  of  being  cured  is  engendered  in  the 
mind  of  the  patient  and  he  denies  that  syphilis  can  possibly  be  in  anv 
way  the  cause  of  his  present  trouble.  The  larger  number  of  cases  of 
brain  syphilis  that  I  have  seen  have  presented  just  such  an  early  his- 
tory. It  is  in  the  class  of  cases  in  which  the  primaries  and  secondaries 
are  slight  as  well  as  too  briefly  treated,  that  tertiary  syphilis  is  so 
likely  to  occur ;  and  so  emphatically  am  I  convinced  of  this  that  when 
I  have,  upon  the  examination  of  the  patient,  formed  a  reasonably  con- 
clusive opinion  that  he  has  brain  syphilis,  his  denial  of  all  early  signs, 
coupled  with  an  admission  of  exposure,  clinches  the  diagnosis  and 
makes  it  positive. 

By  referring  to  syphilis  of  the  brain  as  tertiary  syphilis,  it  is  not 
intended  to  convey  the  idea  that  the  brain  may  not  be  attacked  in  the 
secondary  stage,  or  even  earlier  in  the  disease.  On  the  other  hand, 
this  form  of  tertiary  syphilis  may  not  occur  until  many  years  after  the 
appearance  of  the  primary  lesion.  The  larger  number  of  cases  appear 
about  two  or  three  years  after.  The  recorded  limits  in  which  brain 
troubles  of  this  kind  may  occur  after  infection  are  from  a  few  months 
to  thirty  or  more  years.  It  may  even  follow  hereditary  syphilis.  The 
term  tertiary  has  no  relation,  therefore,  to  the  time  of  the  manifesta- 
tion ;  it  is  merely  a  convenient  way  of  indicating  the  character  and 
location  of  the  lesion. 

Not  all  syphilitics  become  the  victims  of  brain  syphilii».  It  would 
seem  logical  to  look  for  the  cause  of  this  in  the  condition  of  the  nervous 
system  rather  than  in  the  character  of  the  specific  virus.  So  little  is 
know^n  about  the  matter,  however,  that  little  beyond  speculation  can  be 
advanced.  Certain  exhausting  influences,  such  as  excessive  venery, 
mental  wea-r  and  tear,  dissipation,  lack  of  sleep,  alcoholism  and  trau- 
mata, do  seem  to  determine  to  a  certain  extent  an  outbreak  of  brain 
syphilis  in  those  who  have  been  infected.  An  inherited  neuropathic 
tendency  favors  the  parasyphilitic  rather  than  this  form  of  the  disease. 
An  inherited  w^eakness  of  the  circulatory  and  visceral  organs,  a  familial 
tendency  toward  arteritis,  nephritis,  cardiac  and  hepatic  troubles,  may 
predispose  to  brain  disorders  in  a  syphilitic. 

Pathology  and  P.xthogexe.sis. — The  most  common  form  of  brain 
syphilis  is,  without  doubt,  basal  gummatous  meningitis.  This  starts 
usually  in  the  subarchnoid  space  in  the  vicinity  of  the  optic  chiasm 
and  spreads  out  over  the  base  and  up  the  sides  of  the  brain  and  dov/n 
between  the  crura.     It  causes  the  membrane  to  be  thickened,  opaque 


88o 


THE   NOX-NEURONIC  DISEASES 


and  gummy,  and  to  be  covered  with  numerous  knob-like,  round  eleva- 
tions or  tumors,  varying  in  size  from  a  pea  or  hazel-nut  to  a  walnut. 
These  gummata  may  surround  the  neighboring  cranial  nerves,  espe- 
cially the  optic,  the  ocular  and  the  abducens.  Sometimes  the  nerves 
themselves  are  not  injured ;  usually,  however,  they  appear  swollen, 
enlarged,  grayish  or  yellowish  white  on  section  with  atrophy  of  the 
nerve-fibres.  Both  the  small  and  large  arteries  of  the  base  of  the 
brain  are  involved.  Their  walls  ■  are  thickened,  and  their  calibre  is 
diminished  or  occluded.  The  basilar  artery  shows  this  tendency  par- 
ticularly.   As  its  terminal  branches  are  so  often  obstructed,  there  will 

FIGURE  197- 


Syphilitic  basilar  meningitis  and  multiple  gummata  at  the  base  of  the  brain. 
(After  Siemerling.) 


be  observed  numerous  foci  of  softening.  Sometimes  the  remains  of 
old  hemorrhages  are  found.  Instead  of  foci  of  softening  there  may 
be  a  diffuse  softening  over  a  large  area.  This  basal  gummatous  menin- 
gitis may  assume  almost  any  form  and  mode  of  extension.  It  may  be 
associated  with  a  circumscribed  gum.ma.  A  disseminated  extension 
may  take  place  in  the  form  of  yellow  or  gray  plaques  (meningo- 
encephalitic  foci)  or  in  the  form  of  multiple  tumors.  Even  miliary 
gummata  are  now  and  then  seen.  This  same  gummatous  meningitis 
may  appear  on  the  convexity  of  the  brain  either  as  a  separate  process 
or  along  with  the  basal  disease.  As  a  rule  it  is  less  severe  on  the  vertex 
than  it  is  at  the  base.  Yet  with  this  meningitis  the  underlying  cortex 
may  be  involved  (syphilitic  meningo-encephalitis),  disturbing  to  a 
profound   degree   the   cerebral   functions    and   by  extension   into   the 


THE  NON-NEUUOxNIC  DISEASES 


depths  of  the  brain  tissue,  causing  a  widespread  softening,  even  of  a 
whole  hemisphere.  Simple  gummata  within  the  substance  of  the  brain 
are  very  rare.  A  gummatous  neuritis  of  the  cranial  nerves  may  occur 
separately  and  apart  from  any  implication  of  the  brain  or  its  meninges ; 


FIGURE  i( 


Syphilitic  arteritis   of  the   middle  cerebral  artery.      (After   Heubner.) 
Syph.     Sj'philitic  new  growth. 
/.     Lumen  of  the  artery. 
inf.     Original  fenestrated  membrane. 
III.     Muscular  coat. 
a.     Infiltrated  adventitia. 
sb.     Infiltrated  subarachnoid  space. 
cb.     Upper  surface  of  the  brain. 
cl.     Round  cells. 
cp.     Newly  formed  capillary. 
p.     Pigment. 

and  not  infrequently  the  brain  will  remain  intact  while  many  of  its 
arteries  show-  syphilitic  arteritis.  It  is  composed  of  a  cellular,  highly 
vascular  granulation  tissue.  It  is  never  or  rarely  purulent,  though  in 
spots  it  may  be  caseated  or  fibrous.  A  round-cell  proliferation  extends 
directly  along  the  adventitia  of  the  blood  vessels  and  also  along  the 
epineu'rium  of  the  nerves.  Between  the  bundles  of  the  nerve-fibres  the 
thickened  and  infiltrated  epineurium  sends  its  processes  everywhere, 


882  THE  NON-NEURONIC  DISEASES 

like  connective-tissue  septa.  The  nerve  itself  thus  becomes  swollen, 
while  the  individual  fibres  undergo  atrophy- 
In  hereditary  cerebral  syphilis  the  lesions  are  not  unlike  those  of 
the  acquired  form,  though  probably  less  intense.  To  sum  up,  the 
lesions  of  both  hereditary  and  original  brain  syphilis  involve  the 
lymphatics,  capillaries,  veins  and  arteries.  Endarteritis  is  the  lesion 
par  excellence.  This  may  involve  the  dura  or  the  pia,  more  especially 
the  latter.  A  gummatous  new-growth  is  formed,  and  as  a  result  dural 
and  pial  gummata  with  gummatous  leptomeningitis  are  seen.  Focal 
and  diffuse  encephalitis  with  hemorrhages,  necrobiosis  from  obstructive 
disease  of  the  arteries  and  veins,  and  fibroid  indurations  from  chronic 
vascular  disease  are  all  liable  to  occur.  The  wide  extent,  variable 
character  and  changeable  nature  of  these  pathological  findings  make 
clear  the  reason  of  the  great  diversity,  variability  and  swift  changes  in 
the  symptomatology  of  brain  syphilis. 

Symptoms. — I  sometimes  teach  that  among  organic  diseases  the. 
clinical  picture  of  brain  syphilis  is  the  homologue  of  hysteria  among 
the  psychoneuroses.  Brain  syphilis  has  such  a  wide  range  of  symp- 
toms that  it  can  simulate  almost  every  other  known  form  of  cerebral 
disease.  Somewhat  like  hysteria,  its  symptoms  are  remarkable  for  their 
appearance  and  disappearance,  their  transference  from  one  part  of  the 
body  to  another  and  their  involvement  of  all  known  functions  of  the 
nervous  apparatus,  sensory,  motor,  vasomotor  and  trophic.  As  the 
entire  encephalon  is  liable  to  the  disease,  and  as  the  disease  process 
(soft  and  easily  broken-down  gummata,  hemorrhage,  emboli,  etc.) 
itself  is  so  inconstant  in  its  minute  manifestations,  one  can  readily  com- 
prehend how  the  symptoms  or  outward  signs  of  these  changing  and 
shifting  pathological  phenomena  should  also  be  changing  and  shifting. 
It  would  be  quite  an  impossible,  or  at  least  an  herculean,  task 
to  attempt  to  classify  the  symptoms  of  brain  syphilis.  And  yet  there 
is  a  certain  constancy  and  uniformity  in  their  appearance  and  group- 
ing, so  that  after  a  time  one  comes  quickly  to  recognize  the  clinical  pic- 
ture as  being  more  or  less  characteristic. 

Certain  distinctive  features  belong  to  the  symptoms  in  such  a  way 
that  we  can  group  them  somewhat.  The  symptoms  indicative  of  cen- 
tral irritation  are  quite  distinguishable  from  those  indicative  of  de- 
struction of  the  central  nervous  tissue.  Sometimes  these  two  classes 
of  symptoms  exist  simultaneously  in  different  parts  of  the  nervous 
distribution ;  at  other  times  one  or  the  other  set  alone  predominate. 
Usually  they  exist  in  the  same  parts,  the  irritative  being  followed  by 
the  destructive  signs.  Epilepsies  and  stupor,  delirious  and  comatose 
states,  pargesthesia  and  hypaesthesia,  spasms  and  pareses,  all  thus  alter- 
nate or  occur  together  in  the  same  patient  or  follow  one  another  with 
remarkable  persistency. 

Again,  the  symptoms  may  be  subdivided  into  those  that  are  due 
to  the  gummatous  meningitis  involving  the  gray  matter  of  the  cortex 
and  the  basal  nerves  in  the  irritative  and  destructive  process,  and 
those  that  have  to  be  attributed  to  the  closure  of  the  circulation  by 
thrombotic  and  embolic  obstructions  or  to  minute  hemorrhages  and 
inflammatory  foci.    The  former  are  apt  to  be  more  focal  and  localized 


THE   XOX-XLURONIC  DISEASES  883 

in  character  and  implicate  special  nerves  and  individual  functions ;  the 
latter  are  rather  hemiplegic  in  character  and  are  diffuse,  spreading; 
over  segments  of  the  body  known  to  the  patient's  mind  and  not  in  ac- 
cordance with  distinct  anatomico-physiological  arrangements  of  the 
peripheral  neuromuscular  apparatus.  All  this  great  variability  and 
wide  extent  of  the  symptomatology  of  brain  syphilis  are  features  that 
are  almost  pathognomonic  of  the  disease.  And  yet.  as  I  have  tried  to 
emphasize  before,  in  spite  of  all  this  diversity  in  the  details  of  the 
symptomatolog}",  in  its  general  manifestation  there  is  a  remarkable 
constancy,  uniformity  and  individuality. 

I  will  now  discuss  the  clinical  picture  of  the  commonest  form  of 
brain  syphilis,  basal  gummatous  meningitis.  It  must  not  be  assumed 
that  in  these  cases  the  disease  is  limited  entirely  to  the  membranes  and 
vessels  of  the  base.  In  fact,  in  these  basal  cases  there  is  practically 
always  some  disease  of  the  convexity  and  some  neiiritis  of  the  cranial 
nerve  roots.  In  the  clinical  picture,  however,  the  symptoms  of  the 
basal  meningitis  predominate.  These  indicate  irritation,  compression 
and  destruction  of  the  neighboring  nervous  elements.  Foremost  among 
the  general  symptoms  is  headache.  This  is  characteristic  and  peculiar. 
The  pain  is  more  or  less  generalized  over  the  whole  head,  is  paroxysmal 
and  generally  exacerbates  v^ith  great  severity  at  night.  Sometimes  it 
resembles  the  indefinite,  indistmct,  parcesthetic  sort  of  a  headache  com- 
l^lained  of  by  neurasthenics ;  at  other  times  it  is  sharp,  cutj;ing  and 
boring.  It  is  rarely  unilateral  like  hemicrania ;  it  is  less  definitely 
locaHzed  than  the  headache  of  cerebral  tumor  and  abscess;  it  lacks 
the  dependence  upon  mental  states  like  the  clavus  of  hysteria ;  and  it  is 
influenced  by  the  stomach,  the  eyes  and  other  sources  of  peripheral  irri- 
tation which  sometimes  provoke  pain  in  the  head.  It  is  not  accom- 
panied by  fever  as  a  rule,  though  sometimes  the  temperature  rises  in 
cerebral  svphilis.  It  is  a  sort  of  a  cross  between  the  headache  of  brain 
tumor  and  acute  infective  states ;  not  as  wearing  and  constant  as  the 
former;  more  intense,  definite  and  paroxysmal  than  the  latter.  Vomit- 
ing and  vertigo  are  frequent  accompaniments  of  the  cephalalgia.  Con- 
vulsions of  a  generalized  character,  with  unconsciousness,  occur  in 
periodical  attacks.  Between  these  there  may  be  a  progressive  stupor 
as  in  all  forms  of  progressive  intracranial  growths.  Weakness  of  mem- 
ory, failure  of  intellect  and  power  of  attention,  and  general  mental 
apathy  are  not  uncommon.  Even  dementia  of  the  true  type  may  occur. 
In  the  midst  of  all  this  gradual  obliteration  of  the  consciousness,  out- 
bursts of  mania,  severe  attacks  of  excitation,  delirium  alternating  with 
coma  may  be  so  severe  as  to  require  the  incarceration  of  the  patient  irr 
an  asvlum.  The  characteristic  changeability  of  the  symptomatolog}'  o£ 
brain  syphilis  is  shown  in  the  occasional  alteration  of  these  mental 
manifestations  with  periods  of  apparent  mental  restoration  to  health. 
The  coma  may  recede,  only  to  return  again,  however.  It  is  obvious^ 
that  the  gummatous  meningitic  exudation  is  the  cause  of  these  symp- 
toms largely  by  the  intracranial  pressure  it  causes  and  the  encephalitib- 
it  lights  up.  Doubtless  the  same  explanation  will  answer  for  the  oc- 
casional polvdipsia  and  polyuria  that  are  seen  in  this  form  of  brain 


884  '^"Jtil^   NOX-NEUKONIC  DISEASES 

syphilis.  Tubercular  meningitis  of  the  base  is  easily  differentiated  by 
its  general  development  and  more  or  less  elevated  temperature. 

Most  important  are  the  symptoms  dependent  upon  compression 
and  destruction  of  the  cranial  nerve  roots.  The  optic  and  oculomotor 
nerves  are  the  most  frequentl}-  implicated,  usually  somewhat  more  on 
one  side  than  the  other.  The  pathciiciis  and  ahdnccns  nerves  are  the 
next  most  frequently  involved,  but  they  are  apt  to  be  affected  on  one 
side  or  the  other  only.  The  fifth,  seventh,  eighth,  ninth,  tenth,  elev- 
enth and  twelfth  nerves,  as  well  as  the  olfactor}-,  are  all  liable  to  be 
aft'ected,  but  with  decreasing  frequency  in  the  order  in  which  they  are 
enumerated.  Optic  nerve  trouble  is  particularly  common,  which  for 
the  purpose  of  diagnosis  is  fortunate.  The  ophthalmoscope,  together 
with  an  examination  of  the  vision,  shows  in  most  all  cases  some  de- 
gree of  atrophy.  Typical  choked  disc  and  neuritic  atrophy,  with 
neuro-retinitis,  are  frequently  seen  on  one  or  both  sides.  I  have  seen 
cases,  on  the  other  hand,  in  which  the  eye  ground  symptoms  were  p-rac- 
tically  negative  though  the  visual  loss  was  certain. 

Almost  every  variety  of  z'isual  disturbauce  may  be  met  with,  as, 
for  example,  bitemporal  or  homonymous  hemianopsia  :  amaurosis  on 
one  side  with  hemianopsia  on  the  other,  ultimately  becoming  bilateral 
amaurosis,  which  is  not  persistent  as  a  rule,  or  complete.  The  visual 
field,  when  the  optic  nerve  itself  is  diseased,  may  show  an  irregular, 
concentric  contraction,  decrease  of  central  visual  acuity,  etc.  All  of 
these  optic  nerve  symptoms,  exclusive  of  the  atrophy,  show  a  remark- 
able degree  of  cliaiigeability  and  unsteadiness.  The  outlines  of  the 
contracted  visual  field  may  change  from  day  to  day  ;  the  amaurosis 
may  swiftly  vary  or  change  from  one  eye  to  the  other ;  the  bitemporal 
hemianopsia  may  be  of  the  most  fugitive  type. 

Paralytic  symptoms,  involving  all  or  a  part  of  the  third  nerve, 
are  early  and  frequent.  Ptosis  on  one  or  both  sides  is  often  seen. 
■Sometimes  one  branch  of  the  nerve  gives  way  after  another  until  the 
whole  nerve  is  involved.  Oppenheim  declares,  however,  that  a  pure 
ophthalmoplegia,  interior  and  exterior,  is  rare  in  basal  syphilis. 

With  involvement  of  the  olfactory  roots  there  results  anosmia, 
which  may  be  double  or  one-sided. 

I  have  several  times  seen  the  fifth  nerve  involved.  This  most  fre- 
quently occurs  on  one  side  and  may  give  rise  to  hypersesthesia,  anaes- 
thesia or  rather  hypssthesia  of  the  face,  with  weakness  in  the  move- 
ments of  the  lower  jaw.  The  taste  is  disturbed  on  the  anterior  two- 
thirds  of  the  tongue,  and  there  is  often  a  neuroparalytic  keratitis  on 
the  same  side.  Hearing  is  affected  by  involvement  of  the  auditory 
nerve ;  at  times  the  irritation  produces  most  annoying  tinnitus.  When 
the  facial  is  included,  the  paralysis  resembles  the  peripheral  type  of 
Bell's  palsy,  without  the  involvement  of  the  palate,  the  hearing  and 
the  taste.  In  other  words,  the  paralysis  partakes  of  the  nature  of  a 
peripheral  palsy,  without,  however,  alteration  in  the  electrical  reactions. 
Facial  diplegia  occurs. 

The  cranial  nerve  symptoms,  various  and  scattered  and  change- 
able as  they  may  be,  are  so  constant  a  constituent  of  the  clinical  pic- 
ture of  basal  gummatous  meningitis,  that  without  them  the  diagnosis 


THE   NON-NEURONIC  DISEASES  885 

should  be  made  with  much  hesitancy.  It  may  be  that  for  some  brief 
period  in  its  course  basal  gummatous  meningitis  may  exist  and  pro- 
duce other  symptoms  than  those  showing  implication  of  the  cranial 
nerves,  especially  the  optic  and  oculomotorius,  but  such  cases  must 
be  exceedingly  rare  and  such  a  clinical  manifestation  would  probably 
be  very  brief.     I  have  never  seen  either. 

When  the  gummatous  meningitis  is  limited  to  the  convexity  of 
the  brain  of  course  the  cranial  nerves  escape.  Moreover,  the  symp- 
toms are  quite  dissimilar  to  those  of  basal  disease.  The  headache  seems 
to  be  more  superficial  and  localized.  Percussion  on  the  outside  of  the 
skull  will  elicit  sensitive  spots  or  areas,  especially  above  and  behind 
the  ear  and  in  the  occipital  region.  When  the  disease  process  is  of 
wide  extent,  spreading  over  a  large  area,  there  will  be  epileptiform 
manifestations,  conz'ulsions,  muscular  Iremblings  and  slight  muscular 
?-igidif\.  If  the  motor  region  of  the  cortex  is  pressed  upon  by  the 
gummata,  apJiasic  manifestations  or  Jachsonian  epileptic  attacks,  fol- 
lowed by  monoplegia,  Avill  make  their  apearance.  Eye  symptoms, 
like  choked  disc  may  not  be  present  until  the  disease  is  far  advanced. 
Sometimes  the  motor  and  sensory  disturbances  will  be  of  a  very  marked 
character  on  the  opposite  side  of  the  body,  such  as  epileptoid  attacks^ 
tremor,  contracture  and  pains.  In  some  cases  the  mind  is  affected  by 
the  associated  involvement  of  the  gray  cortex.  If  the  meningitis  is 
focal  and  scattered  in  character,  the  symptoms  may  be  of  a  focal  char- 
acter, depending  upon  the  part  of  the  brain  and  its  localization  func- 
tion, pressed  upon.  In  this  way  occipital  meningitis  may  produce 
hemianopsia,  temporary  disturbances  of  hearing,  peripheral  pains  and 
other  sensory  phenomena. 

In  the  larger  number  of  cases  of  brain  syphilis  these  two  forms  of 
meningitis,  that  of  the  base  and  that  of  the  convexity,  occur  together, 
though  for  a  time  one  or  the  other  seems  to  predominate.  Along  with 
the  meningitic  symptoms  are  those  which  may  be  regarded  as  in  a 
way  secondary  to  the  disease  in  the  isolated  vessels.  In  the  larger 
vessels,  especially  those  of  the  base,  like  the  -basilar  artery  and  its 
branches,  an  endarteritis  is  the  particular  form  of  lesion  present,  while 
in  the  smaller  and  terminal  capillaries  of  the  cortex  it  is  more  of  the 
nature  of  a  periarteritis.  In  these  cases  thrombi  form  and  emboli  float 
off  and  occlude  the  circulation  ;  or  the  thickening  of  the  arterial  walls 
brings  about  almost  the  same  result  by  the  narrowing  of  the  calibre 
of  the  vessels.  The  location  and  size  of  the  artery  thus  affected 
will  of  course  determine  the  character  of  the  syniptoms,  but  these  will 
partake  of  the  nature  of  those  of  an  encephalomalacia.  When  the 
softening  is  at  the  base,  the  great  symptom  is  a  progressive  hemiplegia, 
which,  however,  may  come  and  go,  first  in  the  leg,  then  the  arm  and 
finally  the  face,  several  times  before  it  becomes  permanent.  The  sen- 
sory and  mental  functions  as  a  rule  remain  intact.  Premonitory  indi- 
cations, like  twitching,  often  precede  the  hemiplegic  attack;  on  the 
other  hand,  the  paralysis  may  come  on  most  unexpectedly  and  pass 
awav  entirely  in  a  few^  hours  or  days.  I  saw  a  case  where  the  patient 
had 'to  take 'to  his  bed,  and  yet  the  next  day  he  was  walking  around 
almost  as  well  as  if  nothing  had  happened.     Speech  was  affected,  but 


886  '    THE   NOX-NEUROXIC  DISEASES 

there  was  no  loss  of  consciousness.  This  hemiplegia  is,  of  course,  on 
the  opposite  side  from  that  on  which  the  affected  artery  rests.  As 
Oppenheim  well  points  out,  the  laws  of  localization  for  crossed  hemi- 
plegia (superior  and  inferior)  must  be  used  with  some  caution  in 
brain  syphilis. 

Oculomotor  paralysis  of  one  side,  and  hemiplegia  of  the  other, 
are  here  sometimes  caused,  not  by  a  focal  peduncular  disease,  but  by 
the  very  conditions  of  the  basal  meningitic  process.  Involvement  of 
the  basilar  and  vertebral  arteries  give  rise  to  pontile  and  bulbar  symp- 
toms. When  the  arteries  higher  up  are  thus  obstructed,  the  well- 
known  apoplectic  manifestations  occur,  such  as  prodromes  followed 
by  extensive  hemiplegia,  hemianccsthesia,  aphasia,  heniianopsia.  The 
syphilitic  nature  of  these  attacks  is  indicated  by  the  headache  and  ver- 
tigo that  long  precede  them,  by  the  fugitive  character  of  the  apoplecti- 
form outbreaks,  the  stupor,  mental  confusion,  and  dementia  that  follow 
them. 

With  these  forms  of  brain  syphilis,  especially  with  the  basal  type, 
there  is  often  conjoined  syphilitic  meningo-myelitis.  The  latter  dis- 
ease, as  a  separate  affection,  will  receive  special  attention  under  the 
general  head  of  spinal  syphilis.  Here,  however,  a  few  words  must 
be  said  in  regard  to  the  symptomatology  of  the  combined  diseases,  com- 
monly referred  to  as  cerebrospinal  syphilitic  meningitis.  As  a  rule  the 
brain  symptoms  stand  out  in  overwhelm.ing  prominence.  If  a  thorough 
search  be  made,  however,  a  fugitive  girdle  pain,  a  tendency  to  para- 
plegic phenomena,  irritability  of  the  bladder,  localized  spinal  root  pains 
wnth  vasomotor  and  trophic  disturbances,  and  loss  of  one  or  both 
patella  reflexes  will  be  discovered.  Later  on  these  spinal  symptoms 
may  become  more  obvious  and  more  constant.  In  some  cases  they  may 
even  obscure  somewhat  the  cerebral  symptoms.  Almost  any  type  of 
spinal  syphilis  may  thus  present  itself  with  brain  syphilis,  the  more 
common  of  which  are  Erb's  type  of  syphilitic  spinal  paralysis,  multiple 
sclerosis,  Brown-Sequard's  syndrome  or  Oppenheim's  syphilitic  pseudo- 
tabes which  is  not  unlike  tabes  dorsalis  in  many  respects. 

Closely  related,  pathologically  and  symptomatically,  to  this 
cerebrospinal  syphilis  is  the  muliiple  syphilitic  neuritis  of  the  nerve- 
roots  of  Kahler.  There  is  nothmg  distinctive  about  this  to  call  for 
special  consideration  except  the  fact  that  the  paralysis  of  the  various 
cranial  and  spinal  nerves  comes  on  insidiously  and  irregularly,  and  that 
the  trouble  may  readily  be  mistaken  for  a  peripheral  neuritis.  Oppen- 
heim says,  anent  this  multiple  syphilitic  neuritis  of  Kahler,  that  it  is 
just  a  little  too  schematic,  a  remark  which  I  am  inclined  to  apply  to 
the  former's  own  separate  description  of  basilar  and  vertex  forms  of 
brain  syphilis  as  though  they  were  separate  and  distinct  diseases.  To 
"be  sure  they  each  have  a  striking  characteristic  symptomatology  and 
prognosis,  but  that  is  the  result  merely  of  the  location  of  the  disease 
process.  To  found  a  classification  thus  of  the  same  disease  upon  a  mere 
difference  of  location,  is  confusing.  Especially  is  this  true  where,  as 
in  brain  syphilis,  the  disease  process  so  often  occupies  both  and  even 
all  localities  simultaneously. 

The  symptoms  do  not  materially  differ  in  brain  disease  when  the 


THE  NON-NEURONIC   DISEASES  887 

syphilis  is  inherited  from  those  in  which  it  is  acquired.  Occurring  thus 
early  in  life,  however,  it  is  obvious  Vv^hy  many  mental  defects  and 
epilepsy  should  be  so  much  more  prominent  than  they  are  in  the  ac- 
quired form. 

Diagnosis. — It  is  easy  to  confuse  brain  syphilis  with  other  dis- 
eases when  there  is  not  a  clear  history  of  infection.  The  wide  extent 
of  its  pathology  and  consequent  symptomatology  account  for  this  and 
the  great  changeability  and  transitoriness  of  many  of  its  clinical  phe- 
nomena. As  the  error  is  more  often  committed  of  attributing  a  non- 
syphilitic  disease  to  syphilis  than  vice  versa,  the  differential  diagnosis 
is  best  considered  under  the  headings  of  the  diseases  that  are  thus  more 
likely  to  be  mistaken. 

Prognosis. — The  prognosis  of  brain  syphilis,  both  as  to  life  and 
as  to  permanent  disability,  depends  very  largely  upon  the  location  of 
the  disease  process.  When  it  is  most  active  at  the  base  of  the  brain 
the  prognosis  is  worse  than  when  it  is  spread  over  the  convexity.  In 
neither  form,  however,  is  it  absolutely  unfavorable.  Life  is  endangered 
the  more  the  process  approaches  and  affects  the  great  vital  centers  in 
the  pons  and  medulla.  Involvement  of  the  basilar  artery  and  its 
branches  is,  therefore,  a  particularly  unfortunate  event.  This  is  so 
especially  in  old  age,  and  when  the  general  health  is  below  par. 

When  hemiplegia  occurs  it  may  clear. up,  and  later  on  many  re- 
lapses follow.  A  hemiplegia,  however,  is  always  a  bad  sign,  as  it  in- 
dicates both  an  advanced  and  wide  state  of  disease.  If  the  hemiplegia 
does  not  recede,  and  especially  if  contractures  have  begun,  recovery 
is  no  more  to  be  expected  than  in  a  hemiplegia  of  any  other  sort. 

In  regard  to  the  question  of  recovery.  Gowers  has  stated  that 
syphilis  is  practically  an  incurable  disease,  though  he  probably  would 
not  deny  that  by  treatment  its  symptoms  may  be  suppressed  and  its 
destructive  influence  held  in  abeyance.  With  this  view  I  am  in  per- 
fect accord.  Therefore  it  follows  that  recovery  under  treatment — so- 
called  recovery — can  only  be  looked  for  when  the  tissue  changes  are 
strictly  specific  and  have  not  gone  on  to  complete  degeneration,  reor- 
ganization, etc.  An  optic  neuritis,  for  instance,  is  amenable  to  treat- 
ment, but  an  optic  atrophy  is  not ;  a  specific  meningo-encephalitis  may 
be  made  to  clear  up,  whereas  a  necrobiosis  due  to  an  arte- 
rial obliteration  will  not  give  any  response  to  the  most  heroic  medica- 
tion. This  is  the  reason  that  an'tisyphilitic  treatment  gives  such  varia- 
ble results  in  cases  treated  promiscuously  and  consecutively. 

Treatment. — The  prophylactic  treatment  of  brain  syphilis 
should  include  the  education  of  the  young  as  to  the  dangers  of  infec- 
tion and  the  heroic  treatment  of  the  infection  at  once  after  it  has  been 
acquired.  No  half  measures  are  permissible  here.  A  thorough  course 
of  mercury  for  a  long  period,  with  now  and  then  intervals  of  a  few 
weeks'  rest,  should  be  carried  out.  It  is  my  own  practice  to  recom- 
mend treatment  of  this  sort  for  a  period  of  not  less  than  three  years, 
and  sometimes  many  years  more.  The  mercury  may  be  given  by  the 
stomach  or  by  inunction.  I  prefer  the  latter  method  myself.  About 
a  dram  of  unguentum  hydrargyri  is  rubbed  into  the  skin  daily  or 
every  other  day,  for  a  couple  of  weeks,  and  then  a  few  weeks'  rest  is 


888  THE   A'ON-NEURONIC   DISEASES 

allowed  or  the  mercury  is  continued  in  milder  dosage  by  the  mouth. 
It  is  best  to  use  the  ointment  alternately  on  the  inner  side  of  first  one 
arm,  then  the  other,  or  on  the  inner  side  of  one  thigh  and  then  the 
other,  taking  twenty  minutes  or  half  an  hour  to  rub  it  in,  and  covering 
the  part  afterwards  with  a  bandage.  During  this  mercurialization  the 
diet  must  be  attended  to,  excluding  all  acids  and  stimulants ;  the  exer- 
cise must  be  regulated  and  the  use  of  free  bathing  to  promote  the  ac- 
tivity of  the  skin  must  be  enjoined.  A  chlorate  of  potash  mouth  wash 
(about  5  per  cent,  strength)  if  used  often  during  the  day  will  prevent 
stomatitis.  In  a  few  cases  even  the  most  vigorous  early  treatment 
after  the  above  manner,  fails  to  prevent  the  disease  attacking  the  brain 
or  the  trouble  itself  from  relapsing.  When  either  of  these  unfortunate 
events  occur,  the  treatment  must  be  at  once  renewed  and  conducted  to 
the  very  point  of  ptyalism.  It  is  the  patient's  only  hope  of  avoidmg 
the  frightful  ravages  of  the  disease  in  the  wav  of  the  paralyses,  etc. 

In  some  cases  the  iodide  of  potash  may  be  employed  with  or  with- 
out the  mercury.  It  shows  its  effects,  as  a.  rule,  sooner  than  the  mer- 
cury but  the  effects  are  not  so  lasting.  The  dosage  of  the  iodides 
should  be  much  larger  than  is  usually  given.  I  have  myself  given  as 
much  as  one  thousand  grains  a  day.  Beginning  with  twentv  or  thirty 
grains,  well  diluted  in  water  and  taken  after  food,  three  times  a  dav, 
the  dose  should  be  rapidly  increased  daily  until  two  or  three  hundred 
grains  a  day  are  taken.  If  the  remedy  is  well  diluted,  and  the  stom- 
ach assisted  with  a  little  pepsin  and  nux  vomica,  there  is  little  danger 
of  the  manifestations  of  iodism.  In  some  cases  I  have  had  such  mani- 
festations disappear  after  suddenly  advancing  the  dose  to  a  still  larger 
amount,  say  five  or  six  hundred  grains  a  day.  The  average  case  will 
hardly  need  more  than  about  three  or  four  hundred  grains  a  day.  con- 
tinued for  two  or  three  weeks  or  longer.  I  prefer  the  potassium  salt 
to  any  of  the  others,  and  above  all  to  the  many  iodonucleins  and  other 
substitutes  put  upon  the  market. 

Where  atrophy  has  taken  place,  destruction  of  tissue  and  sclerotic 
changes  have  occurred  within  the  nervous  tissues,  of  course  no  treat- 
ment, however  vigorously  applied,  can  be  expected  to  produce  any  ben- 
eficial results.  This  is  the  reason  why  such  varying  reports 
are  made  in  the  treatment  of  consecutive  cases  of  brain  syphilis.  Hem- 
iplegia, contractures,  etc.,  are  to  be  managed  here  on  the  same  lines  as 
when  following  other  general  causes. 

When  complete,  or  what  is  more  frequent,  partial  recoverv,  is 
obtained,  the  patient  should  be  warned  of  the  possibility  of  a  relapse 
and  told  that  the  best  way  to  avoid  such  a  catastrophe  is  to  lead  a 
steady,  regular  life,  to  avoid  all  mental  strain  and  worry,  sunstroke, 
traumata,  stimulants  and  excesses  of  all  sorts,  especiallv  in  eating  and 
sexual  matters. 

DEMENTIA  PARALYTICA. 

Until  quite  recently  this  disease  was  discussed  solely  in  works 
upon  insanity.  This  was  on  account  of  the  apparent  supremacy  of  its 
psychic  manifestations.  Since  we  have  learned  more  about  its  true 
nature,  we  find  that  pathologically  and  symptomatically  it  is  an  organic 


THE   NON-NEUKONIC  DISEASES  889 

brain  disease.  While  there  may  be  some  doubt  as  to  the  strict  apph- 
cabiHty  of  the  name  chronic  diffuse  meningo-encephahtis,  some  still 
regarding  the  disease-process  as  primarily  one  of  degeneration  rather 
than  inflammation,  there  can  be  no  doubt  as  to  the  positive  changes  in 
the  cortex  and  their  relationship  not  only  to  the  psychic  but  to  the 
rriotor  and  other  equally  important  symptoms.  Hence  it  is  proper  to 
now  discuss  general  paresis  or  dementia  paralytica  under  the  head  of 
diseases  of  the  brain.  The  old  name  progressive  paralysis  of  the  in- 
sane ought  to  be  entirely  dropped  as  it  represents  a  conception  of  the 
trouble  not  at  all  in  consonance  with  what  we  know  about  it  to-dav. 

Etiology. — In  a  few  cases  a  neuropathic  heredity  can  be  traced 
but  only  in  a  few.  The  male  sex  fall  victims  to  it  much  more  fre- 
quently than  the  female.  It  occurs  most  commonly  in  the  middle 
period  of  life,  between  the  ages  of  thirty  and  fifty.  It  has  been  seen 
in  childhood.  It  is  very  rare  in  old  age.  Nationality  seems  to  have 
no  deterring  influence  for  or  agamst  it.  It  is  on  the  increase  every- 
where where  the  excitements  and  struggles  of  life  are  at  their  maxi- 
mum. In  the  cities  and  the  crowded  centers  of  civilization  and  in  those 
walks  of  life  where  ambition  to  get  ahead,  mental  strain,  anxieties 
and  hopes  are  the  keenest.  Nascent  races,  like  the  negro,  when  placed 
under  these  conditions  become  subject  to  it.  Fournier  ranks  general 
paresis  along  with  tabes  dorsalis  as  a  parasyphilitic  disease.  In  from 
70  to  90  per  cent,  of  all  cases  a  history  of  syphilis  is  obtainable.  Like 
tabes  it  is  regarded  not  as  a  syphilitic  disease  but  rather  as  a  sequel 
of  or  the  remains  after  the  syphilitic  storm.  Pathologically  and  clin- 
ically locomotor  ataxia  and  dementia  paralytica  are  certainly  closely 
related.  The  difficulty  of  inoculating  paretics  with  the  syphilitic  virus, 
as  shown  by  Krafft-Ebbing,  is  a  strong  point  in  favor  of  the  syphilitic 
theory  of  the  disease.  Acquired  and  congenital  syphilis  has  been 
traced  in  some  of  the  cases  seen  in  childhood.  It  is  probably  this  in- 
fection, together  with  the  strain  and  dissipation  that  lurk  behind  gen- 
eral paresis,  that  determine  such  factors  in  the  etiology  of  it  noted 
above  in  connection  with  sex,  age,  etc.  In  a  happy  epigram  Krafft- 
Ebbing  has  summed  up  the  etiology  of  the  disease  as  covered  by  "civil- 
ization and  syphilization."  The  particular  truth  concealed  in  this 
aphorism  is  that  neither  the  syphilis  nor  the  civilization  alone  is  likely 
to  give  rise  to  the  disease.  The  predisposing  influence  of  the  former 
and  the  exciting  tendencies  of  the  latter  must  cooperate.  And  yet  one 
cannot  elicit  evidence  of  syphilis  in  every  case.  Other  predisposing 
factors  must  be  assumed  in  its  place  by  those  who  are  not  yet  ready  to 
accept  the  dictum  that  all  paretics  are  syphilized.  In  two  instances  in 
which  the  infection  was  strenuously  denied,  and  in  whom  I  could  not 
obtain  the  slightest  evidence  either  in  the  past  or  present  history  of  the 
disease,  typical  dementia  paralytica  developed  soon  after  the  residence 
of  the  patient  was  transferred  from  the  country  to  the  city.  In  both 
instances  the  new  life  was  most  strenuous,  full  of  trouble  and  anxiety 
and  wanting  in  either  happiness  or  contentment.  Nothing  beyond  a 
neuropathic  heredity  could  be  discovered  as  a  predisposing  cause.  It 
is  not  unreasonable  to  suppose  that  in  a  certain  small  percentage  of 
cases  there  mav  be  such  a  congenital  weakness,  such  a  want  of  vital 


890  THE   NON-NEURONIC  DISEASES 

capacity,  in  certain  of  the  central  neurones  that  when  subjected  to 
the  sudden  and  unwonted  strain  of  competitive  civiHzation  they  suc- 
cumb. 

Pathology  and  Pathogenesis. — The  principal  pathological 
changes  are  observed  in  the  cerebrum,  though  there  are  changes  often 
in  the  spinal  cord  also. 

Macroscopically  the  brain  is  smaller,  smoother  and  harder  than 
normal.  There  is  an  atrophic  condition  of  the  convolutions,  making 
the  gyri  smaller  and  flatter  and  the  sulci  less  deep.  This  is  most  no- 
ticeable in  the  frontal  and  parietal  regions,  though  it  may  be  seen  also 
in  the  island  of  Reil  and  in  the  temporal  convolutions.  It  is  sugges- 
tive of  cortical  degeneration.  The  membranes  are  frequently  adher- 
ent to  the  brain  and  when  torn  away  often  peel  off  spots  of  cortical 
substance  with  them.  The  pia  is  thickened  and  clouded  while  the 
dura  looks  as  though  there  had  been  an  internal  hemorrhagic  pachy- 
meningitis. There  is  an  excess  of  cerebrospinal  fluid  and  a  variable 
degree  of  internal  hydrocephalus  with  distention  of  the  ventricles  and 
granulation  of  their  walls. 

The  weight  of  the  entire  brain  is  diminished  and  when  it  is  cut 
into  it  feels  firm  and  cheesy.  The  borderlines  of  the  gray  matter  are 
less  sharply  marked  than  normal  and  the  thickness  of  the  cortex  is 
seen  to  be  decidedly  lessened.  The  degree  of  sclerosis  varies  in  differ- 
ent cases.  The  white  matter  is  also  affected  but  not  as  much  as  the 
gray,  being  firmer  in  consistency  and  seemingly  more  compact.  Areas 
of  softening,  old  hemorrhagic  remains  and  arterio-sclerosis  are  not  un- 
frequently  observed.  In  a  word  the  gross  appearances  are  such  as  we 
might  expect  from  a  prolonged  inflammatory,  degenerative,  sclerotic 
process. 

The  microscopic  appearances  are  striking  and  quite  typical  though 
the  nature  of  the  process  underlying  these  appearances  is  not  clear. 
The  cells  of  the  cortex  are  more  or  less  atrophied  and  the  neuroglia 
and  interstitial  tissue  is  hardened  and  increased.  The  ganglion  cells  are 
variously  altered,  the  nuclei  and  fibres  of  the  neuroglia  are  increased, 
the  spider  cells  are  proliferated,  the  bloodvessels  are  hyaline  and  col- 
loid, and  sclerosed,  and  the  lymph  tracts  are  dilated  and  displaced.  Ac- 
cording to  Tuczek  the  medulated  tangential  fibres  of  the  upper  cor- 
tex, especially  of  the  frontal  lobe  and  island,  are  degenerated.  The 
whole  condition,  as  Wernicke  expresses  it,  suggests  a  chronic  progres- 
sive process  of  the  disease  in  the  cortex  that  causes  an  ultimate  atro- 
phy of  its  constituent  parenchymatous  elements. 

Similar  appearances  are  sometimes  observed  in  the  basal  ganglia, 
and  gray  matter  of  the  crura,  pons  and  medulla.  The  pyramidal  and 
posterior  tracts  may  also  be  implicated.  It  is  not  known  whether  the 
degeneration  of  the  pyramidal  tracts  is  primary  or  secondary.  That 
of  the  posterior  tracts  is  probably  primary  due  to  the  same  cause  that 
produces  the  cerebral  changes.  The  optic  nerves,  and  occasionally  some 
of  the  other  cranial  nerves,  are  wasted.  Even  the  peripheral  cutaneous 
nerves  are  now  and  then  degenerated. 

It  will  be  noted  that  this  pathological  picture  brings  to  mind  very 
forcibly  the  pathological  picture  of  tabes  dorsalis,  the  only  difference 


TPIE  NON-NEURONIC  DISEASES  89 [ 

being  the  location  of  the  primary  focus  of  the  disease.  Fournier  hini- 
-self  suggests  that  the  two  affections  are  but  different  expressions  of 
the  one  and  same  morbid  entity,  possibly  the  one  and  same  disease. 
■Clinically  it  has  long  been  remarked  that  locomotor  ataxia  often  ter- 
minates in  dementia  paralytica  and  that  paretic  dements  not  infre- 
-quently  develop  tabes  dorsalis. 

The  question  of  the  nature  of  the  primary  process  in  the  patho- 
.genesis  of  the  malady  is  quite  as  unsettled  here  as  it  is  in  locomtor 
ataxia.  There  are  strong  contestants  for  the  primary  degenerative 
theory  on  the  one  hand,  and  for  the  meningeal  inflammatory  theory  on 
the  other.  It  is  highly  probable  that  whichever  view  is  ultimately 
proved  to  be  correct,  it  will  apply  to  both  dementia  paralytica  and  loco- 
motor ataxia  alike. 

Following  the  lead  of  Fournier  many  still  maintain  that  as  a  more 
•or  less  remote  result  of  the  specific  infection  a  primary  degeneration 
takes  place  in  the  cortical  cells  and  their  processes,  with  a  secondary 
sclerosis  and  inflammation  in  the  interstitial  tissues  and  cerebral  mem- 
iDranes.  Many  facts  seem  to  lend  credence  to  this  view  and  none  more 
so  than  the  one  overwhelming  fact  that  in  the  true  syphilitic  diseases 
■of  the  central  nervous  system,  which  are  distinctly  meningeal  and 
inflammatory  no  such  characteristic  changes  are  produced  as  are  ob- 
served in  dementia  paralytica.  The  arteritis,  gummata  and  gumma- 
tous meningitis  of  cerebral  syphilis  are  never  seen  in  these  degenera- 
tive diseases,  while  on  the  other  hand  the  characteristic  degenerative 
appearances  of  the  latter  do  not  seem  to  occur  with  the  inflammatory 
processes  of  cerebral  syphilis.  Either  there  must  be  two  distinct  forms 
of  inflammation  resulting  from  syphilis,  the  degenerative  and  the  or- 
dinary, or  the  two  processes  must  be  distinct  and  separate.  In  the 
light  of  modern  pathology  the  latter  seems  to  me  to  be  the  only  answer 
to  the  question.  The  primary  inflammatory  processes  of  syphilis  of 
the  central  nervous  system,  whether  immediate  or  remote,  are  not  the 
same  as  the  degenerative  results  of  syphilis  as  seen  in  dementia  para- 
lytica and  tabes  dorsalis. 

Those  who  contend  that  the  disease  is  primarily  inflammatory  with 
the  parenchymatous  atrophy  as  a  secondary  result  are  tending  back  to 
the  old  view  of  a  primary  sclerosis,  though  they  place  the  initial  stages 
of  the  disease  process  in  the  cerebral  meninges.  This  is  somewhat  in 
line  with  Obersteiner  and  Redlich's  explanation  of  locomotor  ataxia 
'On  the  basis  of  a  particular  form  of  spinal  meningitis.  Bevan  Lewis 
partly  sums  up  this  view  by  stating  that  there  are  three  stages  in  the 
'Cortical  process :  ( i )  the  stage  of  inflammatory  change  in  the  tunica 
adventitia  of  the  arteries;  (2)  the  stage  of  hyper-development  of  the 
lymph-connective  system  of  the  brain,  with  degeneration  and  disap- 
pearance of  the  nerve  elements  and  the  axis-cylinders;  and  (3)  the 
stage  of  general  fibrillation  with  shrinkage  and  extreme  atrophy  of 
the  parts  involved.  In  perfect  consonance  with  this  view  the  disease 
is  sometimes  called  chronic  diffuse  meningo-encephalitis. 

Whether  the  meningitis  is  an  initial,  synchronous  or  terminal  phe- 
nomenon with  the  encephalitis  or  not,  the  primary  inflammatory  na- 
ture of  the  entire  process  is  the  essential  feature  of  this  view.     If  this 


892  THE    .\OX-NEL"R()XIC   DISEASES 

be  SO  we  are  at  once  confronted  by  the  question  as  to  the  nature  of 
the  process  in  the  similar  disease,  locomotor  ataxia.  If  the  two  dis- 
eases are  the  same  then  primary  inflammation,  it  would  naturally  be 
supposed,  underlies  the  pathology  of  the  latter.  Many  declare  that 
it  does  but  that  it  originates  in  the  membranes.  These  theorists  prob- 
ably then  also  believe  that  dementia  paralytica  originates  in  a  chronic 
meningeal  inflammation.  Why  discuss  either  disease  then  outside  of 
the  chapter  or  chapters  devoted  to  cerebral  and  spinal  meningitis?  The 
degenerative  sequelze  can  then  be  easily  treated  of  in  a  special  para- 
graph and  emphasized  as  one  of  the  many  results  of  these  special 
forms  of  meningitis.  If,  however,  the  meningitis  is  not  the  primary 
source  of  the  trouble,  though  it  is  still  affirmed  that  the  process  is 
primarily  an  interstitial  inflammation,  then  it  is  presumably  the  same 
in  locomotor  ataxia,  and  we  are  back  to  the  old  posterior  spinal  sclero- 
sis theory  in  which  the  degeneration  was  affirmed  to  be  a  secondary 
process.  The  only  way  of  escape  from  this  dilemma,  it  seems  to  me, 
is  to  deny  completely  the  relationship  between  the  two  diseases,  tabes 
dorsalis  and  dementia  paralytica,  and  that  we  cannot  do. 

The  whole  question  is  in  need  of  more  light,  though  for  the 
present  we  are  justified,  in  my  opinion,  in  regarding  the  primary  pro- 
cess as  a  degenerative  one  in  the  nervous  elements  in  both  diseases. 
This  degeneration  is  the  result  of  an  exciting  cause  acting  upon  a  nerv- 
ous system  predisposed  by  syphilis.  Secondary  to  the  degeneration  are 
the  interstitial  sclerosis,  meningeal  inflammation,  and  other  vascular 
alterations. 

Symptoms. — It  goes  without  saying  that  the  most  prominent 
symptoms  of  dementia  paralytica  are  the  mental  exhibitions.  For  this 
reason  the  disease  was  formerly  named  and  classified  among  the  pure 
psychoses.  Prominence  and  importance  are  not  synonymous  terms. 
There  are  other  symptoms  so  important  that  were  they  absent,  the 
mental  symptoms  would  lose  much  of  their  significance  as  signs  of 
this  afifection.  The  diagnosis  should  never  be  positively  based  upon 
the  psychic  symptoms,  though  they  may  furnish  the  strongest  clue 
to  the  trouble.  In  every  case  search  shoifld  be  made  for  the  motor 
signs,  evidences  of  apoplectiform  attacks,  speech  disturbances  and 
Argyll-Robertson  pupils.  One  or  more  of  these  will  usually  be  found 
and  when  associated  wath  the  psychic  exhibitions,  the  diagnosis  of 
the  organic  cerebral  disease,  dementia  paralytica,  is  assured. 

The  special  value  that  attaches  to  the  menial  change  is  that  it  be- 
gins to  show  itself  so  early  that  it  almost  assumes  the  role  of  a  prod- 
rome and  awakens  a  strong  suspicion  before  any  of  the  other  symptoms' 
can  be  clearly  detected.  The  panorama  of  the  psychic  disturbances 
moves  through  the  successive  stages  of  gradual  excitable  dementia.  A 
steady  down  grade  in  the  intelligence,  with  a  weakening  of  its  chan- 
nels of  expression,  the  judgment  and  conscience  and  morale,  is  the 
psychic  side  of  the  clinical  picture.  Those  mental  powers,  with  the 
high  obligations  that  accompany  them,  which  have  been  the  last  to 
have  been  laboriously  evolved  during  long  periods  of  evolutionary  de- 
velopment in  the  race  and  in  the  individual,  like  the  apex  of  a  pyra- 
mid, are  the  first  to  topple.    There  is  a  gradual  descent  from  manliness 


THE  NON-NEUROXIC  DISEASES  803 

to  childishness,  from  ahruism  to  egoism,  from  a  high  sense  of  obhga- 
tion  to  a  low  sense  of  responsibility.  While  the  memory,  the  imagina- 
tion and  the  will  may  be  affected,  it  is  the  intelligence,  the  comparing 
.and  relating  faculty,  that  is  especially  damaged.  As  this  faculty  ex- 
ercises an  inhibitory  control  m  health  over  all  of  the  lower  faculties 
of  the  animal  personality,  the  more  it  is  weakened  the  more  the  lower 
faculties  and  their  personality  come  to  the  front.  This  explains  the 
•egoism,  the  selfishness,  the  shamelessness,  the  cunning,  the  unreason- 
able scheming,  the  emotionalism,  the  instability,  unreliability  and  irri- 
tability, the  abnormal  ideomotor  excitement,  almost  resembling  mania, 
the  expansive  imaginativeness  with  its  hallucinations  and  delusions, 
its  volubility,  loquaciousness  and  general  bustling  activity  and  self- 
satisfaction  usually  seen  in  these  patients.  The  guiding  reins  of  the 
intelligence  have  fallen  and  the  steeds  of  the  lower  faculties  are  run- 
ning away.  Only  exhaustion  brings  them  to  a  standstill  in  the  ter- 
minal dementia.  The  whole  picture  is  a  sort  of  psychic  analogue  of 
.spastic  paralysis,  or  a  failure  of  pneumogastric  inhibition  over  the  ac- 
tion of  the  heart. 

So  fine  are  these  psychic  changes  in  the  beginning  that  often  they 
are  not  noticed  except  by  the  closest  observers  and  the  nearest  oi 
kin.  There  is  a  tendency  towards  indifference  to  business,  home  ties 
and  obligations  of  honor.  The  individual  is  not  as  scrupulous  about 
little  matters,  his  dress,  his  word,  his  promises,  his  speech,  his  en- 
gagements as  he  has  been  wont  to  be.  He  is  a  little  impatient  of  re- 
straint and  seems  to  seek  his  own  comfort  and  pleasure  more  deter- 
minedly. He  becomes  fickle  and  frivolous.  He  neglects  his  wife  and 
•children  upon  the  slightest  selfish  whim.  He  grows  inattentive  and 
forgetful.  He  makes  use  of  language  and  performs  acts  that  are  un- 
called for,  unaccountable  and  often  shameless.  At  times  he  is  em- 
barrassingly indelicate,  vulgar,  cynical,'  obscene.  He  seems  to  have 
lost,  as  the  disease  advances,  all  sense  of  the  proprieties,  all  finer  ap- 
preciation of  his  proper  relationship  to  the  world  outside  of  himself. 
He  will  expose  his  person,  urinate  or  defecate  upon  the  highway, 
utterly  indiff'erent  of  publicity.  This  general  apathy  and  indift'erence 
•coupled  with  the  unbridled  egoism  often  brings  him  in  conflict  with 
his  partners  and  associates  in  business,  in  opposition  to  those  who  are 
most  interested  in  his  welfare,  and  even  in  actual  struggle  with  the 
law.  Thus  irritabilities  at  home  and  lawsuits  abroad  are  his  portion. 
Sharpers  and  tricksters  observing  and  taking  advantage  of  his  weak- 
ness, often  lead  him  into  concocting  vast  schemes,  spending  vast  sums 
■of  money,  starting  huge  industrial  undertakings,  developing  unwieldy 
financial  combinations  which  help  to  enrich  them  but  invariably  spell 
ruin  and  disgrace  for,  him.  Who  knows  what  financial  crashes,  in- 
dustrial upheavals  and' great  business  failures  have  not  been  the  legit- 
imate ending  of  the  grand  schemes  of  some  unrecognized  but  irre- 
sponsible paretic  dement !  More  disrupted  family  circles,  more  thiev- 
ery in  the  world  of  high  finance,  more  immorality,  dishonesty,  and 
general  devilishness  of  a  certain  order  may  be  due  to  incipient  general 
paresis  than  we  are  willing  to  admit. 

Not  only  on  the  side  of  moral  apathy  and  ethical  indifference  does 


894  THE    NON-XEUKONIC   DISEASES 

dementia  paralytica  exhibit  itself  but  also  on  that  of  positive  self- 
satisfaction,  unceasing  activity,  restlessness  and  excitement.  The 
calm  egotism  and  self-satisfaction  of  these  patients  is  sometimes  posi- 
tively exasperating.  They  know  it  all,  they  are  absolutely  impervious 
to  instruction.  They  are  therefore  often  apparently  happy  and  pleased 
with  the  world,  themselves  and  things  in  general.  Their  restlessness 
may  exhibit  itself  in  many  ways ;  in  taking  long  walks,  scribbling  whole 
reams  of  paper,  inventing  a  lot  of  useless  gewgaws  or  perambulating 
about  the  house  all  night.  The  environment  of  such  patients  is  in  a 
constant  state  of  turmoil.  Those  about  him  become  worn  out  with 
his  incessant  volubility  and  his  constant  bustling  without  achievement, 
mvoluntarily  irritate  and  cross  him  and  drive  his  weak,  irritable  dis- 
position into  frequent  explosions  of  terrific  anger.  ^  Though  danger-^ 
ous  at  times,  these  passionate  outbreaks  are  not  lasting.  Sometimes- 
they  are  most  violent  and  provoked  by  the  most  trivial  circumstances. 

Loss  of  mojiory  is  characteristic  of  almost  every  case.  It  must 
not  be  confused  with  the  mere  apparent  loss  of  memory  caused  by 
the  overwhelming  force  of  the  selfishness.  One  of  my  patients  was 
given  some  money  by  her  husband,  who  was  a  poor  man,  to  go  out 
and  pay  some  grocery  and  other  bills  in  the  neighborhood.  She  soon 
walked  in  with  nineteen  shirtwaists,  to  purchase  which  she  had  used 
all  the  money  and  declared  she  had  forgotten  all  about  the  shop-bills 
which  she  still  held  in  her  hand.  In  the  true  amnesia,  recent  events 
are  more  easily  forgotten  than  remote.  If  the  patient  is  asked  to 
describe  his  life  he  will  be  very  loquacious  about  his  early  years  but 
very  chary  in  reporting  what  he  did  the  week  before.  Inability  for 
mental  computation  is  particularly  noticeable.  A  previous  lightning 
calculator  will  struggle  over  the  addition  or  multiplication  mentally  of 
a  column  of  two  figures.  Amnesia  is  probably  at  the  basis  of  this 
trouble. 

\\'ith  the  steady  progression  of  the  disease  the  signs  of  psychic 
irritability  and  intellectual  weakness  become  more  and  more  pro- 
nounced. They  assume  the  character  of  grandiose  hallucinations  and 
delusions,  particularly  in  regard  to  himself.  On  account  of  this  folic 
de  grandeur  he  identifies  himself  with  kings,  presidents  and  mighty 
geniuses.  It  is  a  favorite  occupation  with  these  poor  creatures  to 
pose  as  the  reincarnated  Messiah.  Sometimes  they  imagine  they  are 
veritable  Monte  Cristos  with  unlimited  wealth.  The  paretic  dement 
is  always  a  great  artist,  an  inexhaustible  inventor,  a  poet  of  world- 
wide renown,  an  astute  detective  and  the  scientist  of  scientists.  While 
he  does  not  hold  long  to  these  various  poses,  sometimes  he  does  dabble 
in  the  work  of  the  particular  character  he  imagines  he  is.  The  vacuity 
of  all  his  efforts  and  absolute  nothingness  of  the  sum  total  is  at  all 
times  pathetic  if  not  amusing. 

Instead  of  the  feeling  of  well-being  there  is  sometimes  one  of  de- 
pression. Hypochondriasis  or  melancholia  ma}'  occur  early  in  the 
disease,  though  even  these  usually  assume  the  grandiose.  He  is  a 
Byronic  sufiferer  on  account  of  the  cruelty  of  the  world.  The  torments 
oi  Dante's  Inferno  are  nothing  in  comparison  to  what  one  of  my  pa- 
tients declared  he  endured.     They  fancy  they  are  the  victims  of  most 


THE   XOX-XEUROXIC  DISEASES  895 

extraordinar}-  anatomical  and  physiological  conditions.  A  man  told 
me  once  that  the  food  he  ate  flew  out  of  the  top  of  his  head  up  against 
the  ceiling.  Unique,  astonishing,  surpassingly  strange  though  sad  and 
depressing  are  these  delusions,  and  thus  they  are  in  keeping  with  the 
general  psychic  manifestations  of  the  disease.  As  the  excitement, 
volubility,  and  psychic  irritability  approach  their  climax  the  patient  be- 
comes dangerous  and  more  and  more  intolerable.  He  bursts  out  in 
passion,  screams,  rushes  about,  seizes  those  near  him,  scolds  and  pours 
forth  a  volume  of  senseless  words  and  phrases  and  makes  all  sorts 
of  strange  and  wild  grimaces.  The  oncoming  exhaustion  soon  shows 
itself  in  beginning  bodily  emaciation,  especially  as  the  patient  refuses 
all  nourishment,  in  a  more  prompt  appearance  of  the  condition  of  tire, 
in  lessened  volubility,  in  increasing  inattention  and  dullness  and  finally 
in  absolute  stupor  and  dementia.    The  end  is  then  not  far  oft. 

Among  the  non-mental  somatic  symptoms  of  the  disease  the  ear- 
liest to  appear,  and  therefore  of  the  greatest  importance,  are  the 
Argyll-Robertson  pupil,  pupillary  inequality,  tremor,  especially  of  the 
tongue  and  lips,  special  disturbances  of  the  speech  and  alterations  of 
the  handwriting.  These  may  be  present  when  the  mental  manifesta- 
tions are  quite  elusive.  Others  may  precede  the  mental  and  all  other 
symptoms  by  months  and  years.  They  are  never  entirely  absent  when 
the  mental  symptoms  are  noticeably  prominent.  They  should  always 
be  strenuously  sought  for  and  constitute  the  stronger  foundation  for 
the  diagnosis  of  the  disease  in  the  entire  complexus  of  S3'mptoms.  De- 
mentia paralytica  is  an  organic  disease  with  positive  somatic  representa- 
tion. The  prominent  psychosis  that  constitutes  a  part  of  its  clinical  pic- 
ture is  the  direct  result  of  the  organic  damage  in  the  cerebral  cortical 
elements.  It  is  not  entirely  and  wholly  an  insanity  in  the  usual  mean- 
ing of  the  word. 

Pupillary  rigidity  to  light  stimulation,  with  '  preservation  of  re- 
sponse to  accommodation,  the  Argyll-Robertson  pupil,  is  an  early  sign 
of  general  paresis.  It  is  estimated  that  it  occurs  in  sixty  per  cent,  of 
the  cases.  It  may  precede  all  other  symptoms  and  be  the  only  one 
present  for  many  months  and  even  several  years.  It  is  usually  a  con- 
tracted pupil ;  some  ophthalmologists  say  always  a  contracted  pupil. 
]\Iydriasis  may  exist,  however,  in  some  cases.  It  is  usually  bilateral, 
though  it  may  be  more  marked  in  one  eye  than  in  the  other,  or  may  be 
entirely  unilateral.  The  pupils  are  sometimes  unequal  or  irregularly 
contracted.  Hippus  has  been  observed.  The  vision  is  more  or  less 
disturbed  and  on  account  of  the  occasional  headache  with  scintillat- 
ing scotomata  the  disease  for  a  time  has  been  mistaken  for  hemi- 
crania.  Double  vision  from  paralysis  of  the  external  ocular  muscles 
and  even  paralysis  of  accommodation  have  been  rarely  noted  among 
the  earlier  manifestations.  These  eye  symptoms,  and  others  it  will  be 
remarked,  are  much  like  those  sometimes  seen  in  the  preataxic  stage 
of  locomotor  ataxia.  For  a  while  in  some  cases  the  distinction  between 
the  two  diseases  cannot  be  made. 

Soon  a  peculiar,  fine,  fibrillary  tremor  announces  itself.  It  is 
especiallv  noticeable  in  the  sides  and  tip  of  the  tongue  and  in  the  lips. 
When  the  patient  talks  it  can  also  be  slightly  detected.     It  may  be  con- 


896  THE   XOX-XEUROXIC  DISEASES 

fined  to  certain  muscles  or  it  may  appear  in  every  part  of  the  body. 
It  shows  itself  when  the  patient  writes  and  it  is  seen  in  the  hand  and 
foot  sometimes  when  they  are  held  out.  The  oscillations  are  small, 
rapid  and  sometimes  accompanied  by  jerky  movements.  Together 
with  and  partly  on  account  of  the  tremor  and  fine  incoordination,  the 
patient's  speech  and  -ccrituig  are  strikingly  characteristic.  The  former 
is  slow,  blurred,  drawling,  stumbling  and  interrupted.  There  seems  to 
be  difficulty  in  getting  the  words  out  and  consequently  delay  and  hesi- 
tancy. Syllables  and  parts  of  whole  phrases  may  be  omitted  or  slid 
over  indistinctly.  There  is  no  distinct  scanning  of  the  speech,  but 
rather  uncertainty,  jerkiness  and  irregularity.  In  the  articulation  the 
lips  tremble  and  shake  markedly,  unusual  parts  of  the  face  are  worked 
and  a  nasal  tone  is  assumed.  Generally  ordinary  language  will  do  to 
exemplify  these  manifestations.  I  sometimes  demonstrate  them  more 
forcibly  by  getting  the  patient  to  repeat,  as  well  as  he  can  some  such 
phrases  as  these :  Peter  Piper  picked  a  peck  of  pickled  peppers  ;  round 
the  rugged  rock  the  ragged  rascal  ran ;  buy  baby  blue  bottle  of  black- 
berry brandy,  etc.  Familiar,  semi-automatic  speech,  like  reciting  the 
multiplication  table,  can  usually  be  uttered  with  more  facility  than 
speech  requiring  constant  attention  and  thought.  The  latter  is  always 
accompanied  by  a  greater  slowness  of  diction,  partly  on  account  of  the 
growing  dementia.  In  reading  it  is  apt  to  be  more  noticeable  than  it  is 
in  automatic  speech,  but  not  quite  so  marked  as  in  thoughtful  conversa- 
tion. The  same  general  features  seen  in  the  speech  trouble  are  seen  in 
the  handwriting.  There  is  tremulousness.  jerkiness,  irregularity,  slow- 
ness, laborious  efifort,  repetitions  and  omissions.  Incoordination  and 
dementia  are  behind  these.  Sometimes  there  is  absolute  want  of  sense, 
coherency  and  relevancy  in  w^hat  is  penned.  Paralexia  or  irrelevant 
reading  has  been  noted  in  some  cases.  If  the  patient  has  been  a  letter 
writer,  always  ask  to  see  some  of  the  earlier  letters.  In  some  cases 
there  may  be  detected  slight  occasional  lapses,  both  of  thought  and 
diction,  that  now  show  themselves  so  prominently.  As  in  all  examina- 
tions of  this  sort,  involving  the  patient's  intelligence  and  education,  the 
previous  culture  must  be  known  and  taken  carefully  into  consideration. 
A  man  of  mere  ignorance  may  attempt  to  write  and  the  product  bear 
somewhat  a  resemblance  to  that  put  forth  by  an  incipient  paretic. 

So  important  are  the  speech  and  writing  defects  in  the  diagnosis 
of  the  disease  that  their  examination  must  never  be  omitted,  however 
slight  the  other  symptoms  may  appear.  They  alone  are  almost  path- 
ognomonic and  can  ofttimes  be  detected  by  special  examination  when 
otherwise  they  would  not  attract  attention. 

A  history  of  temporary  syncope  and  paralytic  attacks  is  extremely 
suggestive.  These  may  be  either  apoplectiform  or  epileptiform. 
Without  warning  and  without  apparent  immediate  cause,  the  patient 
suddenly  has  a  sinking  spell  with  more  or  less  coma  and  muscular 
w^eakness.  He  may  turn  pale  and  fall,  or  he  may  remain  stationary  in 
a  sort  of  petit  mal  state.  On  the  other  hand,  he  may  have  all  the  indi- 
cations of  a  true  apoplectic  seizure;  sudden  unconsciousness,  a  fall, 
relaxed  extremities  wath  flushing  of  the  face,  stertorous  respiration, 
rapid  heart  action,  elevation  of  temperature  and  death.     Hemiplegia, 


THE   XOX-XEUROXIC  DISEASES  897 

monoplegia,  aphasia  and  all  the  usual  accompaniments  and  sequelae 
of  cerebral  hemorrhage  and  obstruction  may  appear  in  some  cases. 
Usually  these  attacks  are  of  the  temporary  type  and  sooner  or  later 
the  patient  is  almost  back  to  his  old  condition.  The  paralysis  and  the 
aphasia  may  be  very  brief  and  fleeting  or  they  may  be  partially  per- 
sistent. The  phenomenon  repeats  itself,  varying  in  time  and  location. 
True  epileptic-like  seizures,  generalized  and  partial,  usually  without 
aurae,  are  perhaps  more  common  than  apoplectic  strokes.  Sometimes 
these  precede  the  appearance  of  any  of  the  other  typical  symptoms. 
All  forms  of  epilepsy  may  be  simulated  by  them,  even  the  psychic  and 
the  status  types.  After  these  paralytic  and  epileptic  attacks  the  pa- 
tient's general  mental  condition,  speech,  etc.,  are  apt  to  be  worse. 

In  the  cases  that  are  hemiplegic  the  gait  is  characteristic,  pains  are 
absent  and  the  reflexes  of  the  knee  are  exaggerated.  In  some  cases, 
however,  there  will  appear,  if  not  at  first,  then  later  on,  loss  of  the 
knee-jerks,  static  and  motor  ataxia,  lancinating  pains  and  other  sensory 
phenomena  without  much  motor  weakness.  These,  of  course,  are  the 
manifestations  of  tabes  dorsalis.  They  may  appear  before  the  mental 
indications  of  dementia  paralytica ;  in  about  eighty  per  cent,  of  cases 
they  come  on  after  them.  Even  perforating  ulcer,  arthropathies,  bed 
sores,  optic  atrophy  and  other  vasomotor  and  trophic  conditions  obtain 
late  in  the  disease.  With  involvement  of  the  pyramidal  tracts  together 
with  the  posterior,  a  combined  spinal  degenerative  sclerosis  with  its 
usual  clinical  picture  will  be  associated  with  the  general  paresis. 

So  extensive  is  the  clinical  portrayal  of  the  disease  at  times  that 
one  may  well  be  in  doubt  as  to  what  are  the  symptoms  of  the  funda- 
mental malady  and  what  the  symptoms  of  the  complications.  There 
is  ground  evidently  for  the  contention  of  Fournier  that  the  entire 
complexus  of  symptoms,  cerebral  and  spinal,  represents  one  uniform, 
wide  disease  of  the  entire  nervous  system,  with  its  maximum  repre- 
sentation, and  usually  limitation,  in  the  sensory  path. 

Diagnosis. — In  the  earlier  stages  the  diagnosis  of  dementia 
paralytica  is  very  difficult  and  this  is  the  time  when  a  correct  diagnosis 
is  especially  desirable.  To  save  the  patient,  his  family  and  his  property 
a  prompt  recognition  of  the  first  signs  of  the  trouble  should  be  within 
the  ability  of  every  physician.  A  later  diagnosis  is  neither  especially 
brilliant  or  useful.  By  that  time  the  patient  is  apt  to  be  so  far  ad- 
vanced that  no  possible  treatment  will  be  of  any  benefit  and  so  obstrep- 
erous that  the  family  will  already  have  thought  of  putting  him  in  con- 
finement. Be  very  suspicious,  therefore,  when  a  strong,  industrious, 
devoted  man  suddenly  begins  to  neglect  his  engagements,  his  family 
and  his  usual  duties ;  when  he  loses  his  power  of  concentration  and 
attention;  when  his  apperceptions  become  clouded  and  his  judgments 
confused;  when  trifling  causes  excite  him  abnormally ;  when  he  dallies 
and  delays  and  seems  to  want  initiative  force;  when  he  is  easily 
wearied  mentally  and  physically ;  when  he  lets  loose  in  his  sexual  life, 
is  immoral,  obscene  and  indififerent  to  all  law  and  order ;  when  he  is 
unwarrantably  egotistic,  self-satisfied  and  selfish,  or,  on  the  other  hand, 
is  melancholy  and  hypochondriacal. 

If  a  history  of  svphilis  can  be  obtained  in  addition  to  these  mani- 


898 


THE   NON-NEURONIC  DISEASES 


festations  in  a  man  whose  temperament  is  not  of  the  neurotic  type, 
the  suspicion  is  strengthened.  Ask  to  see  some  of  his  letters  and  note 
any  changes  in  their  style,  both  as  to  writing  and  contents.  Especially 
look  out  for  irrelevancy  of  phraseology,  repetition  and  omission  of 
w^ords  and  syllables.     Note  his  surprise  when  his  attention  is  called 

FIGURE  199- 


General   Paresis   with   arthropathies.      (After  Lloyd.) 

to  these  things,  showing  that  they  were  done  absent-mindedly,  as  it 
were.  Search  keenly  for  the  somatic  signs,  such  as  the  Argyll-Robert- 
son or  other  pupillary  defect,  the  tremor,  the  speech  disturbance. 

In  the  early  stage  the  disease  most  liable  to  be  confused  with 
general  paresis  is  neurasthenia.  Very  often  these  patients  are  neu- 
rasthenic and  hysterical;   it  therefore  behooves  the  examiner  to  be  all 


THE   XOX-XEUKOXIC    DISEASES  899 

the  more  careful  to  detect  the  presence  of  the  dementia  and  other  signs- 
of  the  trouble.  The  somatic  symptoms  are  rarely  liable  to  be  mis- 
taken for  signs  of  neurasthenia,  certainly  not  the  pupillary  change"^.. 
In  nervous  exhaustion  there  ma}-  be  a  kind  of  aphasia  or  a  tremulous- 
ness,  but  there  are  none  of  the  paralytic  attacks  of  an  apoplectiform 
or  epileptiform  character. 

In  hysteria  the  latter  may  be  simulated,  but  there  are  sensory  phe- 
nomena as  well  as  absence  of  the  peculiar  tremor  that  determine  the 
latter.  In  neither  neurasthenia  nor  hysteria  is  there  that  strange  and 
almost  weird-like  absence  of  the  old  personality  in  the  midst  of  all 
the  bustling  activity  and  garrulousness.  Something  seems  to  have 
dropped  out  of  the  mental  life  of  the  man  that  represents  not  so  much 
a  loss  of  force  as  a  loss  of  control.  In  neurasthenia,  and  much  more 
so  in  hysteria,  the  personality  may  be  somewhat  changed,  but  it  is  a 
m.ore  radical  change ;  nothing  is  lost,  but  everything  is  altered.  In 
general  paresis  there  is  a  distinct  hiatus  in  the  mental  picture,  and 
that  which  has  left  the  vacancy  is  missed  because  of  the  absence  of 
its  controlling  force  over  the  entire  man,  mental  and  physical.  The 
paretic  dement  does  not,  except  in  very  rare  cases,  worry  about  his 
condition.  He  is  not  introspective  or  the  victim  of  phobias  and  fixed 
ideas,  as  a  neurasthenic  or  hysteric  is.  He  is  objectively  egotistic,  while 
the  latter  are  subjectively  egotistic.  The  paretic  dement  has  the  ego- 
tism of  a  child,  selfish,  grasping,  indift'erent  to  others,  happy  when  its 
wants  are  supplied,  enraged  when  subjected  to  restraint.  The  neu- 
rasthenic and  the  hysteric,  to  a  lesser  degree,  has  the  egotism  of  the 
intense  introspectionist.  The  former  is  then  usually  gay  and  exhilar- 
ated, the  latter  are  more  apt  to  be  sad  and  whining  and  depressed. 

This  dift'erence  between  the  general  mental  states  of  dementia 
paralytica  and  neurasthenia  or  hystero-neurasthenia,  coupled  on  either 
hand  with  the  other  special  symptoms  of  the  two  sets  of  diseases,  ought 
to  aid  very  materially  in  the  making  of  the  dift'erential  diagnosis. 

The  paroxysmal  character  of  the  headache  in  hemicrania,  its 
abrupt  onset  and  cessation,  the  aurae,  the  peculiar  eye  symptoms  and 
the  absence  of  the  t\^pical  psychosis  of  general  paresis,  will  distinguish 
the  former  from  the  latter.  And  yet  there  are  cases  of  the  latter  in 
which  there  are  only  headache  and  neurasthenic  manifestations  early  in 
the  disease,  just  as  in  some  cases  of  hemicrania.  In  even  these  cases, 
however,  the  headache  does  not  come  and  go  periodically,  localize  itself 
closely,  and  be  associated  with  vomiting  as  in  migrame. 

Tumor  has  been  mistaken  for  early  dementia  paralytica.  There 
are  headache,  neurasthenic  symptoms,  sometimes  aphasia,  epileptiform 
seizures  and  mental  changes  in  tumor,  but  there  are  also  choked  disc,, 
absence  of  tremor,  absence  of  Arg}-ll-Robertson  pupil  and  none  of  the 
characteristic  mental  exhibitions.  Mental  stupor  and  slow  pulse  are  the 
traits  of  an  intracranial  neoplasm. 

Gumniata  and  gummatous  meningitis  may  cause  symptoms  that 
closely  resemble  those  of  dementia  paralytica.  And  this  is  not  re- 
markable when  it  is  remembered  that  the  arteriosclerosis  and  meningo- 
encephahtis  set  up  by  syphilis  may  conceivably  provoke  the  degenera- 
tive changes  in  the  nervous  elements  that  are  observed  in  the  para- 


900  THE   XOX-XEUROXIC  DISEASES 

syphilitic  troubles.  In  cerebral  syphilis  there  is  a  sharper  localization 
of  the  symptoms  and  more  of  an  inflammatory  irritative  character 
about  them  than  there  is  in  general  paresis.  The  headache  is  distinct 
and  sharply  localized,  the  paretic  symptoms  are  comparatively  limited 
and  the  somatic  signs  are  more  pronounced  than  the  mental,  whereas 
in  general  paresis  it  is  the  other  way.  Argyll-Robertson  pupil,  tremor, 
speech  difficulty  such  as  are  seen  so  frequently  in  paretic  dementia 
are  not  traits  of  cerebral  syphilis,  but,  on  the  other  hand,  ocular  palsies, 
monoplegias,  sharp  epileptic  seizures  are  more  to  be  expected  in  the 
latter.  In  late  cerebral  syphilis,  particularly  of  the  vertex  type,  quite  a 
typical  form  of  general  paresis  may  supervene ;  but  by  that  time  the 
essential  nature  of  the  disease  will  have  been  well  established. 

Multiple  sclerosis  can  be  differentiated  Avithout  much  difficulty. 
The  mental  symptoms  when  present  are  of  the  stuporous  or  mildly  de- 
lirious type,  not  so  unique  and  sui  genesis  as  they  are  in  general  paresis. 
Xystagmus,  scanning  speech,  intentional  tremor,  paresis  with  sonie 
rigidity,  ocular  palsies  with  diplopia  of  a  transient  character,  will  help 
to  easily  distinguish  a  disseminated  sclerosis. 

Senile  dementia  is  a  disease  of  old  age  and  is  not  abrupt,  but  is 
clearly  a  condition  running  parallel  with  a  slow  wasting  of  the  entire 
organism.  It  has  not  the  more  prominent  somatic  signs  of  general 
paresis. 

Subacute  and  chronic  alcoholism  produce  an  exhilaration,  a 
weakening  of  the  higher  controlling  mental  faculties  and  mild  delirium 
that  in  some  respects  brings  to  mind  dementia  paralytica.  Tremor, 
speech  troubles,  restlessness,  insomnia,  loquacity,  amnesia,  belong  to 
both  diseases.  In  some  of  the  cases  of  alcoholism  that  I  have  seen  I 
have  suggested  the  diagnosis  of  incipient  alcoholic  meningo-enceph- 
litis.  Here,  however,  the  irritative  traits  of  the  psychosis  have  seemed 
to  me  to  be  more  pronounced  than  they  are  in  general  paresis.  There 
are  illusions  and  hallucinations  and  other  typical  phenomena  that  are 
rarely  met  with  in  the  latter  disease.  The  etiolog}-  of  the  trouble  is 
almost  quite  obvious  and  to  a  large  extent  helps  to  determine  the 
diagnosis,  just  as  it  does  in  the  encephalopathy  of  lead  poisoning  and 
bromine,  trional  and  other  forms  of  drug  intoxication. 

Progxosis. — This  is  absolutely  bad.  ]\Iost  cases  die  in  about 
three  years,  others  have  lived  to  eight  and  ten  years.  It  has  been  re- 
ported that  two  or  three  cures  have  occurred.  The  only  cases  tha; 
hold  out  any  possible  hope  of  recovery  are  those  that  are  recognized 
early,  give  a  clear  history  of  recent  syphihtic  infection  and  undergo 
vigorous  antisyphilitic  treatment.  Death  is  caused  hy  exhaustion, 
hypostatic  pneumonia,  bedsores,  genito-urinary  complications  or  other 
intercurrent  trouble.  As  partial  remissions  in  the  course  of  the  dis- 
ease sometimes  occur,  it  is  imperative  to  warn  the  relatives  not  to  mis- 
take these  for  a  cure. 

Treatmext.^A  paretic  dement  is  always  a  nuisance  and  dan- 
ger to  himself  and  his  family.  The  proper  place  for  him  therefore  is 
in  a  sanitarium  or  asylum.  Here  he  will  be  given  careful  nursing, 
plain,  nourishing  food  and  such  occupation  and  diversion  as  will  keep 
him  out  of  harm's  wav  and  in  the  least  excited  state  of  mind.     Tonics 


THE   NON-NEURONIC  DISEASES  gOI 

may  be  emplo3ed  on  general  principles  but  medicinally  the  only  hope- 
ful treatment  is  the  specific.  Large  doses  of  the  iodides  should  be 
given  a  trial.  If  they  show  the  slightest  tendency  to  do  harm,  they 
should  be  withdrawn  at  once.  Temporary  remissions  sometimes  fos- 
tered by  this  treatment  are  mistaken  for  cures.  Early  in  the  disease 
some  improvement  may  follow  massage,  hydrotherapy  and  gentle  ex- 
ercise. No  severe  measures  of  any  sort  should  be  attempted.  Cold 
to  the  head  may  allay  excitement.  Other  symptomatic  measures  in- 
clude the  bromides  for  the  insomnia  and  epileptic  seizures,  hypoder- 
mics of  morphine,  hyoscine,  duboisine  and  ergotin  for  the  delirious 
excitement,  the  usual  measures  for  the  apoplectiform  attacks  and  forci-_ 
ble  feeding  for  the  refusal  to  take  food. 

MULTIPLE      SCLEROSIS.        DISSEMINATED      SCLEROSIS. 
CEREBROSPINAL  MULTIPLE  SCLEROSIS. 

This  is  a  chronic,  progressive  malady  of  the  cerebrospinal  axis, 
occurring  in  the  early  part  of  adult  life  and  notable  for  the  wide 
diversity  of  its  symptoms.  While  in  the  typical  forms  of  the  disease 
there  is  a  certain  degree  of  uniformity  in  its  clinical  picture,  in  many 
of  the  atypical  forms  it  closely  simulates  a  large  number  of  other 
nervous  diseases,  from  which  it  is  sometimes  extremely  difficult  to 
differentiate  it.  On  account  of  the  disseminated  nature  and  wide 
distribution  of  the  lesion,  with  the  consequent  variability  and  wide 
diversity  in  its  clinical  manifestations,  a  concise  definition  of  multiple 
cerebrospinal  sclerosis  cannot  be  satisfactorily  formulated.  When  con- 
fronted with  a  suspected  case,  the  diagnostician  must  keep  well'  in 
mind  the  nature  of  the  lesion  and  apply  most  carefully  his  knowledge 
of  nervous  physiology  and  localization. 

Etiology. — Multiple  sclerosis  is  almost  unique  in  being  the  only 
chronic  progressive  organic  disease  that  occurs  so  early  in  life.  The 
vast  majority  of  the  cases  make  their  appearance  between  the  ages 
of  twenty  and  thirty  years.  It  rarely  occurs  before  fourteen,  and  still 
more  rarely  after  fifty.  Cases  have  been  reported  in  infancy.  In  old 
age  it  is  practically  unknown.  Young  male  adults  are  rather  more 
frequentlv  afflicted  than  females.  Neither  climate,  race  nor  season 
enter  into  its  etiology. 

Heredity  in  some  instances  has  seemed  to  have  played  a  minor 
role  in  the  "transmission  of  a  neuropathic  condition.  Eichhorst  saw 
it  in  an  eight-month's  child  whose  mother  was  a  victim  of  the  disease. 

An  inherited  degeneracy  rather  than  a  mere  neuropathic  state  may 
underly  some  of  these  cases.  There  is  now  under  my  observation^  a 
man,  thirty-two  years  of  age,  who  exhibits  and  gives  a  typical  his- 
torv  of  disseminated  sclerosis,  which  began  about  eight  years  ago. 
His  family  history  is  remarkably  suggestive.  His  grandparents  on 
the  paternal  side  were  first  cousins.  His  father,  an  uncle,  and  an 
aunt,  were  born  deaf-mutes.  His  mother  became  a  deaf-mute  in  child- 
hood after  a  severe  attack  of  scarlet  fever.  The  patient  himself  is 
the  younger  and  weaker  of  twins.  His  twin  brother  and  one  other 
brother  are  apparently  perfect  in  every  way.     There  can  be  discovered 


902  THE   NON-NEURONIC  DISEASES 

no  exciting-  cause  whatever  for  the  onset  of  the  trouble.  He  has  been 
temperate  and  has  led  an  even,  comfortable  life.  He  was  married 
over  ten  years  ago  and  has  two  healthy  daughters. 

Infection  is  the  preeminent  cause  of  multiple  sclerosis.  This  is 
so  true  and  it  so  frequently  follows  the  infectious  fevers  that  it  may 
almost  be  called  a  post-infectious  disease.  This  undoubtedly  explains 
in  part  many  of  the  other  etiological  factors  of  the  disease,  such  as 
the  age  of  the  patient,  sex,  slight  hereditary  influence,  etc.  Typhoid 
fever  and  malaria  seem  to  be  the  more  frequent  infections  that  pre- 
cede it.  Variola,  scarlet  fever,  measles,  pneumonia,  whooping-cough, 
diphtheria,  cholera,  influenza,  erysipelas  and  acute  articular  rheuma- 
tism, has  each  seemed  to  have  borne  a  causal  relationship  to  it.  It 
is  not  the  result  of  syphilis.  The  disseminated  form  of  spinal  syphilis, 
with  its  multiple  foci,  is  another  disease.  The  puerperium  has  been 
followed  by  it  and  so  has  dysentery.  Oppenheim  believes  that  intox- 
ication from  metals  is  sometimes  the  origin  of  the  trouble  and  declares 
he  has  observed  it  follow  carbonic  dioxide  poisoning.  Gerhardt  traced 
it  to  mercurial  intoxication  in  one  case. 

Trauma,  shock  and  sunstroke  are  doubtful  causes.  It  is  probable 
that  infection  underlies  these  alleged  causes.  In  some  cases  it  is 
difficult  to  assign  any  cause  for  the  disease. 

Pathology  and  Pathogenesis. — The  gross  appearance  of  the 
cerebrospinal  axis  in  a  case  of  multiple  sclerosis  is  unique  and  striking. 
Even  before  the  removal  of  the  soft  membranes,  the  glistening,-  hard, 
sclerotic  foci  may  be  seen  irregularly  scattered  through  the  white 
matter  of  the  cord  and  brain.  These  nodules  vary  from  1-25  of  an 
inch  to  an  inch  in  size ;  are  irregular  in  shape ;  and  are  harder  than 
the  surrounding  tissue,  though  not  so  hard  as  connective  tissue.  There 
is  no  uniformity  in  their  distribution.  They  are  found  most  commonly 
in  the  white  matter  of  the  centrum  semiovale,  internal  capsule,  crura 
cerebri,  pons,  medulla  and  columns  of  the  cord.  They  are  not  con- 
fined to  any  tract  or  part  of  a  tract.  They  sometimes  involve  a  quar- 
ter, a  half  or  entire  cross-section  of  the  cord.  By  extension  they  im- 
plicate the  gray  matter,  though  they  never  seem  to  originate  in  the 
gray  matter.  They  are  sharply  outlined,  though  the  neighboring  tis- 
sues may  be  more  or  less  indurated.  This  produces  a  sort  of  diffuse, 
as  well  as  disseminated,  sclerosis  in  some  places. 

Under  the  microscope  these  nodules  are  seen  to  be  fibrous  in 
structure  with  a  proliferation  of  the  neuroglia  and  the  other  changes 
common  in  medullary  degeneration.  They  are  not  connected  appa- 
rently with  the  walls  of  the  bloodvessels,  though  the  latter  may  be 
proliferated  and  their  walls  thickened,  distorted  and  otherwise  sugges- 
tive of  an  inflammatory  process.  The  degeneration  is  not  of  the  sec- 
ondary type  so  that  by  many  the  disease  is  supposed  to  be  a  primary 
form  of-  sclerogliosis.  My  own  observations  lead  me  to  believe  that 
some  cases  are  of  the  nature  of  a  congenital  defect,  in  the  same  way 
that  the  cases  of  syringomyelia  and  Friedreich's  disease  are.  The 
nature  of  the  lesion,  the  marked  influence  of  a  neuropathic  heredity, 
and  the  frequent  absence  of  all  exciting  causes  are  very  suggestive. 

Infections  produce  inflammatory  and  neuronic  degenerative  dis- 


THE   NOX-XEUROXIC  DISEASES 


903 


orders,  but  in  no  other  disease  do  they  cause  the  unique  patches  seen 
in  this  disease.  Infection  probably  acts  as  a  prominent  exciting  cause 
in  most  cases. 

Running  through  the  nodules  may  be  seen  axis  cylinders.  The 
myelin  substance  breaks  down  but  the  axis  cylinders  and'  ganglion  cells 
show  a  great  power  of  resistance  to  the  sclerotic  process.     It  is  not 

FIGURE  200. 


Disseminated  sclerosis  of  the  brain  and  the  spinal  cord.    (Partly  schematic.)     (After  Leyden.) 


probable  that  the  axis-cylinders  midergo  any  regeneration  under  these 
circumstances. 

The  nodules  and  sclerotic  process  implicate  and  surround  some- 
times the  peripheral  nerve-roots  and  cranial  nerves. 

The  origin  of  this  peculiar  form  of  sclerosis  is  hidden  in  much 
mystery.  The  pathological  findings  do  not  give  absolute  validity  to 
any  one  explanation,  though  they  are  highly  suggestive  of  several. 
There  are  three  hypotheses  held  among  the  various  pathologists.  I 
have  alreadv  mentioned  that  one  set  of  authorities  hold  that  the  dis- 


904  THE   NON-NEURON IC  DISEASES 

ease  is  a  primary  proliferation  of  the  neuroglia,  a  sclerogliosis,  and 
that  many  of  the  other  presentations  suggestive  of  inflammation  and 
softening  are  purely  secondary  to  the  irritative  presence  of  these 
sclerotic  nodules.  Other  writers  state  that  the  pathological  process  is 
primarily  a  minute  myelomalacia,  the  result  of  the  presence  of  minute 
infected  emboli.  These  infected  emboli  obstruct  the  circulation  in 
the  minute  terminal  bloodvessels  of  the  brain  and  cord.  The  tissue 
in  spots  softens,  breaks  down  and  is  absorbed.  .The  vacant  area  is 
then  occupied  secondarily  by  the  overgrown  neuroglia.  Still  others 
maintain  that  the  sclerosis  arises  from  an  inflammatory  process  com- 
mencing in  the  arteries.  This  as  well  as  the  preceding  explanation 
is  in  consonance  with  the  infectious  nature  and  origin  of  the  disease 
though  many  of  the  later  findings  do  not  lend  either  of  them  very 
strong  support. 

Symptoms. — Two  significant  facts  stand  out  in  the  symptomatol- 
ogy of  multiple  sclerosis,  and  while  beautifully  indicative  of  the  char- 
acteristic nature  of  the  lesion,  are  even  of  greater  importance  when  it 
comes  to  the  question  of  diagnosis.  The  first  noteworthy  fact  is  that 
the  symptoms,  whatever  they  may  be,  are  rarely  if  ever  complete.  The 
paralysis,  the  anaesthesia,  the  trophic  and  mental  disturbances,  never 
go  on  to  complete  paralysis,  complete  ansesthesia,  etc.  It  is  exceedingly 
rare  for  an  entire  tract,  center  or  cerebrospinal  association  to  be  com- 
pletely severed  or  obliterated.  As  a  rule  some  fibres  and  cells  re- 
main intact,  and  as  a  result  the  symptomatology  exhibits  such  general 
characteristics  as  paresis,  parsesthesiae,  incoordination,  tremor,  jerking 
movements.  This  will  be  brought  out  in  the  further  discussion  of  the 
symptoms. 

The  other  notable  traits  about  the  general  symptomatology  of 
the  disease  are  the  zvide  diversity  and  great  variety  of  the  individual 
symptoms,  showing  more  or  less  implication  of  all  parts  and  all  func- 
tions of  the  cerebrospinal  apparatus.  This  would  naturally  be  looked 
for  from  such  a  lesion  as  multiple  sclerosis  usually  reveals. 

And  yet  in  spite  of  all  this  variability  and  diversity,  the  symp- 
tomatology of  typical  multiple  sclerosis  is  singularly  definite  and  uni- 
form. It  is  this  clinical  picture  that  I  will  now  attempt  to  describe 
and  when  I  have  done  this,  I  will  point  cut  the  possible  variations  in 
the  picture. 

As  a  rule  the  onset  of  the  disease  is  z'cry  insidious.  The  patient 
first  notices  a  little  difficulty  in  his  ivalking.  It  seems  to  be  stiff, 
irregular  and  a  trifle  jerky.  The  lower  limbs  feel  zveak  and  numb. 
As  he  has  probably  come  through  a  severe  infectious  fever,  and  has 
been  convalescing  for  several  weeks,  he  attributes  this  weakness  and 
numbness  to  his  lowered  health  and  vitality ;  and  therefore,  he  does 
not  pay  much  attention  to  it  at  first.  He  notices,  however,  that  it 
does  not  improve  but  seems  to  get  worse.  Moreover  he  begins  to  have 
vertiginous  attacks,  reels  slightly  and  has  to  take  great  care  lest  he 
fall  when  he  turns  suddenly.  He  is  becoming  cognizant  of  a  slight 
tremor  in  his  limbs,  especially  when  he  moves  them  voluntarily.  His 
bladder  appears  to  be  weak  and  he  has  some  trouble  retaining  his 
urine.     All  of  these  manifestations,  not  unlike  the  earlv  manifestations 


THE   NON-NEURONIC  DISEASES 


905 


of  myelitis,  gradually  increase,  or  at  least  continue  unabated,   until^ 
becoming  alarmed,  he  seeks'  the  advice  of  a  physician. 

A  careful  examination  now  reveals  a  partial  paraplegia,  spastic  m. 
type,  with  muscular  rigidity  and  exaggeration  of  the  reflexes.  The 
gait  is  unsteady  and  much  like  that  of  alcoholic  intoxication.  It  is 
spastic  and  paretic,  incoordinate,  ataxic,  and  trembling.  It  may  reveal 
the  characteristics  of  cerebellar  ataxia.  The  tremor  and  incoordina- 
tion may  be  observed  in  all  of  the  movements  of  the  body,  especially 
of  the  limbs,  of  the  eyes  and  the  muscles  of  speech  and  parts  under 
the  more  immediate  control  of  the  will.  The  tremor  is  absent  during 
rest  and  appears  only  upon  voluntary  movement.  It  has  therefore 
been  denominated  an  intentional  tremor.  At  times  it  accompanies  re- 
flex and  automatic  movements.  It  is  irregular,  wobbling  and  occurs 
in  oscillations  of  five  or  six  to  the  second.  Sometimes  the  tremor  is 
coarse  and  choreic  in  appearance.  On  this  account  the  patient  cannot 
carry  a  glass  of  water  to  his  mouth  without  spilling  it,  or  write,  or 
touch  promptly  the  end  of  his  nose.  It  is  impossible  for  him  to  walk  a 
chalk-line  on  the  floor,  climb  a  ladder,  or  kick  squarely  the  leg  of  the 
table.  This  ataxia  is  also  static  in  character  and  the  Romberg  symp- 
tom is  more  or  less  present. 

The  muscular  stiffness,  weakness,  ataxia  and  intentional  tremor  all 
render  the  patient  exceedingly  awkward  in  all  of  his  movements.  The 
head  jerks  and  oscillates,  the  tongue  is  protruded  in  a  jerking  manner, 
the  eyeballs  jerk  {nystagmus)  and  the  speech  is  thick,  slow  and  jerk- 
ing {scanning  or  syllabic). 

With  all  this  muscular  disorder  and  weakness,  there  is  no  atrophy 
or  changes  of  electrical  reaction.  The  reflexes  are  increased  and  usually 
an  ankle  clonus  can  be  easily  elicited. 

The  sensory  symptoms  are  not  of  very  great  significance,  except 
those  of  vision.  There  may  be  numbness  in  the  beginning  and  this 
may  go  on  to  a  considerable  degree  of  hypaesthesia.  Complete  anaes- 
thesia does  not  occur,  although  a  hemiansesthesia  has  been  reported. 
In  such  cases  there  is  always  some  sensation.  The  ataxia  in  this  dis- 
ease is  not  the  result  of  the  sensory  disturbances  so  much  as  of  the 
motor  trouble.  Even  less  frequent  than  the  tactile  disturbances  are  the 
disturbances  of  the  muscular,  temperature  and  pressure  senses.  Neu- 
ralgic pains  are  not  uncommon  and  the  Brown-Sequard  symptom-com- 
plex has  been  observed. 

A  rather  striking  and  confusing  characteristic  of  these  sensory 
symptoms  is  their  instability  and  variability.  They  are  temporary  and 
come  and  go  most  unexpectedly.  In  this  respect  they  bear  a  resem- 
blance to  the  symptoms  of  hysteria  and  cerebrospinal  syphilis.  The 
reason  for  this  is  obvious. 

The  visual  symptoms  of  multiple  sclerosis  are  important  and  should 
be  sought  for  in  every  suspected  case.  Diplopia  occurs  as  the  result  of 
the  involvement  of  the  ocular  muscles.  In  a  very  large  number  of 
the  cases  there  is  irregular  and  partial  atrophy  of  the  optic  nerve.  A 
complete  atrophv  of  the  nerve  is  so  rare  as  to  be  unworthy  of  fur- 
ther consideration.  An  ophthalmoscopic  examination  of  the  fundi 
shows  in  most  of  the  cases  an  atrophic  pallor  of  the  outer  or  temporal 


906  THE   NON-NEURONIC  DISEASES 

halves.  Spots  occur  here  and  there  and  the  two  fundi  never  present 
the  same  appearance.  These  fundus  changes  appear  in  about  twenty 
per  cent,  of  all  cases.  As  a  result  of  these  changes  in  the  fundi,  the 
optic  nerve,  and  the  central  neurones  that  take  part  in  the  visual  act, 
many  symptomatic  phenomena  occur.  The  vision  becomes  blurred 
and  misty  and  may  be  the  first  indication  to  the  patient  of  his  trouble. 
This  diminution  of  vision  scarcely  ever  advances  to  complete  blind- 
ness. The  Held  is  irregularly  contracted  and  central  scotomata,  first 
for  colors  and  then  for  white,  become  prominent.  Scintillating  sco- 
tomata are  sometimes  present,  and  sometimes  there  is  simply  achroma- 
topsia. Neuritic  changes  may  precede  the  atrophy  and  the  visual  dis- 
turbance is  usually  the  outgrowth  of  a  partial  retro-bulbar  neuritis  of 
one  or  both  eyes.  Thus  the  vision  is  sometimes  markedly  impaired 
without  any  noticeable  alterations  in  the  fundi. 

The  pupils  may  be  unequal  and  contracted.  Ophthalmoplegia  has 
been  seen  a  number  of  times,  though  it  is  rare. 

A  very  important  symptom  when  it  does  occur  is  an  apoplecti- 
form attack.  There  is  unconsciousness  and  hemiplegia,  both  very  tem- 
porary and  disappearing  in  a  few  hours  or  days.  Sometimes  the  at- 
tack resembles  an  epileptic  one,  at  other  times  it  is  like  a  severe  stroke 
of  apoplexy  with  prolonged  after  results.  In  such  cases  there  is 
marked  headache  and  vertigo.    Sometimes  the  temperature  is  increased. 

The  mental  faculties  are  not  usually  affected.  There  may  be  dull- 
ness, however,  hebetude,  general  apathy,  with  melancholia  and  weak- 
ening of  the  memory.  The  impulsive  laughter  is  not  a  mental  symp- 
tom. It  is  entirely  involuntary  and  does  not  represent  in  any  way  a 
mental  mood.  Sometimes  it  is  paroxysmal  and  exaggerated,  and  be- 
ing frequently  repeated  greatly  annoys  the  patient.  It  is  exceedingly 
rare  for  illusions,  hallucinations  or  delirium  ever  to  be  present. 

Diagnosis. — The  above  description  represents  a  more  or  less 
typical  case  of  multiple  sclerosis.  Such  cases,  however,  are  not  the 
ones  usually  met  with.  The  atypical  cases,  the  aberrant  cases,  the  so- 
called  aborted  types,  the  "formes  frustes''  are  the  ones  that  too  often 
cause  the  confusion  in  diagnosis.  Moreover,  difficult  is  it  in  practic- 
ally all  cases  to  make  a  diagnosis  early  in  the  disease,  when  an  accurate 
diagnosis  is  especially  desirable. 

Practically  every  case  exhibits  some  approach  to  the  general  clin- 
ical picture  which  I  have  attempted  to  ovitline.  Here  and  there  a 
particular  symptom  may  be  absent,  or  the  grouping  of  the  symptoms 
may  be  quite  unusual.  This  is  all  to  be  expected  when  one  remembers 
the  character  and  distribution  of  the  lesion.  If  the  symptoms  are  in- 
tracranial as  well  as  spinal,  rather  insidious  in  onset,  and  slow  in 
progress,  to  a  certain  extent  variable  and  falling  short  of  completeness, 
and  above  all  suggestive  of  an  interrupting  lot  of  scattered  foci  within 
the  nervous  paths,  the  diagnosis  of  a  disseminated  sclerosis  is  almost 
certainly  indicated. 

In  the  early  period  of  the  disease  one  should  be  keenly  observant 
of  the  motor  zveakness.  As  this  may  be  the  only  symptom  for  many 
weeks  or  months,  it  should  be  closely  studied.  Its  character  is  that  of 
a  spastic  spinal  paralysis.     A  slight  nystagmus,  a  diplopia,  a  failure  of 


THE   XOX-XEUROXIC  DISEASES  9O7 

-eyesight  may  accompany  it.  Sooner  or  later  the  nystagmus  the 
■optic  atrophy,  the  dysarthria,  the  intentional  tremor,  the  vertigo  and  even 
the  temporary  apoplectic  attacks  will  announce  themselves.  Oppen- 
Jieim  saw  a  unilateral  optic  atrophy  as  the  only  symptom  in  a  case  for 
twenty  years.  I  have  seen  a  tremor  with  merely  a  little  vertigo  cause 
a  great  variety  of  diagnoses  to  be  made  during  a  period  of  a  year  or 
more.  In  one  case  that  I  had  under  observation  for  nearly  two  years 
there  were  hysterical  manifestations  with  merely  a  slight'  ataxia  and 
misty  vision.  The  case  had  been  variously  diagnosed  as  hysteria,  loco- 
motor ataxia,  neurasthenia  and  epilepsy  from  a  possible  incipient  intra- 
cranial tumor.  It  gradually  assumed  the  classical  picture  of  a  cerebro- 
spinal disseminated  sclerosis. 

Too  much  caution  therefore  cannot  be  exercised  in  the  earlv 
diagnosis,  and  it  may  be  put  down  as  an  axiom  that  at  this  stage  a 
positive  diagnosis  is  practically  impossible.  It  cannot  be  more  than  a 
-Strong  suspicion. 

The  atypical  forms  of  the  disease  ma}'  show  every  sort  of  com- 
bination in  their  symptomatic  presentation.  The  form  that  resembles 
a  progressive  spastic  spinal  paralysis  is  perhaps  the  commonest.  The 
head  symptoms,  such  as  the  optic  atrophy,  the  diplopia,  the  nystagmus 
and  the  dysarthria,  as  well  as  the  sensory  manifestations,  must  be 
earnestly  sought  for  and  will  usually  be  found,  but  more  or  less  ob- 
scured by  the  more  prominent  spinal  symptoms.  There  is  a  hemi- 
paretic  form  that  has  been  referred  to  by  Oppenheim.  Charcot,  Ed- 
wards, Bickeles  and  others.  A  glycosuria,  tachycardia  and  asphyxia 
may  indicate  a  bulbar  form.  An  acute  ataxia  of  the  upper  extremities 
with  bulbar  symptoms  giving  rise  to  an  alternate  hemiplegia  has  been 
observed. 

Among  the  more  common  diseases  with  which  insular  sclerosis 
may  be  confused  are  transverse  myelitis,  spastic  spinal  paralysis,  loco- 
motor ataxia.  Friedreich's  disease,  bulbar  paralysis,  amyotrophic  lateral 
sclerosis,  post-infectious  disseminated  myeloencephalitis,  chronic  men- 
ingitis, dementia  paralytica,  apoplexy,  epilepsy,  paralysis  agitans  and 
especially  hysteria.  So  large  a  number  of  diseases  is  disseminated 
sclerosis  liable  to  be  mistaken  for.  that  sometimes  its  diagnosis  is  best 
made  bv  exclusion.  A  careful  consideration  of  the  clinical  picture 
presented  by  these  various  simulated  affections,  therefore,  should 
always  be  borne  in  mind.  The  reader  is  referred  to  their  discussion 
in  other  parts  of  the  book.  A  word  must  be  said,  however,  here  in  re- 
gard to  the  differentiation  of  this  disease  from  spastic  spinal  paralysis, 
locomotor  ataxia,  dementia  paralytica  and  hysteria. 

In  spastic  spinal  paralysis  the  head  symptoms,  such  as  the  head- 
ache, the  optic  atrophy,  the  nystagmus,  the  scanning  speech,  are  ab- 
sent. There  is  no  intentional  tremor  and  no  ataxia.  The  gait  is  stitt 
and  paretic,  but  it  is  not  irregular  and  jerky.  There  are  particularly 
no  sensory  or  mental  alterations.  The  muscular  atrophy  is  a  little  more 
marked  than  in  multiple  sclerosis,  though  not  so  marked  as  in  anterior 
poliomyelitis,  or  amyotrophic  lateral  sclerosis,  or  progressive  muscular 
atrophy.  The  spasticity,  together  with  the  exaggeration  of  the  knee- 
jerks,  is  perhaps  a  little  more  pronounced  in  spastic  spinal  paralysis. 


908  THE   >;OX-NEUROXIC  DISEASES 

In  multiple  sclerosis  the  rectal,  and  especially  the  vesical,  functions 
are  apt  to  be  somewhat  disturbed. 

Locoinofor  ataxia  has  been  diagnosed  from  the  ataxia  which, 
sometimes  obtains  in  insular  sclerosis.  The  former  is  a  sensory  dis- 
turbance, however ;  the  latter  a  motor.  In  locomotor  ataxia  Rom- 
berg's static  ataxia  is  promptly  manifested  when  the  patient  is  asked 
to  close  his  eyes  while  standing.  The  mere  closure  of  the  eyes  does 
not  so  seriously  discommode  the  victim  of  disseminated  sclerosis.  The 
absent  knee-jerks,  the  fulgurating  pains,  the  anaesthesia,  the  Argyll- 
Robertson  pupil,  the  early  loss  of  sexual  power  and  other  sensory,, 
degenerative  symptoms  will  help  to  distinguish  tabes. 

Dementia  paralytica  is  a  diffuse  meningoencephalitis  and  has 
some  symptoms  not  unlike  those  of  multiple  sclerosis  in  which  the 
cerebral  symptoms  predominate.  There  is  a  form  of  post-infectious 
disseminated  myeloencephalitis  that  cannot  be  distinguished  from  mul- 
tiple sclerosis,  and  sometimes  changes  into  the  latter.  Dementia 
paralytica  can  usually  be  distinguished  by  the  more  distinctively  mental 
character  of  some  of  its  symptoms  than  the  mental  manifestations  of 
multiple  sclerosis,  though  it  must  be  admitted  that  the  differentiation 
at  times  is  extremely  difficult,  if  not  impossible.  In  dementia  paralytica 
the  growing  irritability,  the  weakening  memory,  the  failure  of  con- 
tinued attention,  the  restlessness  and  excitability,  the  moral  and  sex- 
ual indifference,  the  exaltation  of  ideas  and  folie  de  grandeur,  must 
be  carefully  taken  into  account.  The  incoordination  and  tremor,  as 
shown  in  the  penmanship  and  speech  of  the  paretic  dement,  are  char- 
acteristic. The  finer  and  more  complex  voluntary  movements  of  the 
hands  are  very  noticeable,  as  well  as  the  fibrillary  tremor  of  the  tongue. 
In  multiple  sclerosis  the  tremor  and  incoordination  are  much  coarser. 
The  unequal  pupils,  the  Argyll-Robertson  pupil  and  the  absence  of  nys- 
tagmus characterize  general  paresis. 

Between  no  two  diseases  is  a  mistake  more  liable  to  be  made  in 
some  cases  than  between  multiple  sclerosis  and  hysteria.  Every  symp- 
tom characteristic  of  the  former  may  be  simulated  by  the  latter.  IMore- 
over  the  two  diseases  not  infrequently  coexist  in  the  same  patient. 
When  after  a  most  careful  examination  there  is  still  doubt,  it  is  judi- 
cious for  the  practitioner  to  throw  the  weight  of  his  suspicion  on  the 
side  of  the  organic  disease.  In  hysteria  the  temperament  of  the  pa- 
tient, the  psychic  factors  in  the  etiology,  the  psychic  complexion  of  the 
entire  clinical  picture  and  the  exceeding  variability  and  instability  of 
the  symptoms  speak  plainly.  The  sensory  manifestations  are  more  pro- 
nounced in  hysteria  than  they  are  in  disseminated  sclerosis.  In  the 
latter  the  intentional  tremor,  the  optic  atrophy,  the  characteristic  dys- 
arthria, the  nystagmus  and  the  incoordination  are  to  be  closelv  noted.. 
If  these  symptoms  occur  in  a  hysteric,  excepting,  of  course,  the  optic 
atrophy,  they  can  be  made  to  show  slight  degrees  of  alteration  by 
some  sudden  influence  upon  the  patient's  mind.  It  must  be  admitted 
that  at  times  it  is  next  to  impossible  to  say  whether  a  case  is  hysterical, 
a  case  of  multiple  sclerosis  or  a  combination  of  the  two  diseases.  I 
have  seen  a  case  of  multiple  sclerosis  regarded  for  several  vears  by 
dift'erent  diagnosticians  as  locomotor  ataxia,  hvsterical  ataxia  and  in- 


THE   XOX-XEUROXIC  DISEASES 


9aj 


sanity.  Lately  I  saw  a  case  diagnosed  as  hypertrophic  pachymenin- 
gitis. 

Progxosis.- — The  prognosis  of  disseminated  sclerosis  in  regard  to 
Jife  is  favorable.  Only  when  the  disease  attacks  the  vital  centers  in 
the  medulla  does  it  cause  death  directly.  The  fatal  issue  is  usually 
brought  about  by  some  complication  or  intercurrent  disease.  In  re- 
gard to  ultimate  cure,  the  prognosis  is  not  good.  A  very  few  cures 
have  been  reported.  Usually  the  disease  runs  a  long  course  of  years, 
progressively  getting  worse,  but  with  occasional  intermissions  of  quies- 
cence, or  even  partial  remissions.  Other  degenerative  and  inflamma- 
tory troubles  may  be  lighted  up  in  the  course  of  a  multiple  sclerosis, 
and  the  prognosis  then  becomes  the  prognosis  of  this  particular  disease. 

Treatmext. — The  treatment  is  not  very  satisfactory.  Quiet,  reg- 
ularity of  habits,  hygienic  environment  and  all  the  other  recommenda- 
tions for  slow,  progressive,  chronic  troubles  are  here  in  order.  Above 
-all  avoid  severe,  radical  measures.  Why  electricity  is  recommended 
I  cannot  understand.  In  my  own  opinion  it  had  better  not  be  em- 
ployed. Hot  and  cold  baths,  stimulants  and  over-exertion  must  all 
Ije  prohibited.  Special  forms  of  the  disease  call  for  special  lines  of 
treatment.  Syphilitic  cases  should  be  combated  with  mercurv  and  the 
iodides.  Apoplectic  cases,  myelitic  and  encephalitic  complications  de- 
mand a  certain  amount  of  antiphlogistic  treatmtent.  Local  bleeding  with 
leeches  may  be  of  some  avail  in  such  cases.  In  all  cases  the  stead v  use 
of  the  iodide  of  potassium  is  about  the  best  medicinal  line  of  treatment 
to  be  employed.  iVrsenic,  nitrate  of  silver,  quinine  and  mild  hydro- 
therapy, chiefly  for  their  tonic  effects,  are  useful  at  times.  In  spite 
of  all  treatment  most  of  the  cases  steadily  progress,  often  in  an  irreg- 
ular manner  for  many  years. 

TU^IORS  OF  THE  BRAIN. 

Every  variety  of  tumor  attacks  the  brain,  solid,  granular  and  cys- 
tic. In  fact,  the  intracranial  structures  seem  to  be  a  favorite  seat  for 
new  growths,  whether  they  appear  elsewhere  in  the  bod}'  or  not.  As 
compared  wdth  other  organic  diseases  of  the  brain  they  are  not  so  com- 
mon. They  seem  from  the  reports  to  be  more  frequent  than  tumors 
of  the  spinal  cord.  They  partake  of  the  same  characteristics  in  a  gen- 
-eral  way  as  the}'  do  when  in  other  parts  of  the  body.  The  only  thing 
that  makes  them  of  special  interest  in  cerebral  pathology  is  the  effect 
of  their  presence  upon  the  functions  and  histological  structures  of  the 
iDrain  itself.  Only  in  some  few  particulars  does  their  intracranial  seat 
cause  them  to  exhibit  special  differences.  For  instance,  fatty  tumors 
are  comparatively  less  frequent  in  the  brain  than  they  are  elsew^here : 
gliomatous  tumors  are  never  found  outside  of  the  skull  except  in  the 
retina  and  spinal  cord.  It  is  more  common  for  massive  tubercular 
growths  to  appear  in  the  brain  than  elsewhere.  Aneurism  constitutes 
a  variety  of  tumor  but  it  will  be  discussed  in  a  section  by  itself  as  it 
is  more  of  a  disease  of  the  circulatory  apparatus  than  a  new  growth. 

Etiology. — There  is  nothing  specially  distinctive  about  the  etiol- 
ogy of  brain  tumors  more  than  what  is  true  of  them  when  located 


ylO  THE   XON-XEUROXIC  DISEASES 

elsewhere  in  the  body.  Their  essential  causes  are  but  little  known.. 
The  granulomata,  tubercle  and  syphiloma  are,  of  course,  infectious  in 
origin ;  some  of  the  gliomata  and  fatty  tumors  owe  their  existence  to 
developmental  anomalies  and  other  congenital  influences;  echinococci 
and  cysticcrci  are  parasitic;  acti}ioi)iycosis  is  an  infectious  form  of 
tumor. 

Heredity  is  supposed  to  exercise  a  slight  influence  in  predisposing 
to  the  tumor  itself  and  its  particular  variety.  ]\Iales  suffer  about  twice 
as  often  as  females.  This  ma}-  be  due  to  the  greater  incidence  of  cer- 
tain exciting  influences  in  the  former  than  in  the  latter  in  some  cases 
but  certainly  not  in  all.  The  difference  between  the  sexes  in  this 
respect  varies  with  the  nature  of  the  tumor.  It  is  with  sarcomata 
that  the  sexes  approach  more  nearly  to  an  equality. 

All  ages,  from  six  months  to  advanced  }ears,  are  subject  to  brain 
tumor.  Certain  tumors  exhibit  a  choice  of  age  in  their  appearance. 
In  the  first  twenty  years  of  life,  one-third  of  all  cases  occur.  The 
relative  number  diminishes  then  until  it  becomes  quite  small  after  fifty. 
The  reason  of  this  is  obvious  since  the  infectious  and  other  conditions 
out  of  \s-hich  the  tumor  is  evolved  are  more  common  in  these  years. 
Tuberculous  tumors  are  found  most  frequently  in  childhood  and  early 
adult  life,  though  they  may  be  seen  up  to  old  age.  Parasitic  tumors 
are  incidents  of  early  adult  years.  So  also  are  gummata  and  gliomata. 
In  early  and  middle  life  the  sarcomata  join  the  gummata  and  gliomata 
in  the  frequency  of  their  occurrence.  Carcinomata  have  been  diagnosed 
at  all  ages  but  most  of  them  have  been  seen  between  the  ages  of  forty 
and  sixty.  The  late  tumors  are  the  sarcomata,  gummata  and  carcino- 
n-ata.  The  rarity  of  all  the  other  varieties  of  tumors  renders  their  gen- 
eral etiological  characteristics  of  slight  importance. 

Traumata  of  the  head,  such  as  blows  and  falls,  are  undoubtedly 
in  some  instances  the  excitants  of  a  morbid  growth.  So  also  may  be 
old  cicatrices.  In  some  instances  the  tumor  may  have  been  latent  but 
the  trauma  initiated  the  secondary  disturbances  upon  which  notice- 
able symptoms  arose.  Hence  traumata  must  not  be  given  too  much 
credit  for  the  production  of  intracranial  neoplasms. 

Pathology. — It  is  difficult  to  make  a  perfectly  satisfactory  classi- 
fication of  all  the  tumors  that  attack  the  brain,  for  our  knowledge  in 
regard  to  them  is  not  entirely  adequate  and  they  vary  in  so  many  par- 
txulars.  Neither  their  frequency,  their  location,  their  causation  nor 
their  intimate  structure  wall  form  at  present  a  basis  for  accurate  clas- 
sification. They  may  be  enumerated,  however,  thus:  tuherele,  syph- 
iloma, glioma,  sarcoma,  myxoma,  carcinoma,  -fibroma,  osteoma,  choles- 
ieotoma,  lipoma,  psarnmoma,  neuroma,  echinococciis  and  cysticercu^. 
To  these  may  be  added  erectile  tumors  or  vascular  enlargements,  actin- 
omvcosis,  abscesses  and  cysts  due  to  hemorrhage  and  encephalomalacia, 
and  dermoid  cysts,  w-hich  will  not  be  discussed  here. 

Some  of  these  grow^ths  may  be  single  or  multiple,  simple  or  com- 
plex. They  may  vary  in  consistency  and  intimate  appearance  in  the 
course  of  their  development.  A  broken  down  glioma  looks  not  the 
same  as  an  original  one.  A  sarcoma  may  be  limited  or  diffused  over 
a  considerable  area.    A  tubercle  may  be  single  or  multiple.    An  osteoma 


THE   NON-NEURONIC  DISEASES  .     911 

and  a  fibroma  may  seem  to  be  amalgamated  into  an  osteofibroma.  In 
the  same  way  osteosarcomata,  gliosarcomata,  angiosarcomata  and 
fibrosarcomata  may  be  recorded. 

A  tuberculous  tumor  is  usually  a  single,  rounded  mass,  varying 
in  size  from  that  of  a  nut  to  that  of  a  hen's  egg  or  closed  fist.  These 
tumors  are  not  miliary  as  they  are  seen  to  be  in  tubercular  meningitis 
though  rarely  the  whole  brain  has  been  infiltrated  with  minute  miliary 
concretions.  They  are  the  most  frequent  of  all  the  brain  tumors  and 
are  slightly  more  often  located  in  the  cerebellum  than  in  the  cerebrum. 
There  may  be  more  than  one  tumor.  They  are  readily  detached,  as  they 
do  not  infiltrate  though  they  damage  somewhat  the  encircling  brain 
tissue.  The  tumor  itself  is  not  vascular,  hence  when  it  breaks  down 
it  exhibits  an  opaque,  cheesy  aspect,  som.etimes  softened  here  and 
there,  but  not  very  extensively.  Calcification  and  pus  formation  are 
among  its  possible  late  alterations.  It  may  surround  itself  with  a 
fibroid  capsule.  Apparently  the  growth  starts  in  the  lymphatic  sheath 
of  the  blood  vessels.  \  ascular  obstruction,  thrombosis,  meningitis, 
cerebral  softening  and  inflammation  are  among  its  complications.  The 
tubercle  bacillus  carried  to  the  brain  by  way  of  the  blood  stream  is,  of 
course,  the  immediate  cause  of  the  morbid  development;  hence  tuber- 
culosis of  the  lungs,  articulations  and  other  parts  of  the  body  is  apt 
to  be  present  though  not  necessarily  so.  All  the  usual  characteristics 
of  a  tubercle,  such  as  the  appearance  of  the  cells  and  the  presence  of 
the  bacilli,  belong  to  these  tumors  as  they  do  to  the  same  tumors  else- 
where. 

Sometimes  a  syphiloma  so  closely  resembles  a  tuberculous  tumor 
that  only  the  presence  of  the  specific  bacillus  in  the  latter  enables  one 
to  distinguish  them  apart.  It  varies  in  size  from  a  pea  to  a  walnut 
and  is  irregular  and  nodular  in  shape.  Like  tubercle  it  is  non-vascular 
and  tends  strongly  to  caseation.  It  does  not  become  purulent  like 
tubercle.  On  section  it  exhibits  scattered,  cheesy  spots  separated  by 
firm,  reddish-gray  fibrous  tissue.  The  periphery  is  irregular,  thick 
and  grayish  with  sometimes  numerous  vessels  and  evidences  of  arte- 
ritis. The  surrounding  brain  substance  is  not  infiltrated  though  it  is 
atrophied  and  otherwise  damaged.  Old  gummata  may  be  soft  and 
broken  down  though  less  markedly  so  than  tubercle,  or  they  may  ap- 
pear shrunken,  fibroid  and  encased  in  a.  capsule.  All  of  the  late 
changes  are  different  from  those  of  tubercle  and  help  to  differentiate 
the  two.  In  these  there  is  a  recognizable  connection  with  the  meninges 
and  a  tendency  to  extend  along  the  surface  of  the  brain  in  a  grayish, 
gelatinous  sort  of  membrane.  With  these  is  often  associated  a  gum- 
matous meningitis ;  with  tubercle  there  may  be  a  scattered  miliary 
tuberculous  condition  in  the  vicinity.  Gummata  are  most  frequently 
met  with  in  the  cerebrum  and  pons  A^arolii,  rarely  in  the  cerebellum 
and  basal  ganglia.  They  are  superficial  and  are  attached  to  the  pia 
mater.  Even  deep  gummata  have  their  origin  from  the  pia  usually. 
Like  tubercles  they  may  sometimes  start  in  the  dura  mater  and  thence 
invade  or  only  compress  the  brain.  The  growth  may  start  from  the 
vascular  walls  elsewhere  than  in  the  meninges,  though  this  is  not  often. 

The  sarcomata  are  among  the  most  interesting  and  frequent  of  the 


912  THE   NON-NEURONIC  DISEASES 

brain  tumors.  They  form  a  large  group  and  on  account  of  their  posi- 
tion, combinations  and  integral  changes  they  assume  various  modifi- 
cations. They  range  in  size  from  a  nut  to  a  fist.  They  are  of  connec- 
tive-tissue origin  and  therefore  start  from  various  tissues. 
They  seem  particularly  to  grow  from  the  periphery  into 
the  cranial  cavity.  The  bones  at  the  base  of  the  skull,  for  instance, 
the  sphenoid,  the  temporal  and  the  occipital  often  form  their  nidus. 
The  dura,  the  periosteum,  the  other  membranes  or  the  brain  substance 
itself  may  be  their  starting  point.  They  are  primary  or  secondary  and 
their  internal  changes  and  amalgamations  give  rise  to  myxosarcomata, 
^liosarcomata,  fibrosarcomata,  osteosarcomata,  etc.  Thev  are  of  ail 
shapes  and  may  be  single  or  multiple.  Rapidly  developing,  as  a  rule, 
they  are  grayish  or  white  in  appearance  or  yellowish  according  to  the 
admixture  of  cells  and  bloodvessels.  They  are  harder  than  gliomata 
as  a  rule  and  only  occasionally  reveal  patches  of  caseation  and  disinte- 
gration. They  are  rich  in  cellular  elements,  especially  round  and 
spindle  cells.  Sometimes  they  possess  an  alveolar  structure  and  they 
may  even  break  down  into  cysts.  Pigmentary,  calcareous  and  other 
changes  may  develop  within  them.  They  grow  into  the  cerebral  sub- 
stance but  are  as  a  rule  quite  sharply  defined  from  it.  They  may  even 
be  encapsulated.  As  endothelioma  they  contain  endothelial  cells  from 
the  lymphatics.  Sometimes  they  infiltrate  without  displacnig  the  brain 
substance.  Round  about  them  the  tissues  are  destroyed  somewhat  and 
they  are  often  accompanied  by  meningitis.  A  curious  condition  is  a 
diffuse,  spread  out  sarcomatous  manifestation  in  the  meninges  along 
with  the  tumor. 

Gliomata  are  not  as  frequent  as  seems  to  be  commonly  supposed. 
They  are  strictly  neural  tumors  and  are  often  due  to  congenital 
anomalies.  They  never  involve  the  meninges  and  bones  and  usually 
appear  in  the  cerebrum  or  cerebellum,  rarely  anywhere  else.  They  de- 
velop out  of  the  neuroglia  tissue  and  so  infiltrate  the  brain  substance 
that  they  can  never  be  shelled  out  as  tubercle  can.  They  range  in  size 
from  a  hazel  nut  to  a  hen's  egg.  The  largest  tumors  of  the  brain  are 
the  gliomata.  In  the  middle  they  are  reddish-gray  or  yellowish-white, 
according  to  their  age.  Sometimes  they  look  very  much  like  the  brain 
tissue  itself  and  have  the  same  consistency.  They  undergo  various 
changes  so  as  to  be  mucoid  or  fibrous  in  character.  Especially  prone 
are  they  to  disintegrate  and  being  vascular,  to  exhibit  signs  of  old  hem- 
orrhages. Cysts  and  cavities  are  liable  to  form  in  their  center.  The 
rapidity  of  their  growth  varies  and  they  rarely,  if  ever,  become  en- 
capsulated. 

On  microscopic  examination  the  typical  glia  cells,  small,  spider- 
like cells  with  delicate,  fibrous  prolongations  are  seen,  mingled  with 
an  abundant  supply  of  bloodvessels.  The  formation  of  the  tumor  sug- 
gests strongly  an  inflammatory  process  with  reactive  neurogliosis. 
The  tumors  are  much  more  easily  detected  by  their  appearance  when 
situated  in  the  white  matter  than  when  in  the  gray  matter  of  the  brain. 

Of  course  they  damage  the  tissues  which  they  infiltrate  though 
sometimes  intact  fibres  will  be  seen  coursing  through  them.  The  brain 
is  altered  in  shape  and  enlarged  where  they  are  located.    The  so-called 


THE   NON-NEURONIC  DISEASES 


913 


hypertrophy  of  the  pons,  for  example,  is  simply  a  condition  of  glioma- 
tous  infiltration.  It  has  been  confounded  with  sclerosis  of  the  brain 
and  optic  neuritis  accompaming  hemorrhage  or  softening.  The  tumor 
is  usually  single  though  multiple  glioma  is  a  very  rare  possibility. 
_  _  As  a  primary  growth  carcinoma  of  the  brain  is  very  rare.  Usually 
it  is  secondary  to  cancer  elsewhere.  It  is  a  soft,  vascular,  irregularly 
outlined  growth  that  partly  infiltrates  and  partly  displaces  the  brain 
tissue.  It  may  spring  from  the  dura  and  spread  out  or  it  may  be  a 
circumscribed  or  diffuse  neoplasm  within  the  brain  in  any  situation. 
As  compared  with  other  tumors  it  is  rather  frequent  in  the  central 
ganglia.  It  is  both  single  and  multiple,  sometimes  symmetrical  in 
both  hemispheres.  Its  contents  are  colloid,  consisting  of  large  cells 
sometimes  with  several  nuclei.  AV'ernicke  refers  to  their  tendency  to 
softening  and  destruction  of  all  the  tissues. 

Fibromata  are  small,  very  rare  tumors  of  the  brain,  occurring 
chiefly  in  the  cerebellum  and  cerebellar  peduncles.  They  have  been 
seen  multiple  and  single.  Dana  intimates  that  the  enlarged  and  hard- 
ened pacchionian  bodies  may  be  regarded  as  of  the  nature  of  fibromata. 
Calcification  in  tumors  and  actual  bony  tumors  occur  in  the  brain  and 
may  be  single  or  multiple. 

Osteomata  or  fibro-osteomata  usually  develop  in  the  dura  mater 
and  its  processes. 

Psammomata  are  small  fibrous  growths,  filled  with  calcareous  par- 
ticles, that  develop  in  the  meninges,  pineal  gland  and  choroid  plexus. 
They  are  hemispherical,  smooth,  hard  and  gray.  They  show  no  marked 
tendency  to  grow. 

In  the  hypophysis  adeiioniata  may  develop  and  be  accompanied  by 
acromegalic  symptoms. 

Cholesteatomata  or  pearly  tumors  are  found  sometimes  post  mor- 
tem at  the  base  of  the  brain  in  the  recesses  of  the  skull.  They  are 
composed  of  epidermoid  cells  in  concentric  layers.  They  give  the  ap- 
pearance of  white,  shining  nodules  and  are  said  to  contain  cholesterine 
and  stearine.  Usually  they  are  innocent  but  at  times  they  develop  as 
large  as  a  fist,  growing  into  the  cerebral  substance. 

Neuromata,  small  growths  containing  nerve  elements,  melan- 
omata.  Upomata,  angiomata,  enchondromata,  and  teratoiitata,  are  all 
so  exceedinglv  rare  as  to  be  unworthy  of  lengthened  consideration. 

Cysts  of  the  brain,  excluding  those  due  to  hemorrhage  and  soft- 
ening, are  parasitic  in  origin.  These  are  hydatid  or  cysticcrcous.  The 
former  is  usually  single  and  found  in  the  cerebral  hemispheres,  either 
in  the  ventricles  or  the  white  substance.  Rarely  it  has  been  seen  in  the 
membranes,  the  central  ganglia,  the  crus,  pons,  cerebellum  and  me- 
dulla. The  echinococcus  is  the  cause  of  the  hydatid  cyst.  Those  due 
to  the  cvsticercus  cellulosse  are  apt  to  be  multiple,  as  many  as  fift\^ 
and  a  hundred  cysts  having  been  counted.  They  are  slow  in  growth 
and  are  scattered  over  the  surface  of  the  brain  and  in  the  ventricles, 
are  encapsulated  and  provoke  no  symptoms.  It  must  not  be  forgotten 
that  cysts  are  sometimes  due  to  degenerated  neoplasms,  as  is  seen  so 
frequentlv  in  gliomata. 

As  an  immediate  or  remote  result  of  the  presence  of     the     neo- 


914  THE   NON-NEURONIC  DISEASES 

plasm  in  the  intracraniuni,  certain  changes  are  produced  in  the  brain 
and  surrounding-  structures.  The  gross  appearance  of  the  brain  is 
altered.  There  is  a  flattening  of  the  gvri  and  an  arching  out  of  the 
cortex.  This  is  not  noticed  when  the  tumor  is  cortical  or  meningeal 
in  origin. 

The  softening  and  destruction  of  the  brain  substance  around  the 
tumor  have  already  been  referred  to. 

Displacements  and  distortions  are  effected  by  the  extension  of  the 
growing  mass.  Where  the  space  is  confined,  as  beneath  the  tentorium, 
the  displacements,  as  for  instance  of  the  pons  by  growths  in  the  cere- 
bellum, are  sometimes  very  considerable.  On  account  of  the  obstruc- 
tion of  the  passages  betw^een  the  ventricles  internal  hydrocephalus  of- 
ten results.  Tumors  of  the  cerebellum  and  quadrigemina  act  thus. 
Compression  of  the  vense  Galeni  which  carry  the  blood  away  from  the 
choroid  plexuses  is  responsible  sometimes  for  the  hydrocephalic  con- 
dition. Irritation  and  inflammation,  especially  in  the  meninges,  is  an- 
other effect  of  the  presence  of  the  tumor.  And  sometimes  the  cranial 
bones  are  thinned  out,  actual  perforation  having  been  observed  over  the 
tympanum. 

All  of  these  secondary  results  are  produced  by  direct  pressure  and 
destruction  of  the  growing  mass ;  sometimes  by  remote  and  indirect 
pressure  as  the  result  of  the  foreign  body  being  thus  confined  within  a 
fixed  cavity.  The  choked  disc,  so-called,  and  other  cranial  nerve  in- 
juries are  the  result  of  compression  of  the  nerve  by  the  growth.  In 
children  the  general  intracranial  increase  of  pressure  has  caused  a 
separation  of  the  sutures.  In  a  few  instances  even  spinal  cord  changes 
have  been  observed,  due  possibly  to  the  general  increase  of  pressure 
in  the  cerebrospinal  canal,  to  nutritive  disturbances  and  to  toxic  fac- 
tors. 

Symptoms. — The  brain  is  an  organ  inclosed  within  unyielding 
walls ;  it  is  a  compound  organ  with  special  functions  belonging  to  each 
of  its  constituent  parts.  A  tumor,  therefore,  will  cause  two  distinct 
sets  of  symptoms,  the  general,  due  to  the  general  increase  of  intracra- 
nial pressure,  and  the  special,  or  focal,  due  to  the  particular  location 
of  the  neoplasm  and  the  part  of  the  brain  that  is  damaged. 

The  important  general  symptoms  of  a  tumor  of  the  brain  are 
headache^  choked  disc,  retardation  of  the  pulse,  vomiting,  vertigo  and 
generalized  spasms.  While  the  objective  symptoms  are  the  most  re- 
liable for  diagnostic  purposes,  the  subjective,  especially  the  headache, 
are  usually  the  first  to  appear  or  be  noticed. 

Cephalalgia  occurs  in  about  two-thirds  of  the  cases  and  is  very 
variable  in  character.  It  is  less  paroxysmal  and  more  progressive  than 
most  other  headaches.  It  is  usually  generalized  over  the  whole  head, 
though  there  are  at  times  tender  spots,  especially  upon  percussion  with 
the  fingers.  Very  often,  in  spite  of  its  constancy  it  undergoes  sudden 
and  sharp  exacerbations.  As  a  rule  it  is  dull,  boring,  aching  and  dis- 
tressing. Its  very  constancy  is  exasperating  and  wearing.  At 
other  times  it  is  sharp,  lancinating  and  lightning-like.  Pa- 
tients are  often  driven  to  contemplate  suicide,  so  agonizing  is  it.  It 
breaks  the  sleep  at  night,  it  unnerves  the  patient  and  almost  upsets  his 


THE   NON-NEURONIC  DISEASES 


915 


mmd.  It  is  very  often  worse  at  night  and  occasionally  manifests  S- 
certain  degree  of  periodicity  in  its  daily  appearances.  The  location  of 
the  maximum  point  of  the  pain  is  suggestive  of  the  location  of  the 
tumor.  Occipital  headache  with  the  pain  extending  somewhat  down: 
into  the  neck  is  suggestive  of  a  growth  beneath  the  tentorium,  in  the 
posterior  fossa  or  cerebellum.  Frontal  headaches  occur  when  the 
neoplasm  is  in  the  centrum  ovale  whether  anteriorly  or  posteriorly. 
Superficial  tumors  very  often  lie  immediately  under  the  tenderest  spot 
in  the  scalp.  The  focal  pain  due  to  implication  of  the  origin  of  the 
superior  branch  of  the  trigeminus  often  combines  with  frontal  head- 
ache. Forced  expiration,  sudden  jars,  difficult  defecation,  straining 
of  all  kind,  sneezing  and  coughing  usually  increase  the  headache.  An- 
other peculiarity  about  them  is  that  to  all  forms  of  medication  that 
overcome  other  headaches,  these  are  steadily  resistant.  It 
is  not  clear  entirely  what  is  the  immediate  cause  of  these  headaches^ 
though  it  is  assumed  to  be. a  pressure  and  irritation  of  the  membranes. 
In  all  forms  of  tumor  this  symptom  is  a  prominent  one,  though  it  is 
less  so  perhaps  in  the  gliomatous  variety  and  those  that  grow  more 
slowly. 

The  most  valuable  symptom  of  brain  tumor  for  surety  of  diagno- 
sis is  undoubtedly  the  appearance  of  the  eye-ground.  Choked  disc 
occurs  in  four-fifths  at  least  of  all  cases.  For  obvious  reasons  it  is  not 
always  the  first  symptom  noticed  by  the  patient.  He  tampers  with 
glasses  and  opticians  for  his  failing  sight  for  a  long  time,  often  before 
his  headache,  until  eyesight  and  other  suspicious  signs  finally  drive  him 
to  consult  a  physician.  It  results  from  a  form  of  optic  neuritis  which 
may  be  bilateral  or  less  frequently  unilateral.  Most  commonly  it  is  bilat- 
eral but  more  pronounced  on  one  side  than  the  other,  generally  the  same 
side  as  the  tumor.  It  is  constantly  present  in  tumors  of  the  corpora 
quadrigemina,  and  in  four-fifths  of  the  cerebellar  tumors.  It  is  absenr 
in  nearly  two-thirds  of  the  cases  of  tumor  of  the  pons,  medulla  and 
corpus  callosum.  The  size  of  the  tumor  seems  to  have  very  little  direct 
influence  upon  the  presence,  severity  or  course  of  choked  disc.  It  seems 
to  be  less  frequent,  however,  in  tubercle  and  most  frequent  in  glio- 
r-atous  and  cystic  enlargements.  Irritation,  pressure,  engorgement  of 
the  nerve  sheath  and  associated  meningitis  have  all  probably  something 
to  do  with  the  causation  of  the  optic  neuritis.  The  course  of  the  in- 
flimmation  is  variable  though  generally  progressive.  In  the  end  com- 
plete optic  atrophy  usually  obtains. 

The  use  of  the  term  choked  disc  may  be  misleading,  diverting  the- 
mind  from  the  primary  inflammatory  nature  of  the  trouble,  but  if  this: 
possibility  is  guarded  against  it  is  still  a  good  one  to  employ  in  the  de- 
scription of  the  appearance  of  the  fundus  caused  by  the  neoplastic 
forms  of  optic  neuritis  as  distinguished  from  the  syphilitic  and  some 
other  forms.  Primary  optic  atrophy  never  develops  as  a  result  of 
brain  tumor.  The  sight  is  not  much  impaired  if  the  neuritis  is  moder- 
ate, but  curiously  enough  is  often  diminished  as  the  inflammation  sub- 
sides. The  secondary  atrophy  that  follows  it  is  always  a  late  sign  and', 
may  be  useful  in  indicating  an  older  age  in  the  tumor  when  the  other 
symptoms  have  been  slight  or  only  of  recent  onset. 


9l6  THE   NOX-XEURONIC  DISEASES 

J'ojuifiiig  is  the  next  important  symptom  and  should  probably  be 
added  to  the  headache  and  the  optic  neuritis  as  one  of  the  pathogno- 
monic tripod  of  indications  of  brain  tumor.  It  occurs  in  tumor  of  all 
parts  of  the  brain.  It  is  most  frequent,  pronounced  and  obstinate  in 
cerebellar  and  pontile  neoplasms.  It  is  an  early  symptom  as  a  rule 
though  it  seems  to  be  largely  an  accompaniment  of  the  headache  and 
vertigo.  It  is  a  true  cerebral  phenomenon  and  hence  is  peculiarly  in- 
dependent of  the  taking  of  food  or  of  the  condition  and  contents  of 
the  stomach.  It  may  come  on  at  any  moment  and  is  projectile  in  char- 
acter. A  lad  whom  I  saw  with  a  brain  tumor  had,  before  consulting 
any  physician,  adopted  the  habit  of  always  carrying  a  towel  with  him 
for  he  had  been  often  embarrassed  by  vomiting  under  most  unexpected 
circumstances.  There  is  not  much  nausea  with  the  vomiting  and  the 
examination  of  the  expelled  matter  fails  to  reveal  any  cause  for  it.  In 
a  general  way  it  is  more  characteristic  of  rapidly  growing  tumors. 

In  about  half  of  the  cases  diz;::iiiess  and  persistent  vertiginous,  in- 
toxication distress  are  spoken  of.  In  rarer  instances  there  are  definite 
attacks  of  rotatory  vertigo.  When  the  tumor  is  in  the  cerebellum  espe- 
cially, these  occur  in  conjunction  with  forced  movements.  Sometimes 
the  patient  complains  of  vertigo  only  upon  rising  or  turning  suddenly. 
\'ertigo  is  least  frequent  in  tumors  of  the  cerebral  hemispheres,  some- 
what more  frequent  when  they  are  located  in  the  central  ganglia  and 
most  frequent  when  the  tumor  is  in  the  cerebellum,  cerebellar  peduncle, 
pons  or  corpora  quadrigemina.  It  may  be  explained  partly  and  in 
some  cases  by  the  disturbance  of  those  important  avenues  of  afferent 
irhpulses,  the  optic  and  auditory  nerves,  but  it  cannot  be  entirely  so 
accounted  for.  Under  the  head  of  vertigo  and  Meniere's  disease,  I 
have  discussed  this  symptom  and  its  mechanism  somewhat  more  in 
detail. 

In  nearlv  all  cases,  sooner  or  later,  the  mi)id  is  affected.  This  is 
:a  direct  effect  of  the  pressure  and  irritation  and  not  due  merely  to  the 
prolonged  suffering  caused  by  the  headache.  The  latter,  of  course, 
lias  a  depressing  and  exhausting  effect,  too.  Stupor  and  coma  are  the 
common  terminal  manifestations,  especially  just  before  death.  It  is 
always  a  sign  of  great  significance.  Early  in  the  disease  and  when 
the  tumor  is  small  it  may  be  absent.  In  extracerebral  tumors  it  is  also 
less  frequent.  The  patient  seems  to  be  profoundly  asleep  and  hard  to 
arouse.  He  is  dull,  heavy  and  stupid  when  he  is  aroused.  He  seems 
to  drop  asleep  most  easily  and  on  the  most  extraordinary  occasions. 
At  table  he  will  drop  his  knife  and  fork,  stop  masticating  and  fall  back 
in  his  chair.  Defecation  and  urination  may  occur  in  the  same  way. 
Early  in  the  trouble  there  may  be  only  a  slight  failure  of  memory,  with 
depression  and  partial  lethargy.  In  other  cases  there  is  exhilaration, 
high  emotional  excitement,  silliness,  restlessness,  delirium  or  mania 
with  hallucinations  and  delusions.  Asylum  cases  of  insanity  show  upon 
post  mortem  quite  a  number  of  brain  tumors.  Sometimes  the  disease 
evokes  only  hysterical  manifestations  in  individuals  predisposed  to  this 
psychosis.  Large  tumors  and  froiital  tumors  are  supposed  especially 
to  be  characterized  by  these  psychic  manifestations. 

General  convidsions,  which,  however,  are  not  epileptic  in  character 


THE   NON-NEURONIC  DISEASES  917 

though  they  are  often  associated  with  unconsciousness,  occur  among  the 
general  symptoms  of  brain  tumor.  They  occur  in  all  stages  of  the  dis- 
ease, closely  resemble  epilepsy,  and  m  some  instances  are  even  pre- 
ceded by  prodromata.  One- fourth  of  the  cases  are  subject  to  these 
attacks.  Sometimes  they  are  distinctly  apoplectiform.  True  epileptic 
and  Jacksonian  manifestations  occasionally  occur.  They  may  even  pre- 
cede all  other  symptoms  by  many  years.  These  functional  attacks  may 
range  all  the  way  from  petit  mal  seizures  up  to  those  of  brief,  tetanic 
rigidity.  Oppenheim  suggests  that  when  epilepsy  thus  occurs  it  is  not 
so  much  a  direct  product  of  the  tumor  as  an  independent  disease  in  a 
brain  predisposed  to  the  development  of  both  tumor  and  epilepsy. 

Retardation  of  the  pulse,  to  forty  or  thirty  beats  per  minute,  is  not 
so  very  uncommon  in  intracranial  growths.  It  is  the  result  of  the 
general  intracranial  pressure.  It  is  never  an  earl}'  symptom.  In 
tumors  near  the  region  of  the  vagus  nucleus  the  pulse  rate  tends  to 
unwonted  rapidity. 

It  has  been  found  by  Gray,  Mills,  Lloyd  and  others  that  the 
cranial  temperature  is  often  somewhat  raised.  As  the  normal  tempera- 
ture of  the  scalp  is  uncertain,  the  abnormal  cannot  be  employed  very 
successfully  as  a  means  of  distinguishing  the  presence  of  a  tumor. 

According  to  Bruns,  a  typanitic  or  cracked-pot  sound  is  obtained 
sometimes  by  percussion  of  the  cranium  immediately  over  the  site  of 
the  tumor.  In  a  limited  experience  I  have  not  been  able  to  observe 
this  symptom.  Oppenheim  says  it  occurs  under  other  conditions  and 
is  always  present  in  sucklings. 

Before  the  days  of  cerebral  localization  it  was  not  possible  to 
carry  the  diagnosis  of  a  tumor  of  the  brain  much  beyond  its  mere  pres- 
ence. Under  such  circumstances  the  above  symptoms  constituted  prac- 
tically the  whole  of  the  clinical  picture  so  far  as  the  diagnostician  was 
concerned.  The  order  of  their  appearance,  the  relative  frequency  of 
sensory,  motor  and  special  sense  phenomena,  their  limitations,  degree 
of  severity  and  other  incidents  in  regard  to  them,  were  matters  of  in- 
terest, but  of  little  practical  value.  Since  the  development  of  our 
knowledge  in  regard  to  the  special  functions  of  the  various  parts  of 
the  brain  all  of  this  has  been  reversed.  It  is  not  enough  now  to  diag- 
nose the  presence  of  a  tumor ;  we  must  attempt  a  definite  localization 
of  it  within  the  intracranial  mass.  This  undertaking  presupposes  a 
thorough  knowledge  of  the  anatomy  and  physiology  of  the  brain,  the 
chapters  upon  which,  as  well  as  the  chapter  upon  cerebral  localization, 
should  be  consulted  by  the  reader.  Here,  however,  a  few  words  upon 
the  focal  diagnosis  of  intracranial  growths  are  in  order  to  comprehend 
what  is^said  elsewhere  and  to  emphasize  the  clinical  picture  produced 
en  masse  by  the  peculiar  localization  of  the  tumor. 

Whereas  the  study  of  the  general  symptoms  upon  which  the  diag- 
nosis of  the  mere  presence  of  the  tumor  is  based  takes  precedence 
always  in  point  of  time,  the  search  for  and  study  of  the  particular 
manifestations  upon  which  the  definite  localization  of  the  growth  is- 
found  far  outrank  it  in  importance.  As  the  signs  of  localization  pre- 
suppose and  include  all  those  that  indicate  the  existence  of  the  tumor. 


9l8  THE   NON-NEUKONIC  DISEASES 

they  alone  would  constitute  the  basis  for  the  diagnosis  if  they  were 
always  present. 

Localizing  symptoms  are  not  always  present.  Their  absence 
is  to  be  accounted  for  in  three  different  ways.  In  some  cases  the 
morbid  growth  is  so  large,  and  the  intracranial  pressure  is  so  high 
that  the  general  symptoms  overwhelm  and  completely  mask 
all  localization  signs  when  they  are  present.  In  other  cases  the  neo- 
plasm, small  and  capable  of  provoking  sharply  defined  localization 
symptoms,  is  embedded  in  one  of  the  so-called  silent  parts  of  the  brain, 
as,  for  instance,  the  frontal  and  temporal  lobes  of  the  right  side. 

Multiple  tumors  may  produce  such  a  confused  clinical  picture  that 
the  focal  signs,  though  present,  are  of  little  use  in  the  diagnosis.  Dana 
affirms  that  one-seventh  of  all  tumors  are  multiple,  including,  chiefly, 
tuberculous,  cancerous  and  melanotic  growths.  And  finally  in  still 
other  cases  there  may  be  all  the  while  fine  and  definite  localizing  mani- 
festations present  which  our  knowledge  of  brain  physiolog}^  falls  short 
of  interpreting.  Much  as  we  know  of  the  functions  of  the  brain,  there 
is  much  still,  as,  for  instance,  in  the  production  of  the  mental  phe- 
nomena, that  we  do  not  yet  know.  A  few  gross  motor  and  sensory 
manifestations  do  not  exhaust  all  of  the  functional  activities  of  this 
w^onderful  organ  and  in  our  localization  researches  upon  it  we  have 
only  entered  the  outer  portals  of  its  mysteries.  Not  more  than  one- 
third  of  its  cortex  and  its  constituent  elements  are  in  direct  communi- 
cation with  the  outer  parts  of  the  body  by  way  of  the  nerves,  and  most 
of  our  symptomatologies  are  drawn  from  the  body  and  neural  mani- 
festations. What  symptoms,  beyond  the  few  mental  symptoms  now  in 
our  possession,  we  are  to  attribute,  directly  or  remotely,  to  the  mys- 
terious workings  of  the  remaining  two-thirds  time  alone  can  tell. 

In  many  cases  of  brain  tumor  none  but  general  symptoms  occur 
throughout  the  entire  course.  In  others  the  localizing  signs  are  dis- 
tinct and  definite,  even  in  some  instances  overshadowing"  the  general 
symptoms.  As  a  general  axiom  it  may  be  said  that  the  smaller  the 
tumor  and  the  less  marked  the  signs  of  intracranial  pressure,  the  more 
definite  and  direct  will  the  focal  symptoms  likely  be.  A  small  tumor 
may  rarely  be  located  in  a  functionally  known  part  of  the  brain  and 
yet  no  localization  symptoms  be  manifested.  Such  a  growth  in  the 
white  substance  of  the  cerebrum  has  slowly  separated  the  fibres  without 
functionally  damaging  them.  Again,  what  is  called  action  from  a  dis- 
tance may  lead  to  an  erroneous  focal  diagnosis,  but  this  is  exceedingly 
rare.  Much  more  important  among  these  indirect  manifestations  of  the 
tumor  are  what  are  called  the  neighborhood  symptoms.  If  carefully 
studied,  these  indirect  symptoms  sometimes  add  to  the  value  of  the 
direct  and  so  confirm  the  focal  diagnosis. 

The  best  way  to  discuss  the  focal  symptoms  of  brain  tumor  is 
perhaps  to  take  up  seriatim  the  old  established  anatomical  divisions  of 
the  encephalon,  the  fossae  of  the  skull  and  finally  some  particularly 
prominent  centers  of  the  brain. 

Frontal  Lobe. — Tumors  in  the  anterior  part  of  the  frontal  lobe, 
the  prefrontal  region,  do  not  produce  any  characteristic  motor  or  sen- 
sory symptoms.     There  is  a  change  in  the  character  and  temperament, 


THE   XOX-XEURONJC  DISEASES 


919 


generally,  of  the  patient.  He  is  demented,  is  dull  or  extremely  emo- 
tional. He  laughs  and  cries  easily,  is  silly  and  quickly  angered!  This 
is  more  apt  to  be  the  case  when  the  left  lobe  is  affected ;  tumors  of  the 
right  lobe  are  as  a  rule  absolutel}-  silent.  As  the  tumor  grows  and 
compresses  and  extends  backward  and  downward  other  symptoms  are 
added  to  the  mental.  Encroachment  upon  the  posterior  part  of  the 
frontal  lobe  and  the  central  convolutions  causes  irritative  motor  signs 
such  as  muscular  spasm.  The  speech  center  may  be  involved  in  the 
third  left  frontal  convolution  causing  aphasia,  preceded  by  a  sort  of 

FIGURE  201. 


(From   Spratling.) 

distaste  for  speech,  a  mutism.  Tumors  in  the  inferior  part  of  the  lobe 
may  produce  olfactory  and  visual  disturbances  by  compressing  the 
olfactory  and  optic  nerves.  In  this  way  hemianopsia  and  optic  neu- 
ritis of  a  severe  type  may  be  produced.  Even  the  orbit  may  be  in- 
vaded and  the  ocular  globe  paralyzed  and  protruded.  When  there  is 
conjugate  deviation  of  the  eyes  with  muscular  spasm  in  the  arms  or 
face,  the  diagnosis  of  frontal  tumor  is  positive.  Bruns'  investigations 
have  revealed  to  us  why  frontal  tum.ors  sometimes  produce  cerebellar 

Parietal  Lobe. — Excluding  the  posterior  central  convolutions,  tu- 
mors of  the  parietal  lobe  cause  preeminently  sensory  manifestations. 
Thev   are  not  prominent   and  with   them  are  mingled   neighborhood 


920  THE   NON-NEURONIC   DISEASES 

symptoms.  The  muscular  sense  is  lost,  as  a  rule,  and  therefore  the 
gait  is  ataxic.  xA.s  with  the  frontal  lobe,  if  the  growth  encroaches  upon 
the  central  convolutions,  spasms,  contractions,  convulsions  and  paraly- 
ses may  occur  in  the  related  muscles.  The  lower  limbs  are  affected 
by  high  situated  tumors,  the  arms,  neck  and  head  by  the  lower  ones. 
As  many  tracts  between  the  occipital  lobe  and  the  central  course 
through  the  white  areas  of  the  parietal  lobe,  tumors  in  its  lower  part 
give  rise  to  alexia  and  visual  aphasia.  Still  deeper  growths  may  cause 
hemianopsia.  Near  the  angular  gyrus  is  the  cortical  representation 
of  the  third  nerve  and  its  damage  has  resulted  in  paralysis  of  this 
nerve.  This  may  explain  some  rare  cases  of  vertex  g'ummatous  men- 
ingitis with  motorocular  palsy.  I  once  saw  such  a  case.  The  symp- 
toms of  the  specific  meningitis  pointed  clearly  to  the  vertex  of  the 
brain  and  the  only  cranial  nerve  that  was  involved  was  the  third. 
Some  symptoms  of  a  sensory  character  due  to  implication  of  the 
parietal  cortex  are  probably  neighborhood  symptoms  and  due  to  the 
close  connection  between  the  cortical  elements  of  the  parietal  lobe  and 
those  of  the  central  convolutions.  Astereognosis  is  a  symptom  of  parie- 
tal tumor  in  nearly  all  cases. 

Central  Convolutions. — These  are  the  most  responsive  areas  of 
the  brain  from  the  standpoint  of  localization.  Being  chiefly  motor 
in  function,  and  grouping  the  entire  musculature  of  the  body  in  their 
representation,  their  injury  can  be  studied  objectively  and  in  detail. 
They  constitute  the  motor  zone  and  exhibit  most  pronounced  focal 
manifestations.  With  the  size  of  the  tumor,  of  course,  will  vary  the 
extent  of  the  manifestations  throughout  the  movements  of  the  body. 
Irritative  signs  are  among  the  first  to  appear  and  as  a  result  Jack- 
sonian  epilepsy  obtains.  Sensory,  aurje  often  precede  the  local  spasms. 
If  the  tumor  is  small  the  epileptic  condition  may  be  without  disturb- 
ance of  consciousness  and  be  confined  to  the  face  or  the  arm  or  the 
leg.  As  the  neoplasm  enlarges,  however,  the  muscular  convulsions  be- 
come more  extensive  and  the  consciousness  may  be  lost,  the  whole 
clinical  picture  assuming  the  complexion  of  a  typical  grand  mal  seiz- 
ure. Even  in  these  elaborate  cases,  the  consciousness  is  not  lost  at  first 
and  the  aurse  and  spasm  usually  begin  always  in  the  one  place,  thus 
enabling  the  localization  to  be  made.  The  hemiplegic  character  of  the 
primary  manifestations  should  be  carefully  noted.  As  the  destructive 
action  of  the  tumor  goes  on,  the  spasms  are  replaced  by  a  gradually 
deepening  paralysis.  Monoplegias  and  hemiplegias  are  the  forms  that 
this  assumes.  Sensory  disturbances  usually  accompany  them,  con- 
sisting of  various  pareesthesise  such  as  numbness,  pricking,  pins-and- 
needles  sensation,  loss  of  pain,  touch  and  temperature  sense,  and  even 
complete  hemianesthesia.  Even  the  muscular  sense  may  be  involved 
and  the  stereognostic  sense.  Local  twitchings  in  certain  muscular 
groups,  followed  by  spasm  and  paralysis  in  the  same  groups,  asso- 
ciated with  similar  sensory  phenomena  in  approximately  the  same 
localities,  are  the  sign  manual  of  a  growing  neoplasm  in  the  central 
lobule.  Aphasia  and  agraphia  may  also  be  present.  The  exact  point 
of  the  cortex  impinged  on  and  the  details  of  the  localization  can  be 
worked  out  by  reference  to  the  chapter  on  cerebral  localization.      It 


THE   XOX-XEL'ROXIC  DISEASES 


921 


must  be  remembered  that  the  tumor  may  not  actually  be  in  the  cen- 
tral cortex.  ^  It  may  be  in  the  meninges  over  the  center  or  in  the  white 
substance  of  the  brain  beneath  it.  Under  such  circumstances  irritative 
symptoms  of  the  motor  centers  will  be  very  gradual  in  onset,  paroxys- 
mal in  character  in  the  beginning  and  only  very  late  become  posi- 
tively and  permanently  paralytic  in  character'  However,  there  is  great 
uncertainty  about  this  as  Avell  as  about  the  age  and  size  of  the  tumor 
from  such  localizing  indications.  A  very  large  tumor,  for  instance, 
of  the  centrum  ovale  may  just  touch  the  motor  centers,  as  it  were, 
and  produce  only  slight  irritative  symptoms. 

It  is  thus  obvious  that  impHcation  of  the  motor  zone  of  the  cor- 
tex furnishes  us  with  our  happiest  localizing  symptoms.  Their  origin, 
their  location  and  their  onward  march  from  slight  twitching  to  com- 
plete paralysis  are  seen  in  no  form  of  lesion  so  beautifully  and  regu- 
larly characteristic  as  in  tumor  in  or  about  this  region. 

Temporal  Lobe. — In  right-handed  people  the  right  temporo- 
sphenoidal  cortex  is  practically  latent.  In  the  left  temporal  cortex 
are  the  centers  for  hearing  and  smell  and  taste.  Word-deafness  occurs 
with  tumor  of  the  first  and  second  convolutions,  also  amnesic  aphasia 
and  various  forms  of  paraphasia.  Pressure  by  a  temporal  tumor  on  the 
neighboring  parts  of  the  brain  may  cause  a  variety  of  symptoms. 
Posteriorly  it  may  provoke  optic  aphasia ;  anteriorly  it  may  disturb 
the  centers  for  taste  and  smell  both  in  itself  as  well  as  in  the  comu 
ammonis.  If  the  tumor  is  very  low  in  the  lobe  so  as  to  compress  the 
medulla  and  adjoining  parts  it  may  cause  attacks  of  vertigo  with  forced 
movements  and  a  mixed  type  of  aphasia.  Hemianesthesia,  hemiplegia 
and  hemianopsia  may  all  be  caused  by  such  a  localization  of  the  neo- 
plasm. The  reason  is  clearly  the  implication  of  the  great  conducting 
tracts  in  the  brain  stem. 

Occipital  Lobes. — The  visual  centers  of  the  cortex  are  the  great 
characteristics  of  these  lobes.  A  bilateral  tumor  in  them  produces 
complete  amaurosis.  Hemianopsia  is  the  distinguishing  feature  of  a 
tumor  in  one  of  the  lobes.  As  lesions  of  the  optic  tract  m^ay  cause 
the  same  visual  disturbance,  it  is  not  a  particularly  valuable  sign  for 
locating  the  tumor  in  the  occipital  lobe.  When,  however,  it  is  accom- 
panied by  sharp  occipital  headache,  extending  down  the  neck  the  pre- 
sumption is  strong  that  the  growth  is  occipital.  Psychic  blindness, 
word-blindness,  soul-blindness  or  the  incapacity  to  comprehend  the 
nature  of  things  seen  are  some  of  the  curious  results  of  tumors  in  the 
occipital  lobe.  Extension  of  such  a  tumor  into  the  parietal  lobe  and 
impingement  upon  the  internal  capsule  may  be  surmised  by  the  hemi- 
ansesthesia.  unilateral  ataxia,  and  even  hemiplegia. 

Central  Ganglia.— Tumors  of  this  region  like  those  of  the  corpus 
callosum  are  only  obscurely  diagnosed  and  from  the  standpoint  of 
surgical  intervention  are  of  no  interest  whatever.  ^Most  of  the  symp- 
toms are  due  to  the  damage  done  to  the  internal  capsule,  either 
directly  or  through  pressure.  Gradual  and  partial  hemiplegia  is_  the 
distinctive  svmptom  or  there  may  be  unilateral,  indefinite  twitchings 
from  a  tumor  in  the  striate  body  or  the  thalamus  irritating  the  cap- 
sule and  its  fibres  that  go  coursing  down  between  them.    Hemichorea, 


922  THE   XOX-XEUROMC   DISEASES 

athetoid  movements  on  one  side  of  the  body,  involuntary  and  automatic 
jactitations,  hemianassthesia  and  hemianopsia  of  the  opposite  side,  are 
all  possible  and  their  mechanism  easily  understood.  There  are  no 
known  symptoms  produced  by  a  growth  confined  solely  to  the  cor- 
pora striata  or  optic  thalami.  unless  it  be  located  in  the  posterior 
part  of  the  latter  or  pulvinar.  Growths  in  the  pulvinar  cause  hemian- 
opsia with  distinctive  hemiopic  pupillary  reaction  or  inactivity,  a  fact 
which  distinguishes  this  form  of  hemianopsia  from  that  produced  by 
disease  in  the  occipital  lobe.  Tumor  of  the  basal  ganglia  is  usually 
marked  by  a  considerable  degree  of  stupidity. 

Corpus  Callosum. — Tumors  here  are  not  frequent  and  their  focal 
svmptoms  are  not  very  distinctive.  There  is  a  peculiar  mental  state 
consisting  of  intense  stupidit}-.  drowsiness,  sopor,  mutism  and  mental 
deadness.  For  hours  the  patient  will  sit  immobile,  seemingly  lost  to 
every  stimulation  from  the  outer  world.  The  absence  of  most  of  the 
localizing  signs  of  tumor  and  the  gradual  increase  of  those  that  are 
present  are  two  of  the  more  striking  features  of  tumor  in  this  re- 
gion. Absence  of  cranial  nerve  disturbances  and  absence  of  anaes- 
thesia are  especially  noteworthy.  Hemiplegia  with  a  lesser  degree  of 
paralysis  on  the  other  side,  or  bilateral  hemiplegia  of  equal  intensity 
on  both  sides,  is  suggestive.  Coma  usually  terminates  these  cases. 
Dana  thinks  that  symptomatically  tumors  of  the  great  commissure  are 
the  same  as  or  closely  correspond  with  tumors  situated  in  the  third 
and  lateral  ventricles.  In  other  words  they  belong  to  ajl  of  that  class 
of  tumors  which  begin  in  the  central  parts  of  the  brain  and  gradually 
extend  outwards  toward  the  periphery. 

Corpora  Oiiadrigeinina. — Tumors  here  usually  involve  also  the 
crura  cerebri  and  pineal  gland,  or  vice  versa.  These  structures  are 
very  complex  and  important  organs.  In  them  are  located  the  pri- 
mary centers  of  sight  and  hearing.  Their  occupation  by  a  tumor 
therefore  causes  hemianopsia  or  blindness,  impaired  hearing  or  deaf- 
ness. With  this  hemianopsia  there  is  paralysis  of  the  ocular  muscles 
as  a  rule.  The  pupillary  reflex  is  lost  and  there  is  nystagmus.  Ambly- 
opia may  occur  and  the  same  ocular  muscles  may  be  paralyzed  bilat- 
erally. Incoordination,  forced  movements  and  an  intention  tremor, 
as  well  as  a  tremor  like  that  of  paralysis  agitans,  may  often  be  ob- 
served. Most  of  these  are  neighborhood  symptoms  and  occur  whether 
the  tumor  have  its  origin  in  the  pineal  gland,  the  gemina  or  the  crura. 
A  special  characteristic  of  implication  of  the  latter  is  superior  alter- 
nating hemiplegia,  a  condition  in  which  there  is  oculomotor  paralysis 
of  one  side  with  paralysis  in  the  extremities  of  the  other  side.  A 
curious  and  rare  analogue  of  this  is  the  alternation  of  oculomotor 
palsy  with  a  hemiataxia  of  the  other  side,  due,  according  to  Krafft- 
Ebing,  to  a  tumor  in  the  tegmentum.  These  latter  conditions  are  ex- 
tremely rare. 

C erebeUum.—CereheWar  tumor  of  a  certain  type  is  perhaps  the 
most  definite  of  the  localizable  lesions.  Its  diagnosis  is  therefore  com- 
paratively easy.  Tumors  in  the  lateral  lobes  of  the  little  brain  are 
usually  silent  until  they  press  upon  the  medulla,  the  pons  and  the  re- 
lated cranial  nerves,  when  they  produce  close  neighborhood  symptoms. 


THE   XOX-XEUROXIC  DISEASES  923 

A'ertigo  and  incoordination  are  the  distinctive  symptoms,  though  not 
-Strictly  focal,  of  a  neoplasm  in  the  middle  lobe  or  vermis.  Cerebellar 
ataxia  is  a  reeling,  drunken  gait.  It  has  been  called  a  titubating 
gait.  It  is  unfortunate  that  the  term  unstable  equiUbrium  is  not  used 
instead  of  ataxia,  because  the  gait  is  not  the  same  as  that  seen  in  tabes. 
A  true  ataxia  may  develop  rarely  in  the  extremities  and  be  bilateral 
or  unilateral.  Sometimes  closing  of  the  eyes  increases  the  disturb- 
ance of  equilibrium  and  on  account  of  it  the  patient  may  actually  fall. 
A  distressing  and  constant  vertigo  accompanies  usually  this  symp- 
tom. Vomiting,  appearing  early  and  continuing  during  the  entire 
disease,  is  a  typical  symptom.  Forced  movements,  turning  involun- 
taril}"  and  automatically  one  way  or  the  other,  are  also  quite  prominent 
in  some  cases.  The  general  symptoms  of  this  tumor  are  strongh- 
jnaiiced,  as  a  rule.  The  headache  is  occipital  and  extends  with  mus- 
cular rigidity  into  the  neck.  It  may  be  frontal  in  some  cases.  Optic 
neuritis  is  sharp  and  well  defined.  Opisthotonos,  general  convulsions, 
tetanic  rigidity  of  the  whole  body,  unilateral  and  bilateral  hemiple- 
gia, may  all  occur  from  extreme  pressure  upon  the  great  tracts  run- 
Tiing  through  the  medulla.  Other  medullary  symptoms  that  may  not 
be  unlooked  for  are  glycosuria,  cranial  nerve  and  nuclei  disturbance 
and  the  usual  signs  of  bulbar  paralysis.  Internal  hydrocephalus  is 
also  possible  from  pressure  on  the  venai  Galeni. 

Pons  Varolii  and  Medulla  Oblongata. — These  parts  of  the  brain 
are  subject  more  frequently  to  tuberculous  and  gliomatous  tumors 
than  to  any  other  variety.  Occasionally  no  symptoms  are  produced 
by  them  for  a  long  time  but  sooner  or  later  a  very  characteristic  clin- 
ical picture  is  presented.  The  details  of  this  picture  may 
undergo  a  great  variety  of  presentations  but  in  the  main 
its  chief  outline  is  quite  uniform.  The  prominent  feature  in  the 
symptomatolog}-  of  tumors  of  the  brain  stem  is  the  combination  of 
cranial  nerve  palsies  and  hemiplegia.  In  most  tumors  the  cranial 
■nerve  palsy  will  be  on  the  same  side  as  the  tumor,  the  paralysis  of  the 
limbs  on  the  opposite  side.  This  is  the  well-known  alternating  hemi- 
plegia and  is  easily  comprehended  by  a  glance  at  the  physiological 
anatomy  of  the  parts.  The  paralysis  of  the  Hmbs  will,  of  course,  be 
of  the  cerebral  or  central  neurone  type,  while  that  of  the  cranial 
-nerves  will  be  of  the  spinal  or  peripheral  neurone  type.  The  size  and 
exact  location  of  the  tumor  must  be  worked  out  by  a  study  of  the 
particular  cranial  nerves  involved  and  the  extent  of  the  hemiplegia. 
In  about  one-quarter  of  the  cases  the  cerebral  nerves  alone  are  in- 
volved, in  another  quarter  the  limbs  are  affected,  in  nearly  a  half 
are  both  the  nerves  and  limbs  involved.  In  almost  eighty-five  per 
cent,  of  the  latter  the  paralysis  is  of  the  alternating  variety.  In  high 
tumors  of  the  pons  the  hemiplegia  is  combined  with  oculomotor  paraly- 
sis; in  low  tumors  with  trigeminal  paralysis.  Lower  down  still  in 
the  medulla  the  other  nerves  may  be  involved  seriatim  such  as  the 
facial,  the  abducens,  the  auditory,  etc.  Bilateral  cranial  nerve  palsy, 
iDilateral  hemiplegia  and  all  the  symptoms  of  a  true  progressive  bulbar 
paralvsis  mav  appear  when  the  tumor  is  large,  bilateral  or  centrally 
located.     If  it  is  situated  very  laterally  forced  movements  may  be  a 


924 


THE   iVON-NEURONlC   DISEASES 


FIGURE  202. 


Men 


Schematic  representation  of  the  course  of  the  pyramidal  tract  for  the  face  and 
for  the  extremities.  A  lesion  above  the  facial  decussation  causes  paralysis  of  face- 
and  extremities  on  the  side  opposite  the  lesion ;  a  lesion  below  the  facial  decussa- 
tion causes  paralysis  of  the  face  on  the  same  side  and  of  the  extremities  on  the 
side  opposite  the  lesion.  The  latter  condition  is  known  as  "crossed  paralysis'*" 
or  alternate  hemiplegia.     (Diagram  modified  from  Edinger.) 


THE   NON-NEURONIC  DISEASES  925 

ieature  of  the  case  with  general  unilateral  or  alternating  convulsive 
-movements.  In  pontile  tumors  sensory  symptoms  with  hemiataxia 
may  also  occur.  Most  unexpected  and  extraordinary  combinations 
are  liable  to  occur.  The  conjugate  deviation  of  the  eyes,  sometimes 
accompanied  by  facial  palsy,  is  toward  the  side  opposite  that  of  the 
lesion,  and  thus  is  different  from  the  conjugate  deviation  from  a  cere- 
bral lesion,  in  which  case  it  is  toward  the  side  of  the  lesion.  Disarthria 
and  dysphagia  may  occur  with  pontile  tumors. 

When  the  growth  is  below  the  pons  in  the  medulla  bulbar  symp- 
toms stand  prominently  forth.  Hemiplegia,  hemianaesthesia  with 
paralysis  of  the  ninth,  tenth,  eleventh  and  twelfth  nerves  constitutes 
the  essential  elements  in  the  clinical  presentation.  All  those  symp- 
toms usually  associated  with  implication  of  the  floor  of  the  fourth 
ventricle  may  be  expected  such  as  dysphagia,  dysarthria,  aphonia, 
•deafness,  etc.  Irregular  heart  action,  respiratory  embarrassment,  vom- 
iting, retraction  of  the  head  and  neck,  glycosuria,  vasomotor  phenom- 
ena are  among  the  usual  signs  of  tumors  in  this  part  of  the  encephalon. 
The  gait  may  be  unsteady  as  in  so-called  cerebellar  ataxia,  or  the  limbs 
may  be  unilaterally  or  bilaterally  paralyzed  both  in  motion  and  sensa- 
tion. General  intracranial  pressure  may  or  may  not  be  developed. 
Convulsions  usually  close  the  scene  in  most  cases. 

Tumors  of  the  base  of  the  brain  are  conveniently  localized  into 
those  of  the  anterior,  middle  and  posterior  fossae  of  the  skull.  The 
main  symptoms  of  such  tumors  have  been  referred  to  when  the  cor- 
responding lobes  of  the  brain  were  discussed.  There  are  a  few  pecu- 
liarities about  basal  tumors  that  deserve  further  mention,  however. 
They  may  break  through  into  the  cavities  of  the  forward  part  of  the 
skull.  The  nose,  the  pharynx,  the  antrum,  the  tympanum  have  all 
thus  been  entered  and  the  functions  of  the  corresponding  and  ad- 
joining organs  damaged.  In  such  instances  palpation,  as  through  the 
mouth,  reveals  an  unusual  sensitiveness  of  the  brain  in  that  situation. 
Debris,  hemorrhage  and  pieces  of  the  broken  down  tumor  may  be 
thus  extruded  and  the  nature  of  the  groAvth  be  accurately  diagnosed. 
Optic  neuritis,  optic  atrophy,  less  frequently  than  in  other  tumors, 
choked  disc,  cranial  nerve  implication  are  all  to  be  observed  in  cases 
of  basal  tumor.  If  the  growth  is  extradural,  there  may  be  no  local- 
izing signs  until  late. 

Anterior  Fossa. — In  addition  to  what  has  already  been  said  about 
intrusion  of  the  orbital,  nasal,  pharyngeal  and  maxillary  cavities  by 
tumors  growing  in  the  anterior  fossa,  symptoms  occur  that  are^  the 
sam.e  as  those  when  the  growth  is  in  the  frontal  lobes.  Especially 
characteristic  are  the  mental  and  temperamental  changes.  Olfactory, 
optic  and  oculomotor  disturbances  are  particularly  suggestive.  Paros- 
mia may  be  present  for  a  brief  period  but  anosmia  occurs  sooner  or 
later  from  destruction  of  the  olfactory  lobes.  Loss  of  smell,  it  must 
be  remembered,  has  occurred  from  tumors  elsewhere  in  rare  cases; 
aue,  according  to  an  unproved  hypothesis,  to  a  neuritis  of  the  olfac- 
tory such  as  occurs  in  the  optic  nerves.  The  same  may  be  said,  ex- 
cepting the  hypothetical  nature  of  the  nerve  lesion,  of  the  optic  neu- 
ritis that  is  seen  in  tumors  of  the  anterior  fossa.     As  these  neoplasms 


ij26  THE   NON-NEURONIC   DISEASES 

rarely  remain  confined  to  the  anterior  part  of  the  skull,  symptoms  may 
occur  in  them  showing  implication  of  the  optic  chiasm  and  even  of  the 
crura. 

Middle  Fossa. — These  tumors  may  cause  erosion  into  the  tym- 
panum with  complete  loss  of  hearing,  or  the  deafness  may  be  due 
to  the  extension  of  the  tumor  and  implication  of  the  auditory  nerve. 
The  fifth  nerve  and  the  Gasserian  ganglion  are  particularly  exposed 
to  the  damaging  infiuence  of  these  tumors.  Neuroparalytic  ophthal- 
mia is  a  very  characteristic  symptom.  With  the  extension  of  the 
tumor  the  facial  is  usually  involved  with  the  auditory  nerve.  Symp- 
toms of  optic  nerve  and  chiasma  involvement  are  particularly  char- 
acteristic. The  hypophysis  is  often  the  seat  of  tumors  that  cause 
these  visual  disturbances.  The  condition  is  observed  in  acromegaly 
and  will  be  again  referred  to  in  the  discussion  of  that  disease.  Bitem- 
poral hemianopsia,  unilateral  and  bilateral  amblyopia,  unilateral 
amaurosis  with  hemianopsia  in  the  other  eye.  complete  blindness  and 
other  pronounced  phenomena  may  occur.  The  case  whose  chart  is 
shown  in  the  chapter  on  acromegaly  had  at  one  time  blindness  of  the 
two  lower  half-fields,  horizontal  hemianopsia.  This  was  so  curious 
that  hysteria  was  one  of  the  early  diagnoses  made  in  the  case.  It 
proved'  to  be  sarcoma  of  the  hypophysis  with  complete  atrophy  later  on 
of  the  optic  nerves. 

For  a  while  sometimes  the  fundi  of  these  cases  show  no  changes. 
Signs  of  injury  to  the  optic  chiasm  are  almost  pathognomonic  of  tu- 
mors of  the  middle  fossa.  The  third  nerve,  however,  is  frequently 
included  though  less  so  than  the  optic.  Exophthalmos  with  contrac- 
tion of  the  pupil  may  be  the  only  signs  in  the  beginning  that  can  be 
detected  objectively.  Reflex  twitchings  in  the  facial  may  be  another 
earlv  sign.  Extension  of  these  middle  tumors  forward  may  provoke 
slight  mental  exhibitions  or.  if  they  reach  backward,  crural  symp- 
toms such  as  hemiplegia,  hemian^esthesia  and  rarely  convulsions  may 
be  observed. 

Posterior  Fossa. — With  neoplasms  in  the  posterior  fossa,  cere- 
bellar, pontile,  medullary  and  cranial  symptoms  occur  in  a  great 
variety  of  combinations.  They  may  be  unilateral  or  bilateral.  As 
the  growth  begins  outside  of  the  brain  stem  and  extends  inward,  the 
cranial  nerves  are  apt  to  be  affected  before  the  hemiplegia  appears, 
which  is  the  reverse  or  at  least  different  from  what  obtains  in  internal 
tumors.  It  is  obvious  also  why  in  such  tumors  facial  and  auditory 
nerves  are  implicated  together,  and  internal  strabismus  occurs  in  one 
eye  with  the  conjugate  deviation  of  the  other,  as  will  occur  if  the 
sixth  nucleus  is  the  primary  seat  of  the  trouble.  A  general  com- 
pressive bulbar  paralysis  is  the  typical  picture  produced  by  these  pos- 
terior cranial  growths. 

Speech  may  be  affected  in  several  ways  by  intracranial  neoplasms 
according  to  their  location.  When  the  site  is  the  third  left 
frontal  convolution  or  the  immediate  vicinity,  motor  aphasia  is  the 
character  of  the  disturbance.  Amnesic  aphasia  and  paraphasia  occur 
from  tumors  in   the   first  left  temporal  convolution   and  its  vicinity. 


THE   NON-NEURONIC  DISEASES  927 

Dysarthria,  anarthria  and  aphonia  may  result  from  tumors  in  the 
middle  oblongata  or  in  the  posterior  fossa  of  the  skull. 

I'  isual  disturbances  are  varied  and  numerous  from  intracranial 
neoplasms.  The  visual  impulse  after  it  leaves  the  retina  traverses 
a  long  tract  and  through  many  parts  of  the  brain  before  it  finally 
reaches  the  occipital  cortex.  Hemianopsia  must  always  be  studied 
in  conjunction  with  the  other  symptoms  if  it  is  to  be  employed  in 
making  a  focal  diagnosis.  It  may  be  the  result  of  a  lesion  anywhere 
in  the  tract  behind  the  optic  chiasm.  If  the  tumor  is  in  the  optic  tract 
proper,  other  cranial  nerves,  especially  the  oculomotorius,  are  apt  to 
be  included.  If  the  thalamus  is  the  site  of  the  trouble,  the  conduct- 
ing paths  in  the  capsule  are  involved  and  hemiana^sthesia  and  hemi- 
plegia are  associated  with  the  hemianopsia.  When  the  growth  nests 
in  the  corpora  quadrigemina,  external  and  internal  ocular  paralysis 
occurs.  Aphasia  with  hemianopsia  indicates  implication  of  the  optic 
tract  as  it  courses  backward  to  the  left  occipital  lobe.  A  tumor  of 
the  occipital  lobe  itself  produces  hemianopsia  as  the  only  visual  symp- 
tom. If  the  tumor  is  bilateral  or  so  large  as  to  injure  the  cuneus  in 
both  occipital  lobes  amaurosis  obtains.  Mind-blindness  occurs  with 
occipital  tumors. 

The  sphincters  of  the  bladder  and  bowel  are  not  affected  by  brain 
tumor  though  evacuation  may  seem  to  take  place  involun- 
tarily in  the  state  of  stupidity  and  mental  apathy  that  more 
or  less  accompanies  all  intracranial  neoplasms.  The  polyuria, 
glycosuria  and  albuminuria  that  may  occur  in  tumors  of  the 
brain  stem  have  been  mentioned.  As  they  may  be  due  to  the  general 
intracranial  disturbance  they  are  only  of  limited  value  as  localizing 
symptoms. 

Diagnosis. — The  diagnosis  of  a  tumor  of  the  brain  is  never  a 
simple  matter,  though  it  is  easier  in  some  cases  than  in  others.  It 
should  always  be  made  upon  the  complexus  of  symptoms  in  toto, 
rather  than  upon  any  one  or  two  of  them.  As  many  signs  should  be 
discovered  therefore  as  possible.  Some  cases  are  latent  and  present 
no  signs  at  all,  for  a  long  time  at  least.  Others  exhibit  only  one  or 
two  symptoms,  like  headache,  for  instance,  long,  even  years,  before 
the  appearance  of  others.  Some  cases  present  only  the  general  symp- 
toms ;  now  and  then  a  rare  case  may  exhibit  merely  some  one  or  two 
focal,  without  general,  manifestations.  Most  cases  present  both  gen- 
eral and  focal  symptoms  sometime  in  their  course  though  the  loca- 
tion of  the  tumor,  its  age,  its  nature  and  many  other  factors  will  vary 
very  greatly  the  relative  values  of  the  respective  general  and  focal 
symptoms.  '  Subjective  symptoms  are  commonly  the  first  to  be  no- 
ticed;  objective  symptoms  are  the  most  rehable  for  diagnostic  pur- 
poses. Though  the  patient  usually  presents  himself  on  account  of 
the  headache,  the  examiner  should  at  once  institute  a  minute  search 
for  objective  signs.  The  most  important  of  the  latter  is  without  doubt 
optic  neuritis.  No  headache  should  be  allowed  to  pass  without  a  careful 
examination  of  the  eye-grounds.  From  eighty  to  ninety  per  cent._  of 
the  cases  of  intracranial  tumor  have  optic  neuritis  and  choked  disc. 
It  is  a  characteristic  condition  and  is  not  exactly  like  other  forms  of 


928  THE   XOX-NEUROts^lC  DISEASES 

Optic  neuritis.  It  is  practically  confirmatory  of  the  trouble.  A  some- 
what similar  choked  disc  occasionally  appears  in  meningitis,  cerebral 
abscess,  renal  disease  and  hydrocephalus,  but  these  can  be  distin- 
guished by  other  symptoms.  Papillitis  may  be  due  to  other  causes 
than  tumor,  especially  when  chlorosis,  lead  poisoning,  polyneuritis 
or  alcoholism  are  present.  A  central  scotoma  for  colors  speaks  for 
alcoholic  intoxication.  With  the  headache  cerebral  vomiting  is  almost 
always  present.     Vertigo  is  also  a  frequent  accompaniment. 

The  headache  must  be  studied  from  every  possible  point  of  view. 
It  is  usually  characteristic  in  brain  tumor  though  often  it  varies  from 
the  typical  and  by  resembling  other  forms  of  headache,  like  hemi- 
crania,  the  cephalalgia  of  hysteria,  neurasthenia,  constipation,  infec- 
tion and  toxjemia,  may  add  much  confusion  to  the  diagnosis.  It  is  well 
in  such  cases  to  diagnose  the  neoplastic  headache  by  exclusion.  A 
search  should  be  made  for  all  possible  causes  of  the  headache  apart 
from  tumor.  If  then  papillitis  and  vomiting  can  be  added  to  the  symp- 
tomatology the  diagnosis  is  complete.  Cephalalgia,  optic  neuritis, 
cerebral  vomiting,  constitute  strong  grounds  for  the  opinion  that  a 
tumor  is  present.  As  these  symptoms  are  not  always  present  all  to- 
gether there  are  others  that  when  added  to  any  one  of  these  makes 
the  diagnosis  strongly  presumptive,  practically  positive  in  some  cases. 
\'ertigo  is  not  of  much  importance.  Progressive  stupor  is,  however ; 
so  also  are  retardation  of  the  pulse,  general  convulsions,  epileptic 
attacks  of  a  particular  type  and  various  speech  disturbances.  The 
progressive  character  of  the  symptomatology  is  a  significant  feature.  It 
will  be  noticed  that  all  of  these  symptoms  except  the  optic  neuritis 
may  occur  in  certain  non-organic  diseases,  such  as  hysteria,  neuras- 
thenia, epilepsy  and  certain  psychoses.  It  is  necessary  to  exclude 
these  first,  therefore,  which  may  be  generally  readily  done  by  search- 
ing for  the  other  s^nnptoms  of  these  various  neuroses.  It  is  to  be 
remembered,  however,  that  as  a  rare  possibility  a  latent  tumor  may 
be  present  with  all  the  signs  of  a  mere  neurosis  or  psychosis.  Of 
course,  no  differentiation  can  be  made  then. 

An  organic  disease,  and  that  a  tumor  of  some  sort,  being  finally 
decided,  the  location  of  it  is  the  next  question  to  be  considered.  I 
have  shown  tmder  the  head  of  symptoms  how  the  focal  diagnosis  may 
be  both  clear  and  obscure.  I  have  also  dwelt  upon  its  supreme  im- 
portance. \\'hile  so  strongty  suggestive  of  a  neoplasm,  focal  symp- 
toms are  sometimes  produced  by  other  diseased  conditions,  as  for 
instance,  a  focal  meningitis,  an  aneurism,  an  old  hemorrhagic  cyst 
or  spot  of  necrobiosis.  Even  in  hysteria,  epileps)^,  alcoholism,  uraemia 
and  paralytic  dementia  localized  manifestations  both  of  a  motor  and 
sensory  character  in  various  parts  of  the  body  may  occur  in  such  a 
way  as  to  closely  simulate  the  focal  symptomatology'  of  brain  tumor. 
The  progressive  character  of  the  latter  taken  in  conjunction  with 
the  characteristic  general  symptoms  helps  much  in  the  differential 
diagnosis.  It  seems  incredible  how  closely  even  focal  organic  symp- 
toms may  be  simulated  by  the  neuroses  and  dift'use  organic  diseases. 
Gowers  mentions  the  case  of  a  hysterical  little  girl  who  after  watch- 
ing for  some  time  a  genuine  case  of  brain  tumor,  mimicked  it  almost 


THE   XOX-XEUROXIC  DISEASES  929 

perfectly.  :Monoplegias,  focal  anaesthesia,  limited  irritative  and  de- 
structive simulacra  and  actualities  may  occur  under  manv  other  cir- 
cumstances, functional  as  well  as  organic,  than  those  of  an  intracra- 
nial growth.  The  keeping  close  to  the  typical  symptomatolog}-  of 
tumor  and  contrasting  it  with  the  total  symptomatolog}-  or  entire  clin- 
ical picture  of  these  other  diseases  is  the  only  safe  way  to  determine 
the  origin  and  focal  value  of  the  former. 

The  presence  of  a  tumor  and  its  location  having  been  established, 
it  remains  only  to  fix  its  nature.  As  multiple  tumors  are  always  in- 
operable, whatever  their  location  may  be,  they  must  be  carefullv  dis- 
tinguished from  single  growths.  Such  tumors  do  not,  as  a  rule, 
afford  any  definite  localizing  symptoms  by  which  an  operation  can  be 
guided  anyway  and  so  the  diagnosis  of  the  single  tumor  is  the  great 
desideratum  after  all.  It  is  not  always  easy  by  any  means  to  deter- 
mine what  sort  of  a  growth  the  patient  is  afflicted  with.  Certain  gen- 
eral infectious  states,  such  as  syphilis  and  tuberculosis,  will  afford  a 
strong  presumption  as  to  the  nature  of  the  neoplasm.  The  existence 
of  tumors  in  other  parts  of  the  body,  like  cancer  of  the  breast,  actino- 
mycosis of  the  jaw,  hydatids  of  the  liver,  presupposes  the  same  sort 
of  a  tumor  in  the  brain.  Tubercle  and  gliomata  occur  most  frequently 
in  the  cerebellum  and  brain  stem ;  sarcomata  at  the  base  of  the  brain 
and  outside  of  it;  syphilomata  in  the  cortex.  The  rapidity  of  growth, 
general  course  and  extension  of  the  tumor  help  slightly  to  suggest  its 
nature.  Cerebral  gliomata  are  slow  and  gradual  in  their  development. 
Tumors  that  are  rapid  at  first  and  then  stationar}-  are  probably  tuber- 
culous. The  results  of  treatment  will  occasionally  determine  a  syph- 
ilitic neoplasm  from  all  other  varieties. 

The  main  diseases  from  which  intracranial  tumor  is  to  be  care- 
fullv dift'erentiated  are  epilepsy,  migraine,  hvsteria.  alcohoHsm,  lead 
intoxication,  abscess,  intracranial  aneurism,  dementia  paralytica,  acute 
encephalitis,  disseminated  cerebrospinal  sclerosis  and  melancholia.  The 
reader  is  referred  to  the  sections  upon  these  various  affections  for 
their  dififerentiation  from  tumor. 

Lumbar  puncture  has  been  found  useful  in  the  diagnosis  of  a  few 
obscure  cases.  Increased  pressure,  leucocytosis  and  the  presence  of 
bacteria  mav  point  to  a  tumor  and  meningitis,  though  their  absence 
does  not  exclude  the  former. 

Latelv  skiagraphy  has  been  em-ployed  to  locate  a  cerebral  tumor. 
In  some  instances,  particularly  when  the  growth  was  superficial  or 
near  the  vertex,  the  shadow  was  reassuring.  In  deep  tumors_  the 
Rontgen  rav  does  not  seem  to  be  of  much  availability.  Metal  objects 
such  as  shot  and  bullets  are  much  more  distinctly  seen  in  skiagraphs 
than  are  the  ordinarv  tumors. 

Progxosis. — The  course  of  brain  tumor  is  usually  a  prolonged 
one,  ranging  from  a  few  months  to  a  number  of  years.  Jackson  re- 
ported a* glioma  that  had  apparently  lasted  for  ten  years,  and  Osier 
one  in  which  Jacksonian  symptoms  had  persisted  for  fourteen  years. 
Most  of  the  cases  run  their  career  in  about  two  or  three  years.  The 
duration  of  the  tumor  depends  upon  its  nature  somewhat  and  the  ter- 
mination of  the  case  is  often  effected  by  the  destruction  of  the  neigh- 


930  THE   NON-NEURONIC  DISEASES 

boring  brain  substance.  Glioniata  and  fibromata  are  the  most  en- 
during tumors.  Especially  prolonged  are  cholesteotoma  and  angioma. 
Carcinoma,  some  varieties  of  glioma  and  soft  sarcoma  are  apt  to  be 
rapid.  Tubercle,  especially  when  it  appears  in  childhood,  and  even 
other  forms  of  tumor,  have  become  stationary.  Syphiloma  is  the  only 
tumor  that  seems  capable  of  disappearing  entirely,  and  then  only  un- 
der treatment.  It,  as  well  as  partly  degenerated  gliomata,  may  leave 
permanent  residua.  By  discharging  their  degenerative  debris  through 
the  nose  and  mouth,  the  effects  of  certain  growths  have  been  quite 
ameliorated.  Very  rarely  a  brain  tumor  m.ay  become  encapsulated 
or  atrophied,  with  a  recession  of  its  symptoms.  In  other  cases  after 
a  long  period  of  quiescence  or  slow  progress  it  may  suddenly  light 
up  most  violent  symptoms  with  coma  and  the  patient  pass  quickly  to 
his  death.  Altogether  tubercle  in  cliildren  and  gummata  in  adults 
offer  the  most  favorable  prognosis ;  rapidly  progressing  gliomata  and 
sarcomata  the  most.  A  sarcoma  may  prove  fatal  in  six  months.  Lo- 
cation of  the  tumor  has  much  to  do  with  the  prospect  of  the  patient's 
continued  existence.  Bulbar  tumors  are  particularly  dangerous. 
Subsidence  of  the  headache,  and  recession  of  the  optic  neuritis,  are 
favorable  signs  of  a  possible  recession  or  stationar}'  condition  in  the 
neoplasm,  or  at  least  its  environment.  Marked  mental  stupor,  con- 
vulsions, severe  vomiting,  rapid  and  intense  optic  neuritis  and  apoplec- 
tic seizures  are  bad  omens.  I  have  seen  a  marked  recession  of  all 
symptoms  with  an  ultimate  optic  atrophy  remaining  in  a  case  which 
several  years  ago  had  been  told  by  several  competent  neurologists  that 
he  could  not  possibly  live  the  year  out. 

Our  prognosis  should  always  be  made  guardedly  in  cases  of  brain 
tumor.  A  slow,  chronic  optic  neuritis  indicates  that  the  disease  will 
probably  be  of  slow  progression. 

Spontaneous  recovery  has  been  seen  in  the  parasitic  tumors,  and 
spontaneous  metamorphosis  and  retrogression  are  believed  by  some 
to  occur  sometimes  in  tubercle. 

It  is  believed  that  some  reported  cases  of  the  disappearance  of 
all  symptoms  of  brain  tumor  were  cases  of  Quincke's  serous  menin- 
gitis or  idiopathic  internal  hydrocephalus. 

Death  results  from  bulbar  symptoms,  exhaustion,  mfection,  com- 
plications and  intercurrent  maladies. 

Treatment. — Every  case  of  tumor  presents  a  study  for  medical 
and  surgical  treatment.  In  this  is  included  the  question  of  radical 
cure  or  only  amelioration.  In  most  cases  the  entire  treatment  of  the 
case  resolves  itself  into  the  management  of  the  patient  and  his  comfort, 
without  any  hope  or  attempt  at  modifving  in  the  least  the  morbid 
growth. 

The  administration  of  medicines  Avill  have,  therefore,  for  its 
twofold  object  the  eradication  of  the  tumor  and  the  relief  of  the  pa- 
tient's sufferings.  A  clear  comprehension  of  the  limitations  of  the 
medical  treatment  of  brain  tumor  will  not  only  lead  to  the  avoidance 
of  some  ridiculous  errors  and  absurd  logic  but  it  will  enhance  the 
value  and  efficacy  of  the  small  powers  with  the  limitations.  A  mere 
temporary  relief  of  the  headache  will  not  be  interpreted  then  as   a 


THE   XOX-NEUROXIC  DISEASES 


931 


cure, _  a  diminution  of  the  convulsions  will  not  be  looked  upon  as  a 
hopeful  sign  of  the  disappearance  of  the  neoplasm,  nor  will  the  diag- 
nosis previously  well  founded  be  shaken  by  mere  temporary  changes 
in  the  general  clinical  picture.  On  the  other  hand,  what  can  be  done 
by  medicinal  agents  in  a  tew  cases  will  be  so  sharply  defined  that  there 
will  be  no  hesitancy  or  lack  of  energ>-  in  applying  the  few  effective 
measures  in  the  properly  selected  cases.  Therapeutic  sins  of  omis- 
sion as  well  as  commission  are  sometimes  strikingly  enacted  in  cases 
of  brain  tumor.  In  no  disease  is  prompt,  thorough,  correct  treatment 
so  much  of  a  desideratum,  and  in  no  disease  are  the  indications  for 
it  more  obscure  sometimes.  Time  must  not  be  wasted  with  medicines 
if  the  tumor  falls  into  the  operable  class  soon  to  be  mentioned.  Sur- 
gery must  not  be  coquetted  with  if  the  tumor  is  amenable  to  medical 
treatment  or  is  inoperable.  Symptomatic  relief,  by  all  available  and 
surgical  means,  must  be  promptly  and  fulsomely  given  if  all  hope  of 
affecting  the  tumor  itself  is  past.  In  a  word,  given  a  correct  diagno- 
sis of  the  location  and  nature  of  the  growth,  and  a  thorough  appre- 
ciation of  its  proper  relationship  to  medical  and  surgical  interven- 
tion, the  treatment  should  be  prompt,  thorough,  rational  and  perma- 
nent. 

The  treatment  of  syphUomata  by  appropriate  medication  is  not 
only  successful  but  it  furnishes  us  sometimes  with-  some  of  the  most 
brilliant  results  known  to  medical  science.  The  disappearance  of  some 
of  the  most  threatening  symptoms  is  accomplished  almost  as  if  bv 
magic.  The  more  recent  the  tumor  and  the  shorter  the  time  that  the 
focal  symptoms  have  existed,  the  more  complete  and.-  satisfactorv  is 
the  cure.  After  a  syphilitic  growth  has  existed  for  a  long  time  and 
irreparable  changes  have  taken  place  in  the  brain  tissue,  no  treatment 
can  be  expected  to  banish  the  manifestations  that  depend  upon  those 
changes.  And  yet  even  in  many  advanced  and  old  cases  of  this  sort, 
a  decided  and  grateful  retrogression  of  the  symptoms  is  often  brought 
about  by  antisyphilitic  treatment.  Every  case  that  presents  a  history 
or  suspicion  of  syphilis  should  be  at  once  put  upon  antispecific  reme- 
dies. The  iodide  of  potash,  started  at  twent\-  grains  three  times  a  day, 
should  be  rapidly  increased  until  two  or  three  hundred  grains  a  day 
are  administered.  If  in  a  week  or  two  this  is  not  accompanied  by  some 
change  for  the  better  in  the  symptoms,  mercurial  inunctions  should 
be  added  to  the  regimen.  For  details  of  the  treatment,  consult  the 
chapter  on  cerebral  syphilis.  In  the  case  of  tumor  there  is  not  any 
ground  for  fear  in  the  use  of  this  heroic  antisyphilitic  medication  as 
there  may  be  in  the  degenerative  conditions  of  the  parasyphilitic  dis- 
eases, locomotor  ataxia  and  paretic  dementia.  Within  reasonable  lim- 
its, such  as  would  undoubtedly  show  some  results  in  a  genuine  case  of 
syphiloma,  it  can  do  no  possible  harm  whatever  the  tumor  may  be. 
Nay.  more,  it  is  a  fact  that  even  in  non-syphilitic  neoplasms  the  iodide 
of  potash  has  very  often  caused  a  noticeable  amelioration  of  the  head- 
ache and  other  symptoms.  Hence  it  is  good  practice  to  test  for  a 
short  time  with  antisyphilitic  medication  all  cases  of  tumor  in  which 
there  is  a  shadow  of' a  doubt  about  its  specific  origin,  and  in  which 
the  evidences  do  not  point  most  emphatically  aAvay  from  syphiloma. 


932  THE   NON-NEURONIC  DISEASES 

By  such  a  procedure  under  these  circumstances  there  is  everything  to 
gain  and  nothing  to  lose. 

It  is  extremely  doubtful  whether  any  other  than  syphilitic  tumors 
can  be  directly  affected  by  internal  medication.  Cases  of  improve- 
ment and  even  cure  have  been  reported  in  tubercle  by  the  use  of  cod 
liver  oil,  tonics,  rest  and  a  general  hygienic  mode  of  life.  Gowers  says 
that  more  than  once  he  has  known  the  symptoms  of  cerebral  tubercle, 
steadily  increasing  under  country  air  and  abundant  food,  to  become 
permanently  arrested  when  the  patient  was  taken  into  a  London  hos- 
pital and  cod  liver  oil  and  iron  given.  It  is  known,  however,  that  this 
class  of  morbid  growths  very  often,  after  a  period  of  rapid  and  rather 
violent  activity,  become  stationary,  and  especially  so  when  the  gen- 
eral constitution  is  put  in  the  best  condition  of  health.  These  happy 
results  are  most  attainable  in  children,  in  whom  it  is  believed  that 
tubercle  has  been  miade  to  disappear  completely.  Little  as  we  know 
about  the  reparative  processes  of  the  treatment  in  these  cases,  the 
latter  is  apparently  so  fortunate  in  some  few  instances,  that  it  recom- 
mends itself  for  all  cases  of  tubercle.  The  general  hygienic  and  tonic 
treatment  can  only  be  of  advantage  to  all  cases  of  tumor,  tuberculous 
or  otherwise.  It  is  to  be  hoped  that  some  specific  remedy  will  be  dis- 
covered some  day  to  act  upon  these  tubercles  as  the  iodides  act  upon 
syphilomata.  The  tuberculins  that  have  lately  been  experimented 
with  in  tuberculosis  of  the  lungs  and  joints,  have  not  succeeded  in 
giving  any  very  promising  results  in  cerebral  tuberculosis. 

Arsenic  has  been  recommended  and  said  to  have  shown  a  cura- 
tive power  in  a  few  cases  of  sarcoma.  It  is  a  tonic^  as  we  all  know, 
and  affects  powerfully  the  metabolism  of  the  body.  If  it  only  strength- 
ens the  organism  so  as  to  give  it  a  fighting  capacity  against  these 
growths,  or  if  it  assists  in  their  transformation  into  more  stationary 
forms  such  as  fibrosarcoma,  it  is  a  most  available  agent  and  should 
be  given  a  fair  trial.    The  same  statements  apply  to  phosphorus. 

No  other  tumors  than  those  just  mentioned  respond  to  medical 
treatment  and  so  far  as  v/e  know  no  other  remedy  has  any  direct 
effect  whatever  on  intracranial  neoplasms.  Symptomatic  treatment 
therefore  constitutes  the  only  field  for  the  further  use  of  internal 
medication.  This,  however,  is  of  great  importance  and  may  be  called 
for  whether  an  operation  be  a  part  of  the  question  or  not.  The  head- 
ache is  the  chief  symptom  that  calls  for  relief.  Most  of  the  remedies 
that  are  useful  in  other  forms  of  cephalalgia  are  distinguished,  as  a 
rule,  for  their  inefiicacy  in  this  form.  Hence  in  most  cases  nothing 
but  morphine  will  avail.  To  be  sure  there  is  always  the  danger  of 
the  formation  of  the  morphine  habit  to  be  taken  into  serious  consider- 
ation. If  the  nature  and  location  of  the  tumors  are  not  clear  and  if 
there  is  a  probability  that  it  may  prove  to  be  operable  when  it  an- 
nounces itself  a  little  more  definitely,  morphine  had  better  be  with- 
held and  temporizing  undertaken  with  other  drugs.  Unless  the  head- 
ache is  excruciating,  threatening  to  drive  the  patient  to  suicide,  as  it 
almost  does  sometimes,  all  other  possible  means  of  relief  had  better 
be  tried  first  before  morphine  is  resorted  to.  I  prefer  to  try  the  fol- 
lowing remedies  in  the  order  mentioned:  cannabis  indica,  phenacetin. 


THE   NON-NEURONIC  DISEASES  933 

acetanelid,  antipyrin  and  large  doses  of  sodium  salicylate.  Other 
measures  commonly  employed  in  the  management  of  headache  should 
not  be  neglected.  An  ice  bag,  cold  water  coil  or  hot  cloths  may  be 
applied  to  the  head.  A  mustard  foot  bath  and  a  sinapism  to  the  back 
of  the  neck  may  help  somewhat.  Purgation,  free  diuresis  and  diaphor- 
esis, even  leeches  and  venesection  may  be  considered.  x\s  a  rule  the 
case  will  prove  to  be  desperate  and  resort  will  have  to  be  had  to  mor- 
phine. In  inoperable,  severe  or  moderately  severe  cases  with  an  un- 
favorable prognosis  constantly  hanging  over  them,  it  seems  to  me 
more  beneficent  to  establish,  if  need  be,  the  morphine  habit  and  give 
the  patient  some  comfort  the  few  months  or  years  he  has  to  live,  than 
to  allow  him  to  be  harassed  and  worn  out,  perhaps  sooner  than  he 
would  be  even  with  the  morphine  habit,  by  the  increasing  and  intol- 
erable headache,  vertigo,  vomiting  and  convulsive  seizures.  For  these 
latter  symptoms  there  is  sometimes  mitigation  in  full  doses  of  the  bro- 
mides, chloral  and  other  narcotic  antispasmodics. 

In  nearly  all  cases  the  question  of  surgical  intervention  will  arise. 
In  not  more  than  five  per  cent,  of  the  cases  will  the  tumor  be  found 
to  be  operable.  The  early  enthusiam  following  the  work  of  Hors- 
ley,  Macewen,  Godlee  and  others  has  calmed  down  considerably,  but 
yet  when  we  consider  what  is  being  done  at  the  present  day  by  such 
operators  as  Wernicke,  Horsley,  Bergmann,  Keen  and  others,  and 
compare  the  promising  outlook  offered  by  their  results  with  the  utter 
hopelessness  with  which  these  cases  were  regarded  only  a  few  decades 
ago,  we  may  congratulate  ourselves  without  undue  elation  upon  the 
splendid  advances  of  surgery. 

Five  per  cent,  is  not  a  large  number  of  cases  amenable  to  oper- 
ation but  that  is  not  the  fault  of  surgery,  it  is  in  a  large  measure  the 
result  of  the  location  and  nature  of  these  tumors.  Multiple  tumors  are 
inoperable ;  so  also  are  malignant  and  metastatic  growths.  Deep 
neoplasms  usually  cannot  be  reached  without  almost  certain  risk,  hence 
they  cannot  be  undertaken.  Large  infiltrating  growths  must  also  be 
left  alone.  The  infiltration  of  a  small,  superficial  tumor  is  not  a  ground 
for  its  being  regarded  as  inoperable.  The  most  favorable  tumors  are 
those  that  are  single,  superficial,  not  too  large,  more  or  less  encapsu- 
lated and  distinctly  localizable.  These  are  the  fibromata,  growing  from 
the  dura  and  compressing  the  brain  in  and  about  the  motor  zone. 
Small  tumors,  early  diagnosed,  offer  the  best  chances  also,  though 
large  growths  have  been  removed  piecemeal  in  successive  operations. 
In  some  cases  in  which  the  localization  of  the  tumor  is  somewhat  in 
doubt  an  exploratory  operation  is  to  be  recommended.  Tumors  of 
the  occipital  lobe,  causing  hemianopsia,  and  those  in  the  temporal 
lobe  which  cause  auditory  disturbances  may  be  regarded  as  amenable 
to  the  knife.  As  the  opening  of  the  cranial  cavity  is  always  a  serious 
procedure,  the  relatives  should  always  be  informed  of  all  possible 
accidents.'  Thev  should  also  be  made  well  acquainted  with  the  se- 
quelae that  are  fikelv  to  follow  the  removal  of  the  tumor  or  excision 
of  the  brain  substance  with  its  removal.  The  continuance  of  the 
paralysis   should  be  carefully  explained  beforehand  to   them,   if   the 


934  THE    NON-NEURONIC  DISEASES 

Operator  wishes  to  avoid  most  awkward  questions  after  the  recovery 
of  the  patient  from  the  operation. 

In  some  cases,  focal  symptoms  alone  may  justify  an  operation. 
A  persistent  aphasia,  especially  if  it  be  progressive,  may  well  suggest 
a  trepanation  over  the  third  left  frontal  convolution. 

Cerebellar  tumors  do  not  encourage  one  very  much  to  operate. 
Their  removal  may  be  possible  in  adults  but  is  not  to  be  thought  of  in 
children.  The  trouble  is  that  if  the  tumor  is  in  the  lateral  lobe  it  does 
not  usually  produce  symptoms  until  it  is  too  large  for  surgical  in- 
tervention, and  if  it  is  in  the  middle  lobe  where  it  usually  causes  the 
liveliest  symptoms,  it  is  in  too  close  proximity  to  vital  centers  that  are 
liable  to  be  damaged  in  the  handling  of  the  growth.  Xevertheless  it 
is  to  be  remembered  that  both  Macewen  and  Parkin  operated  success- 
fully upon  a  cerebellar  tumor. 

The  symptomatic  treatment  of  brain  tumor  by  operation  is  always 
to  be  considered  when  the  removal  of  it  is  out  of  the  question.  Tre- 
phining, withdrawing  some  of  the  fluid  and  thus  lessening  the  intra- 
cranial pressure  have  afforded  teniporary  relief  of  the  headache,  stu- 
por and  optic  neuritis.  When  symptoms  are  severe  and  blindness  is 
threatened  one  can  readily  see  the  commendability  of  such  a  procedure, 
though  the  benefit  may  be  only  temporary. 

In  some  cases  the  ventricles  have  been  tapped  in  the  hope  of  re- 
lieving the  pressure  symptoms.  The  results  have  been  very  doubtful, 
however.  The  same  is  to  be  said  of  lumbar  puncture,  a  most  doubt- 
ful procedure. 

INTRACRANIAL  ANEURISM. 

« 

An  aneurism  is  a  variety  of  tumor,  soft,  pulsating,  attached  to  a 
bloodvessel,  and  terminating  usually  in  rupture  and  hemorrhage.  In- 
tracranial aneurisms  may  be  within  the  brain,  on  the  minute  terminal 
arterioles  that  penetrate  its  substance,  or  between  the  brain  and  the 
skull  on  the  large  arteries  foimd  there.  The  former  are  called  miliary 
aneurisms,  are  small  and  produce  no  symptoms  until  they  rupture  and 
allow  the  blood  to  pour  out  into  the  brain  substance.  They  are  of 
interest  chiefly  in  connection  with  intracranial  hemorrhage,  under 
which  head  they  have  been  considered.  The  large  aneurisms  may  be 
formed  anywhere  where  there  is  a  large  vessel  in  the  intracranial 
cavity.  By  far  the  greater  number  of  them  occur  on  the  large  arteries 
at  the  base  of  the  brain. 

Etiology. — The  causation  of  intracranial  aneurisms  is  in  the 
main  the  same  as  that  of  aneurismal  dilatations  elsewhere  in  the 
bod>^  Men  are  more  subject  to  the  disease  than  women,  in  the  pro- 
portion of  about  three  to  two.  The  reason  for  this  is  probably  not  an 
inherent  difference  between  the  sexes,  but  a  difference  in  their  modes 
of  life.  The  greater  tendency  to  exposure,  strain  and  dissipation  in 
men  leads  to  a  greater  deterioration  of  the  walls  of  their  arteries. 
This  is  shown  in  another  wa}'  when  the  age  at  which  these  aneurisms 
occur  are  considered.  For  instance,  they  all  appear  between  the  years 
of  ten  and  sixtv,  and  within  this  period  the  greater  number  show 
themselves  during  the  first  half  or  when  exposure,  strain  and  dissipa- 


THE   NON-NEURONIC  DISEASES  935 

tion  are  most  rife.  In  some  families  there  seems  to  run  a  slight  in- 
heritance toward  arterial  disease.  This  has  been  mentioned  before  in 
connection  with  intracranial  hemorrhage.  The  nature  of  this  con- 
genital influence  we  know  absolutely  nothing  about.  It  is  an  inheri- 
tance not  of  the  disease  itself  but  of  the  predisposition  to  the  disease, 
a  very  important  distinction  to  keep  always  in  mind.  With  or  with- 
out such  a  predisposition  an  aneurism  may  be  initiated  by  various 
eX'Citing  causes  chief  of  which  are  blows,  shocks  and  other  traumata  to 
the  head. 

The  immediate  cause  of  the  dilatation  is  a  diseased  state  of  the 
arterial  walls.  The  muscular  and  elastic  tissue  is  diminished  and  re- 
placed by  a  fibroid  and  otherwise  degenerated  tissue.  Under  the 
pulsations  and  pressure  of  the  blood  stream  the  wall  distends  but  does 
not  contract  again  as  it  should.  In  the  course  of  time  the  bulging  be- 
comes larger,  more  permanent  and  finally  constitutes  an  aneurism  with 
thin  walls,  pulsating  and  variable  in  shape. 

Primary  degeneration,  syphilis  and  emboli,  especially  when  in- 
fected, are  the  chief  factors  in  the  production  of  the  disease  of  the 
vascular  walls.  The  first  is  largely  an  accompaniment  of  old  age 
and  with  traumatism  is  perhaps  the  cause  of  most  of  the  aneurism.s 
in  other  parts  of  the  body;  the  second  and  third  are  conditions  of  early 
adult  and  middle  life  and  are  the  principal  elements  in  the  produc- 
tion of  intracranial  dilatations.  The  primary  degeneration  may  be 
ahroid  or  atheromatous ;  even  extensive  fatty  and  calcareous  break- 
down may  be  seen.  Specific  arteritis  is  a  condition  so  well  known 
that  it  need  only  be  mentioned  here.  Emboli,  especially  infected  em- 
boli, are  the  products  of  endocarditis.  Minute  vegetations  break  off 
from  the  diseased  valves  of  the  heart,  float  away  to  the  brain  on  the 
blood  current  and  finally  become  lodged  at  the  bifurcation  of  some 
artery.  Obstruction  takes  place,  the  vessel  becomes  closed  and  oblit- 
erated in  front  of  the  obstruction,  inflamed  and  degenerated  behind 
it.  The  cause  of  this  inflammation  is  irritation  and  infection.  These 
causes  of  the  arterial  disease  explain  clearly  why  the  basilar  and  ver- 
tebral system  of  vessels  are  so  much  more  frequently  affected  in  ad- 
vanced years  while  the  anterior  and  middle  cerebrals,  especially  the 
latter  on  the  left  side,  are  seen  to  be  the  choice  site  of  the  aneurism  in 
earlier  years. 

Pathology. — Scarcely  more  need  be  said  upon  the  pathology  of 
this  condition  than  what  has  been  mentioned  under  the  etiology.  The 
arteries  that  are  affected  in  the  order  of  their  frequency  are  the  mid- 
dle cerebral,  basilar,  internal  carotid,  anterior  cerebral,  posterior  com- 
municating, anterior  communicating,  vertebral,  posterior  cerebral  and 
inferior  cerebellar.  Those  of  the  left  side  far  outnumber  those  of 
the  right.  Within  the  central  ganglia  or  ventricles  aneurism  is  very 
rare. 

Usually  the  sweUing  is  single  though  a  multiple  condition  may 
obtain.  Its  histological  attributes  are  the  same  as  all  aneurisms  and 
need  not  be  discussed  here.  In  developing  it  compresses  and  more  or 
less  damages  the  neighboring  brain  tissue.  Nerves  in  juxtaposition 
may  also  undergo  destruction.     Even  the  bone  tissue  may  be  eroded 


936  THE   NON-NEURONIC  DISEASES 

by  its  steady  pressure.  The  presence  of  the  tumor  is  generally  rec- 
ognized by  the  symptoms  of  this  collateral  damage  to  bone,  brain  and 
nerve. 

After  a  time  the  aneurismal  sac  bursts  and  a  superficial,  com- 
pressing, severe  hemorrhage  occurs,  the  blood  escaping  in  most  cases 
into  the  membranes  at  the  base  of  the  brain.  This  hemorrhage  may 
be  continuous  or  intermittent,  through  a  small  or  a  large  opening.  The 
ventricles  may  become  gradually  filled  with  the  outpouring  blood,  or 
the  latter  may  tear  or  disintegrate  its  way  into  the  brain  matter.  From 
the  internal  carotid  it  may  burst  into  the  cavernous  sinus. 

Symptoms. — The  symptoms  of  an  intracranial  aneurism  are  prac- 
tically those  of  a  tumor.  They  are  general  and  focal.  The  terminal 
hemorrhage  has  its  ow^i  special  symptomatology  which  is  closely  sim- 
ilar to  that  of  meningeal  apoplexy.  Headache  is  of  a  pulsating  char- 
acter, constant,  intense  and  accompanied  often  by  local  tenderness  in 
some  spot.  Vertigo,  giddiness,  vomiting,  projectile  in  character,  stu- 
por and  occasional  convulsions  are  all  characteristic  symptoms  and 
are  due  to  the  general  intracranial  increase  of  pressure.  Cranial 
nerve  palsies  are  frequent,  though  optic  neuritis  is  not  common.  The 
usual  aneurismal  murmur  is  not  often  produced  by  the  intracranial 
variety  of  dilatation.  It  was  noted  in  aneurism  of  the  internal  carotid 
and  left  vertebral  arteries.  So  many  conditions  give  rise  to  cranial 
murmurs  that  the  symptom  is  not  very  valuable  here  for  diagnostic 
purposes.  A  pulsating  vascular  murmur  may  be  heard  sometimes  in 
cases  of  tumor  located  near  and  compressing  a  large  artery.  It  mav 
be  noted  in  hvdrocephalus,  anaemia,  rachitis,  and  even  in  perfectly 
healthy  children.  Exophthalmic  goitre  and  neoplastic  compression 
of  the  sympathetic  nerve  have  provoked  cephalic  murmurs. 

These  general  symptoms  are  the  offspring  mostly  of  moderately 
large  aneurisms.  With  them  may  be  associated  certain  focal  symp- 
toms indicating  where  the  tumor  is  located.  In  small  aneurisms  it 
may  rarely  happen  that  slight  focal  symptoms  are  presented  but  no 
general  manifestations. 

The  localisation  of  an  aneurism  by  means  of  its  focal  exhibitions 
follows  the  same  general  rules  that  the  localization  of  an  ordinarv  tu- 
mor follows.  Motor  and  sensory  disturbances  should  be  carefully 
noted  and  compared  with  one  another  and  their  correlation  with  the 
areas  of  the  brain  should  be  made  in  accordance  with  the  known  facts 
of  brain  physiology. 

When  the  aneurism  is  in  the  internal  carotid  artery  there  is  com- 
pression of  the  optic  nerves,  the  oculomotor  nerves,  the  olfactory  and 
the  trigeminus.  The  sight  of  one  eye  therefore  fails,  ptosis  occurs 
on  the  same  side,  the  sensibility  of  the  eye  is  lost  with  all  its  usual 
consequences  and  the  power  of  smelling  is  damaged.  Hemiplegia  may 
occur  from  the  pressure  backward  on  the  crus  cerebri.  On  the  left 
side  the  speech  center  may  be  implicated  with  the  production  of  motor 
aphasia.  The  free  communication  between  the  ophthalmic  and  facial 
veins  usually  quickly  relieves  what  transient  fullness  may  occur  in 
the  retinal  veins  from  pressure  on  the  cavernous  sinus.  Michel  finds 
that  the  occasional  optic  neuritis  that  is  seen  is  not  due  to  compression 


THE   NON-NEURONIC  DISEASES  937 

but  to  extension  of  inflammation  from  the  vicinity  of  the  aneurism. 
When  rupture  takes  place,  as  it  does  in  a  Httle  less  than  half  the  cases, 
the  cavernous  sinus  is  invaded  and  a  pulsating  exophthalmus  may 
result. 

Swellings  on  the  anterior,  middle  and  posterior  cerebral  arteries 
can  be  surmised  from  symptoms  pointing  to  implication  of  the  ad- 
jacent cortical  centers.  With  the  first,  for  instance,  the  symptoms  are 
the  same  as  those  in  aneurism  of  the  internal  carotid  except  for  the 
involvement  of  the  third  nerve.  Aneurism  of  the  middle  cerebral,  or 
artery  of  the  Sylvian  fossa,  provokes  hemiplegic  convulsions  and 
speech  disturbances  especially.  The  cranial  nerves  are  notably  free 
from  involvement.  Being  near  the  motor  zone,  Jacksonian  symptoms, 
followed  by  monoplegia  and  hemiplegia,  are  the  characteristic  features. 
Sometimes  they  cause  no  outward  evidences  of  their  presence.  About 
two-thirds  of  them  rupture.  A  posterior  cerebral  aneurism  is  apt  to 
compress  the  upper  part  of  the  pons,  the  crus  cerebri  temporo-sphe- 
noidal  lobe,  the  third  and  sixth  nerves.  Alternating  hemiplegia  there- 
fore is  to  be  expected. 

An  enlargement  of  the  anterior  coniniunicating  artery  produces, 
as  a  rule,  no  symptoms,  because  it  is  usually  small  and  compresses 
merely  the  inner  sides  of  the  frontal  lobes.  If  it  is  large  the  olfactory 
and  optic  nerves  may  be  affected. 

When  the  posterior  communicating  vessel  is  the  seat  of  the  dilata- 
tion hemianopsia  may  be  produced  by  compression  of  the  optic  tract. 
The  temporo-sphenoidal  lobe  and  basal  ganglia  may  be  compressed. 
The  third  nerve  is  the  one  most  commonly  implicated.  Hemiplegia 
is  rare. 

Vertebral  aneurisms  do  not  often  cause  serious  trouble.  In  fact 
the  condition  in  these  arteries  is  usually  one  of  gradual  extensive 
dilatation  of  the  artery  than  that  of  a  typical  aneurism  and  the  symp- 
toms, such  as  they  are,  are  notable  for  their  slowly  progressive  char- 
acter. The  symptoms  are  more  or  less  similar  to  those  of  basilar 
aneurism. 

The  basilar  artery  is  a  frequent  site  of  both  aneurism  and  uniform 
dilatation.  Its  close  proximity  to  the  pons,  the  medulla  and  the  cere- 
bral crura  indicates  the  possible  symptomatology.  The  general  s}-mp- 
toms,  especially  the  headache  and  vertigo,  are  unusually  pronounced. 
Pontile  symptoms,  such  as  alternating  hemiplegia,  upper  cranial  nerve 
involvement,  and  forced  movements,  occur  when  the  swelling  is  high 
up.  Bulbar  symptoms  with  dysarthria,  dysphagia,  cardiac  and  respira- 
tory difficulties  combined  with  hemiplegia  appear  when  the  enlarge- 
ment is  lower  down.  Internal  hydrocephalus  occasionally  occurs.  Con- 
vulsions are  rare.  Occasional  apoplectic  attacks  sometimes  happen. 
About  half  the  cases  rupture. 

Cerebellar  aneurisms  are  of  no  interest  clinically. 

Prognosis. — An  intracranial  aneurism  is  a  most  dangerous  pos- 
session. The  greater  number  of  those  that  have  produced  sufficient 
symptoms  to  enable  them  to  be  diagnosed  during  life  have  sooner  or 
later  terminated  by   rupture.     The   duration   of     these   enlargements 


938  THE   NOX-NEURONIC  DISEASES 

ranges  from  a  few  weeks  to  six  years.  An  occasional  spontaneous 
cure  has  resulted  from  the  filling  of  the  sac  with  a  clot. 

Treatment. — The  dyscrasia  that  causes  the  disease  in  the  walls 
of  the  arteries  would  seem  to  invite  treatment  but  it  is  hardly  to  be 
expected  that  such  treatment  will  modify  an  aneurism  after  it  has  once 
developed  from  such  a  vascular  condition.  Syphilitic  history  there- 
fore recommends  the  use  of  potassium  iodide  and  mercury  to  prevent 
at  least  the  extension  of  the  disease  in  the  arterial  walls.  Atheroma 
and  other  degenerative  conditions  may  be  attacked,  but  little  real  benefit 
will  accrue  thereby  to  the  aneurism.  The  use  of  potassium  iodide  in 
moderate  dosage,  thirty  or  fort}-  grains  a  day,  has  seemed  to  favor 
intra-aneurismal  coagulation  and  spontaneous  cure  in  a  few  instances. 
It  should  be  tried.     Ergot  is  useless  and  irrational. 

In  the  general  regimen  and  mode  of  living  everything  should  be 
done  to  avoid  momentary  or  continuous  increase  in  the  intracranial 
blood  pressure.  Tight  bands  about  the  neck  must  be  eschewed.  Strain- 
ing at  stool,  giving  way  to  passionate  anger,  coughing,  running  to 
catch  a  train,  must  not  be  permitted.  Stimulants,  like  alcohol  and 
coffee  and  tea,  must  be  left  alone.  An  even,  quiet  existence  with  a 
bland,  nutritious  dietary  and  little  drink  should  be  constantly  main- 
tained. In  sleeping  the  head  should  be  elevated  and  in  waking  never 
extended  or  flexed  on  the  body  too  far. 

Surgical  measures  have  been  tried  for  the  cure  of  these  aneurisms 
but  without  any  very  flattering  results.  Only  in  the  rarest  cases  is 
the  diagnosis  sufficiently  precise  to  cause  surgery  even  to  be  thought 
of.  Dilatations  on  the  internal  carotid  have  been  diagnosed  and  the 
artery  itself  ligated  with  success.  The  vertebrals  have  been  tied  for 
a  basilar  aneurism.  The  risk  of  the  operation,  great  as  it  is,  is  less 
than  that  of  the  aneurism.  Lumbar  puncture  must  be  discountenanced. 
IMost  disastrous  results  have  followed  it.  When  rupture  occurs,  the 
physician's  special  services  are  at  an  end. 

HYDROCEPHALUS. 

This  is  another  term  representing  merely  a  symptomatic  con- 
dition, which,  it  is  to  be  hoped,  will  ere  long  be  allowed  to  follow 
the  terms  paralysis,  apoplexy  and  Landry's  paralysis  in  neurological 
nosology^  It  means  merely  dropsy  of  the  brain,  represents  an  accu- 
mulation of  fluid  and  is  the  result  of  a  considerable  number  of  dis- 
eased conditions.  It  is  never  strictly  a  primary  condition.  Its  imme- 
diate causes  may  be  congenital,  developmental  anomalies,  mechanical 
obstructions  or  meningeal  inflammations.  It  is  therefore  both  a  con- 
genital and  an  acquired  condition.  From  the  standpoint  of  duration, 
the  former  is  sometimes  spoken  of  as  chronic,  and  the  latter  as  acute, 
hydrocephahts.  This  is  clearly  an  injudicious  use  of  adjectives,  for 
acquired  hydrocephalus  may  be  chronic  and  a  congenital  form  may  run 
a  rapid,  acute  course.  On  the  basis  of  pathology,  when  the  fluid  occu- 
pies the  ventricles,  the  hydrocephalus  is  said  to  be  internal;  when  it 
is  outside  of  the  brain  in  the  subdural  space  it  is  spoken  of  as  external. 
Internal  hydrocephalus  has  a  varied  etiology,  as  will  be  seen  later  on. 


THE  NON-NEURONIC  DISEASES  939 


External  hydrocephalus,  or  hydrocephalus  ex  vacuo,  is  seen  in  senile 
conditions,  atrophy  of  the  brain,  hemorrhages,  encephalomalacia  and 
sclerotic  conditions,  in  cancer  and  other  cachetic  diseases,  in  chronic 
nephritis,  chronic  alcoholism,  rickets,  meningeal  cysts  and  other 
■chronic  troubles  and  pathological  residua.  This,  of  course,  is  not  a 
true  dropsv,  but  rather  a  pathological,  secondary  effusion. 

It  will  be  practically  convenient,  though  somewhat  arbitrary,  to 
-discuss  the  malady  under  the  three  subheads,  as  Osier  does,  Serous 
Meningitis,  Congenital  Hydrocephalus  and  Acquired  Chrome  Hydro- 
cephalus These  are  all  internal  types  of  hydrocephalus.  The  ex- 
ternal types  might  be  added  as  a  fourth  subhead,  but  as  they  are  merely 
symptomatic  of  so  many  different  disease  states,  their  discussion  would 
be  an  unnecessary  recapitulation  of  what  has  been  said  under  the  head 
of  these  diseases  elsewhere.  ,     ,     ,  ,    , 

Serous  Meningitis.— This  is  a  form  of  internal  hydrocephalus 
whose  pathogenesis  is  obscure.  Quincke  has  studied  it  very  closely 
and  arrived  at  the  conclusion  that  it  is  due  to  a  simple  serous  inflam- 
mation of  the  meninges  of  the  ventricles  with  effusion,  analogous  to 
serous  pleuritis.  It  is  thus  an  ependymitis  and  one  wonders_  at  the 
significance  of  the  name  sometimes  applied  to  it,  idiopathic  internal 
hydrocephalus.  So  much  doubt  is  there  in  regard  to  its  inflammatory 
Tiature  that  Quincke  himself  likens  the  process  to  that  of  angioneurotic 
<Edema  of  Sie  skin,  and  speaks  of  it  as  an  angioneurotic  hydro- 
<:ephalus.  It  is  easy  to  understand  the  secondary  nature  of  the  effusion 
in  this  form  of  ventricular  dropsy  but  the  cause  and  nature  of  the 
primarv  trouble  in  the  ependyma  or  related  structures  are  far  from 
Ling  established.  In  acute  cases  the  ependyma  exhibits  "o  abnormal 
appearance  whatever;  in  the  chronic  cases  it  is  rough  and  thickened. 
tS'some  cases  distinct  signs  of  mflammation  appear,  not  only  m  the 
intracerebral  pia,  the  choroid  plexus,  but  in  the  cortical  pia  also  In 
he  latter  case'th;re  is  also  an  external  hydrocephalus.  One  hypothesi^ 
though  far  from  being  a  satisfactory  one,  attributes  the  ventricular 
effulon  to  the  closure  of  the  foramen  of  Magendie  by  the  simple 
S  meningitis.  The  disease  occurs  almost  as  frequent  y,  however, 
without  any  indications  of  meningitis,  interna    or  external. 

The  exudate  is  believed  to  arise  chiefly  from  the  choroid  plexus 
and  the  wahs  of  the  ventricles.  It  does  not  materia  ly  dififer  from 
?he  normrcerebrospinal  fluid.  If  its  specific  gravity  should  be  above 
1009  wTth  albumin 'present  m  larger  amo.mt  than  two  per  thousand, 
tumor  or  stasis  is  more  likely  to  be  the  original  cause  of  the  drops 
In  some  cases  it  has  been  thought  that  the  entire  disease  owed  its 
inception  to  a  trauma,  mental  strain,  alcoholism,  various  acute  infec- 

^-^-S."^^^^^  of  knowledge,  to  ^c. 

.atel^^rsify  this^orm  of  Mroceph.us^^^^^^^^^^^^^^ 


940  THE   XOX-XEUROXIC  DISEASES 

some  cases  inflammation,  in  others  mechanical  obstruction,  and  appa- 
rently in  a  considerable  number  of  cases,  a  developmental  functional 
defect  may  be  at  the  bottom  of  it.  Xo  name,  beyond  hydrocephalus, 
that  has  hitherto  been  given  to  it  is  strictly  correct. 

Symptomatically  there  seem  to  be  various  well-marked  types  of 
the  affection.  As  an  acute  trouble  it  closely  resembles  sometimes  either 
a  purulent  or  a  tuberculous  meningitis.  It  is  not  improbable  that  some 
reported  cures  of  the  latter  disease  have  been  cases  of  this  form  of 
hydrocephalus.  Headache  is  present.  There  are  signs  of  increased 
intracranial  pressure.  The  discs  are  choked.  The  pulse  is  retarded. 
The  neck  is  retracted.  The  fever  is  slight,  inconstant  and  usually  ab- 
sent. It  may  be  present  at  first  and  then  disappear.  In  some  cases 
loss  of  the  knee-jerk  has  been  observed.  Lumbar  puncture  may  aid 
much  in  the  making  of  a  differential  diagnosis.  In  meningitis  of  the 
purulent  or  tuberculous  type,  the  cephalalgia  is  apt  to  be  keener,  the 
retraction  of  the  neck  more  forcible  and  all  the  other  well  known 
signs,  such  as  occur  in  the  pupils,  m  Kernig's  phenomena,  in  the  stu- 
por, in  the  gait,  more  pronounced.  Excessive  visual  disturbance  points 
rather  to  the  hydrocephalic  condition.  Bacilli  in  the  cerebrospinal  fluid 
and  the  discovery  of  tuberculosis  or  local  infection  elsewhere  may 
clinch  the  diagnosis.  Sometimes  a  differential  diagnosis  is  absolutely 
impossible.  This  acute  hydrocephalus  usually  recovers  completely  or 
partially  in  a  few  weeks  or  passes  into  a  chronic  form  of  the  trouble. 

When  it  has  become  chronic,  this  form  of  cerebral  dropsy  is  very 
liable  to  be  mistaken  for  tumor  of  the  brain  and  cause  a  false  notion 
of  a  cure  of  the  latter  when  the  symptoms  have  disappeared.  Like 
tumor  it  provokes  both  general  and  focal  symptoms.  The  former  in- 
clude intense  headache,  slight  fever,  vomiting,  vertiginous  attacks,, 
somnolence,  stupor,  delirium,  retardation  and  acceleration  of  the  pulse. 
Optic  neuritis  with  choked  disc,  and  later  on  atrophy,  are  very  fre- 
quent manifestations.  Exophthalmos  may  occur.  Hemianopsia,  local 
spasms,  muscular  rigidity,  temporary  monoplegias  and  hemiplegias  and 
signs  of  cranial  nerve  involvement  are  among  the  more  important  focal 
symptoms.  As  the  clinical  presentations  of  this  hydrocephalus  have 
the  remarkable  property  of  undergoing  exacerbations  and  varying 
degrees  of  intensity  from  day  to  day,  they  can  be  distinguished  from  the 
progressive  symptoms  of  tumor.  Moreover  the  hydrocephalic  skull 
is  in  evidence  in  most  of  the  cases,  showing  that  though  the  cases, 
occur  mostly  in  adults  in  this  chronic  form  of  the  trouble  there  has 
been  all  along  a  congenital  predisposition.  This,  of  course,  is  not  the 
case  in  tumor. 

The  diagnosis  of  this  hydrocephalus  rests  primarily  upon  its 
pressure  symptoms,  its  characteristic  remissions  and  intermissions,  its 
temporary  focal  exhibitions  or  absence  of  them,  its  congenital  hydro- 
cephalic predisposition,  and  its  cranial  nerve  involvements.  The  nor- 
mal character  of  the  cerebrospinal  fluid  as  distinguished  from  the 
albuminous  fluid  of  tumor  is  helpful  in  making  a  differentiation  in  some 
cases.  In  children  the  diagnosis  is  less  difficult  than  in  adults  because 
the  hydrocephalic  deformities  of  the  head  are  more  prominent  in  them. 
The  total  clinical  picture,  studied  in  everv  possible  way  and  with  all 


THE   XOX-NEUROXIC  DISEASES  94I 

possible  aids  to  examination,  must  form  the  basis  for  the  diagnosis 
of  so  obscure  a  disease  rather  than  one  or  two  symptoms  only.  This 
picture  must  be  both  broadly  and  minutely  contrasted  with  that  pre- 
sented by  intracranial  tumor,  purulent  meningitis,  tuberculous  menin- 
gitis and  some  other  diseases.  Even  then,  unfortunately,  the  diagnosis 
cannot  be  made  positively  in  a  good  many  cases. 

Recovery  frequently  follows,  in  these  cases,  many  weeks  of  suf- 
fering. In  spite  of  the  presence  of  intense  headache"^,  vomiting,  stu- 
por and  optic  neuritis,  mercurial  treatment  has  eventuated  in  a  com- 
plete cure  after  several  weeks  or  months.  The  course  of  the  disease 
is  always  remittent.  Sometimes  it  becomes  chronic  and  in  children 
cannot  be  distinguished  from  the  ordinary  form  of  congenital  hydro- 
cephalus.    Death  occurs  rather  infrequently. 

Here  could  be  discussed  logically  some  cases  of  acquired  hydro- 
cephalns  that  run  a  course,  and  in  many  respect  are,  similar  to 
Quincke's  type  of  the  disease.  This  is  especially  true  of  some  of  the 
cases  of  secondary  external  hydrocephalus.  One  form  of  the  latter 
has  already  been  referred  to,  as  it  is  sometimes  regarded  as  primary 
and  aligned  with  similar  cases  of  so-called  angioneurotic  hydro- 
cephalus. Alost  of  the  cases,  however,  are  associated  with  atrophy 
of  the  brain,  which  is  supposed  to  cause  a  vacuum  with  resulting  effu- 
sion between  the  brain  and  the  skull.  Hence  the  name  hydrocephalus 
ex  vacuo.  Other  cases,  both  internal  and  external,  are  attributed  to 
trauma,  insolation,  congestion,  obstruction  of  the  ven^e  Galeni.  of  the 
aqueduct  of  Sylvius,  or  of  the  foramen  of  ^Monroe  by  various  neo- 
plasms, cysticerci,  cicatrices,  etc.  Purulent  and  tuberculous  menin- 
gitis after  the  same  manner  may  be  accompanied  by  dropsy  of  the 
brain,  as  also  may  phthisis,  nephritis,  marasmus  and  various  cachexige. 
In  many  of  these  cases  a  slight  hydrocephalus,  or  at  least  hydrocephalic 
tendency,  has  probably  existed  from  birth  and  the  causes  mentioned 
have  only  awakened  it  from  its  latency.  At  all  events  the  cases  'are 
not  in  any  way  distinctive  and  are  of  no  special  clinical  interest  be- 
yond that  of  the  disease  with  which  the  hydrocehalus  is  associated. 

Acquired  Chronic  Hydrocephalus. — This  then  is  the  affection  to 
which  what  has  just  been  said  is  largely  applicable.  It  is  always  sec- 
ondary, even  in  what  is  sometimes  called  the  primary  Or  idiopathic 
form  which  is  in  great  need  of  thorough  pathological  reinvestigation. 
Mechanical  obstructions  and  meningitis  are  the  primary  cause  of  the 
trouble  in  nearly  all  of  the  cases.  All  of  the  etiological  factors  in  this 
form  of  the  trouble  take  their  cue  from  the  etiology  of  the  primary 
cause.  In  adults,  of  course,  the  head  will  not  be  enlarged  though  there 
may  be  an  intense  degree  of  dropsy  present.  In  children  the  skull  may 
and  usually  does  undergo  early  and  steady  expansion.  Even  in  them 
the  enlargement  may  not  be  commensurate  with  the  severity  of  the 
other  symptoms.  The  brain  substance  may  be  so  compressed  and 
attenuated  that  the  ventricles  are  enormously  distended  while  the  gen- 
eral size  of  the  head  remains  about  normal.  The  external  appearances 
are  often  the  same  in  children  as  they  are  in  the  ordinary  congenital 
type  of  the  disease.  The  symptoms  are  extremely  numerous  and  varia- 
ble,  especially  in   the   adult.      They   are  those   chiefly  of   intracranial 


942  THE   XOX-XFX'RONIC  DISEASES 

pressure.  In  children  idiocy  and  imbecility  occur,  in  adults  stupor^ 
delirium  and  maniacal  outbreaks.  In  rare  instances  acquired,  men- 
ingitic  external  hydrocephalus  is  sacculated  on  account  of  the  ad- 
hesions between  the  pia  and  the  dura.  The  condition  is  a  veritable- 
meningeal  cyst.  The  limited  pressure  upon  the  brain  by  such  cysts 
may  give  rise  to  pronounced  pressure  focal  symptoms.  There  is 
hardly  any  need  of  dwelling  here  upon  the  headache,  the  vertigo  and 
vomiting,  the  optic  neuritis,  the  cranial  nerve  palsies,  the  tremors,  the 
spasms,  the  stupor  and  coma  that  are  observed  in  these  cases.  Tumor 
of  the  brain  probably  causes  the  greatest  difficulty  in  the  differential 
diagnosis.  (See  the  discussion  of  this  in  the  preceding  paragraphs 
under  the  head  of  internal  meningitic  hydrocephalus.) 

Congenital  Hydrocephalus. — This  is  the  typical  form  of  the  trou- 
ble, the  most  common  and  the  one  generally  referred  to  when  the  term 
hydrocephalus  alone  is  used.  It  is  practically  always  internal.  Its 
course  may  be  acute  or  chronic.  The  etiology  of  the  disease  is  ex- 
ceedingly obscure.  It  seems  to  be  more  than  merely  congenital  at 
times.  The  appearance  of  the  condition  in  several  members  of  the 
same  family  and  in  two  and  three  successive  generations  indicate  a 
purely  hereditary  influence.  In  conjunction  with  this  fact  it  is  sug- 
gestive that  various  cachexije,  alcoholism  and  syphilis  have  been  reck- 
oned among  its  etological  incidents.  I  have  seen  it  in  syphilitic  fam- 
ilies. Oppenheim  has  several  times  observed  a  moderate  hydro- 
cephalus in  hereditary  syphilitics  with  severe  symptoms  coming  on 
later  in  life.  Of  the  direct  prenatal  causes  that  are  responsible  for  it 
we  know  nothing.  Psychic  excitement  and  traumata  sustained  by  the 
mother  while  she  is  carrying  the  fcetus,  uterine  disease,  etc.,  are  some 
of  the  hypothetical  causes  that  have  been  enumerated. 

The  pathology  of  the  disease  is  capable  of  being  described  but 
its  pathogenesis  is  still  completel}'  in  the  dark.  The  essential  fact 
in  its  pathology  is  the  excessive  accumulation  of  fluid  in  the  ventricles. 
The  fluid  varies  but  little  from  the  normal.  It  is  clear,  colorless,  has  a 
specific  gravity  of  from  looi  to  1009  and  contains  a  small  and  variable 
amount  of  albumin,  a  slight  quantity  of  sodium  chloride,  occasionally- 
some  urea,  cholesterin  and  other  unimportant  substances.  The  amount 
varies  in  different  cases  from  a  few  ounces  to  several  pints.  It  usually 
distends  all  of  the  ventricles,  particularly  the  lateral.  It  may  be  lim- 
ited to  particular  ventricles  by  the  mechanical  obstruction  or  inflam- 
matory closure  of  the  inter-communicating  ducts. 

The  other  pathological  findings  are  the  direct  result  of  the  con- 
stant pressure  and  distention  exerted  by  the  fluid.  The  most  remark- 
able of  these  is  the  atrophy  and  wasting,  the  thinning  out  and  displace- 
ment of  the  brain  substance.  It  is  astounding  at  times  to  what  an  ex- 
tent the  wall  of  the  hemispheres  can  be  reduced.  Both  compression 
and  stretching  is  the  cause  of  this.  The  entire  brain  may  seem  to  be 
transformed  into  a  huge  cavity  inclosed  by  walls  not  more  than  a  few 
millimeters  thick.  It  is  said  that  Cardinal,  Bright's  famous  patient, 
lived  to  be  twenty-nine  years  of  age,  with  a  hydrocephalic  head  per- 
fectly translucent  when  the  sun  was  shining  behind  it.  The  convolu- 
tions and  sulci,  of  course,  are  obliterated.     The  corpus  callosum  is  car- 


THE  NON-NEURONIC  DISEASES  943 

ried  upwards,  the  central  ganglia  are  flattened  out  and  the  floor  of  the 
third  ventricle  bulges  beneath.  Sometimes  the  convolutions  are  only 
partially  obliterated  and  the  basal  ganglia  are  found  at  the  bottom  of 
the  sac.  The  skull  is  uniformly  enlarged  in  correspondence  with  the 
cerebral  distention.  The  falx  is  stretched  and  the  tentorium  is  elevated 
anteriorly.  The  space  beneath  the  tentorium  is  increased  in  size  and  is 
incompletely  filled  by  the  cerebellum.  Either  fluid  or  connective  tissue 
may  occupy  the  space  between  the  cerebellum  and  the  membranes. 
The  choroid  plexuses  are  thickened  and  seem  to  have  been  inflamed 
while  the  ventricular  ependyma  is  often  finely  granular  in  appearance 
and  sodden. 

The  external  appearance  of  the  head  is  striking  and  characteris- 
tic. It  is  uniformly  enlarged  with  a  strong  tendency  towards  being 
dolichocephalic  or  boat-shaped.  As  the  face  remains  small  the  front 
part  of  the  cranium  hangs  over  it  like  a  beetling  brow.  The  promi- 
nences are  all  enlarged,  smooth  and  rounded.  A  balloon-like  appear- 
ance is  thus  strikingly  given  to  the  upper  part  of  the  head.  The  cir- 
cumference, measuring  normally  in  the  newborn  about  thirty-five  to 
forty  centimeters,  may  reach  the  enormous  size  of  a  hundred  and 
sixty-seven  centimeters.  The  bones  are  thin,  the  sutures  gaping,  the 
fontanelles  large  and  bulging.  On  account  of  the  downward  pressure 
on  the  orbital  plates,  the  eyeballs  protrude  and  the  eyes  are  directed 
downward  and  partially  covered  by  the  lower  lids.  Wormian  bones 
sometimes  develop  in  the  sutures  of  the  skull.  The  entire  shape  of 
the  head  is  such  that  it  can  be  readily  distinguished  from  the  square- 
shaped,  angular,  rachitic  head.  Ofttimes  developmental  defects  are 
seen  in  other  parts  of  the  body,  such  as  encephalocele,  hare-lip,  spina 
bifida,  club-foot  and  a  general  condition  of  dwarfism.  Albinism  has 
been  noted. 

In  addition  to  the  physical  appearance  of  the  child,  other  symp- 
toms enter  into  the  composition  of  the  clinical  picture  of  this  disease. 
The  head  may  be  so  large  as  to  obstruct  the  act  of  parturition;  very 
often,  however,  it  does  not  begin  to  be  very  noticeable  until  the  child 
is  several  weeks  or  months  old.  From  that  time  on  there  is  then  a 
steady  increase  in  the  size  of  the  cranium.  The  veins  appear  prom- 
inently beneath  the  skin.  The  hair  fails  to  grow.  Auscultation  en- 
ables one  to  detect  a  brain  murmur  and  percussion  reveals  a  fluctua- 
tion wave.   . 

Idiocy  and  imbecility  is  the  lot  of  these  children.  The  intellect  is 
weak  even  in  the  mildest  cases  and  the  speech  slowly  acquired.  Rarely 
a  hvdrocephalic  child  will  be  bright  mentally ;  the  disease  becomes  ar- 
rested ;  and  adult  life  may  be  reached  with  normal  faculties.  In  still 
rarer  instances  the  mental  faculties  have  been  retained  with  a  high  de- 
gree of  hvdrocephalus. 

General  spasms  and  epileptiform  convulsions  are  common.  The 
head  cannot  be  held  erect,  partly  on  account  of  its  weight,  partly  on 
account  of  the  weakness  of  the  muscles.  The  voluntary  movements 
are  never  learned,  so  that  the  child  carries  his  limbs  about  in  an  awk- 
ward manner.  The  legs  are  usually  somewhat  spastic,  causing  a  de- 
cided difficultv  in  the  gait.    Many  children  never  learn  to  walk.    Others 


944 


THE   NON-NEURONIC  DISEASES 


wabble  and  shift  about   in  the  most  ungainly  way.     Incontinence  of 
urine  and  feces  is  a  mental  rather  than  a  motor  trouble.     Choked  disc 

FIGURE  203. 


Hydrocephalus.     Dr.    Fitch's    case. 


and  optic  atrophy  are  very  frecjuent  accompaniments  of  the  disease, 
caused,  of  course,  by  the  pressure  upon  the  optic  nerves.  Sensation 
is  not  as  often  affected  as  motility  and  seldom  are  the  cranial  nerves 


THE   XOX-XEUROXIC  DISEASES 


945 


except  the  optic,  implicated.       Profound  stupor,  fever,  vomitino-  and 
coma  may  herald  the  end.  ^ 

FIGURE  204. 


Hydrocephalus. 

The  outlook  for  these  children  is  bad.  They  usually  die  within 
the  first  four  or  five  years  of  life.  This  is  a  blessing  in  disguise  if  the 
case  is  a  severe  one  at  all,  for  the  prospect  of  idiocy,  if  i,'fe  continues, 


946  iiii-:  .\(_)X-xt:uROXic  diseases 

is  strong.     In  some  cases  evacuation  of  the  fluid  has  occurred  through 
a  spontaneous  rupture,   with  amehoration   of   the  symptoms.      In  the 

FIGURE  205. 


Hydrocephalus. 


mildest  cases  hfe  has  been  prolonged  to  old  age,  the  disease  having 
doubtless  become  permanently  arrested.  The  prognosis  of  hydro- 
cephalus is  therefore  always  serious  and  full  of  uncertainty. 


'  THE   XOX-XEURONIC  DISEASES  947 

Treatment.— The  treatment  of  hydrocephalus  of  all  forms  is 
far  from  satisfactory.  In  the  acute  and  chronic  acquired  forms  it  is 
more  hopeful  than  in  the  congenital.  It  is  always  uncertain,  however, 
how  much  of  the  recovery  was  due  to  the  therapeutic  measures  insti- 
tuted and  how  much  to  the  natural  events  of  the  disease.  In  the  ac- 
quired types  of  the  trouble,  treatment  should  always  be  directed,  so 
far  as  possible,  to  the  underlying  primary  disease.^  Quincke  advises 
mercurial  treatment  in  all  of  these  cases,  especially  the  internal  men- 
ingitic  cases,  w^hether  a  history  of  syphilis  be  obtainable  or  not.  Medi- 
cines cannot  remove  the  fluid.  Purgatives  and  diuretics,  so  much 
vaunted  in  earlier  days,  accomplish  practically  nothing,  and  are  often 
dangerous  if  used  with  necessary  vigor  in  the  weakened  state  of  these 
patients. 

Surgical  measures,  therefore,  as  a  rule,  are  our  onlv  resort  and 
these  are  not  very  promising.  They  consist  of  steady  compression  of 
the  hea,d,  partial  withdrawal  of  the  ventricular  and  spinal  fluid  by  punc- 
ture, violent  revulsive  measures  and  ventricular  drainage. 

It  does  not  seem  very  rational  to  transfer  the  pressure  of  the  ac- 
cumulating fluid  from  the  skull  around  it  to  the  brain  within  it  by  ex- 
ternal compression  of  the  head.  And  yet  that  is  a  practice  that  is 
honored  both  by  age  and  by  a  few  apparent  cures.  Trousseau,  and 
others  to-day,  recommend  the  application  of  strips  of  adhesive  pias- 
ter up  over  the  vertex  from  one  mastoid  process  to  the  other,  from  the 
nose  to  the  occipit,  and  then  in  circles  around  the  head  horizontally. 
The  case  must  be  closely  watched  and  the  strips  removed  upon  the 
first  indication  of  undue  pressure  upon  the  brain.  It  was  first  hoped 
that  this  would  favor  the  reabsorption  of  the  fluid.  Then  a  check  to 
the  enlargement  of  the  head  was  all  that  was  anticipated.  Neither  of 
these  results,  however,  are  accomplished,  whereas  an  increase  in  the 
symptoms  of  compression  almost  always  takes  place.  West  recom- 
mends the  use  of  a  broad  elastic  band  instead  of  the  diachylon  plaster. 
He,  with  most  other  clinicians,  however,  recognizes  the  general  futil- 
ity of  this  method  of  treatment. 

Withdrawal  of  the  fluid  by  puncture  is  the  most  direct,  but  also 
the  most  dangerous,  mode  of  attempting  relief.  Hippocrates  recom- 
mended puncture  of  the  ventricles.  Simple  puncture  under  the  strict- 
est kind  of  antisepsis,  withdrawal  of  not  more  than  an  ounce  of  fluid 
at  a  time,  and  the  operation  not  repeated  at  too  close  or  frequent  in- 
tervals, have  in  a  few  instances  seemed  to  have  resulted  in  a  cure. 
In  sixty-three  cases,  Henschen  reported  fifteen  recoveries,  twelve  im- 
provements and  twenty- four  deaths.  Often  the  first  operation  is  borne 
well  but  the  second  or  third  proves  fatal.  Puncture,  with  after- 
drainage,  and  puncture  with  iodine  injections,  seem  to  have  been 
particularly  dangerous.  The  insertion  of  the  aspirating  needle  or  tro- 
car is  usually  best  made  at  the  outer  angle  of  the  anterior  fontanelle. 

Much  safer,  though  slower  in  action,  is  puncture  of  the  sub- 
arachnoid sac  of  the  spine  between  the  third  and-  fourth  lumbar  ver- 
tebrae. This  measure  has  proved  to  be  both  curative  and  palliative,, 
especially  in  acquired  hydrocephalus. 

Revulsive   measures   consist  of  the  use  of  the   seton,   inunctions 


948  THE   NOX-NEURONIC  DISEASES 

with  ointments  of  tartar  emetic  and  even  the  once  so  popular  appH- 
cation  of  spirit  of  turpentine  freely  to  the  scalp  and  then  setting  it  on 
fire.  These  heroic  measures  unfortunately  do  not  cure  and  only  too 
often  fail  to  relieve.  It  must  be  admitted,  to  the  chagrin  of  both 
medicine  and  surgery,  that  the  treatment  of  hydrocephalus  is  not  a 
brilliant  success  and  only  too  often  nature  and  a  laissez-faire  policy 
accomplish  about  as  much  as  do  science  and  art. 

DISEASES  OF  THE  PONS  VAROLII  AND  MEDULLA 
OBLONGATA. 

It  is  not  necessary  to  give  a  minute  description  of  the  pons  and 
medulla  here,  for  the  main  points  in  their  anatomy  have  been  touched 

FIGURE  206: 
vc     ^i    !-^ 


ajt    '  Ji 


a.c 


Diagrammatic  representation  of  a  section  of  the  medulla  at  the  level  of  the 
decussation  of  the  pyramidal  tracts  :  fp.,  posterior  fissure ;  f,  anterior  fissure ; 
p,  crossing  of  the  pyramidal  tracts;  fg,  fasciculus  gracilis;  a,  anterior  horn; 
pc,  posterior  horn;  R,  substantia  gelatinosa  of  Rolando;  1,  lateral  column;  ac, 
anterior  column;  ap,  pyramid.      (From  Quain.) 

upon  in  the  earlier  accounts  of  the  anatomy  of  the  brain  and  of  the 
neuronic  architecture  of  the  nervous  system. 

The  medulla  is  but  an  upv^^ard  extension  of  the  spinal  cord.  Its 
tracts  and  gray  matter  are  the  same,  wdth  but  a  slight  alteration  in 
their  relative  positions.  Usually  that  part  is  called  the  medulla  which 
extends  from  the  edge  of  the  foramen  magnum  up  to  the  lower  border 
of  the  pons.  As  the  tracts  of  the  medulla  continue  to  course  on  up- 
wards to  be  prolonged  into  the  crura  cerebri,  they  are  embraced  ven- 
trally  and  crossed  transversely  by  the  great  commissural  fibres  of  the 
cerebellum.  These  transverse  fibres  and  all  that  lies  behind  them  is 
known  in  gross  anatomy  as  the  pons  varolii. 

It  is  better  to  regard  the  upward  extension  of  the  medulla,  lying 
behind  the  transverse  tracts  of  the  pons,  as  the  preoblongata.  What 
IS  commonly  called  in  anatomy  the  medulla  may  then  well  be  called 
the  postoblongata.  Behind  the  preoblongata  is  the  fourth  ventricle, 
with  the  aqueduct  of  Sylvius  above  leading  to  the  third  ventricle. 


THE   NON-NEURONIC  DISEASES 


949 


There  are  three  important  facts  to  be  noted  in  connection  with 
the  rearrangement  of  the  spinal  cord  tracts  in  their  upward  extension 
mto  the  medulla.  The  first  is  that  there  is  a  sort  of  an  antero-posterior 
flattennig  out  of  the  cord,  with  a  gradual  posterior  displacement  of  the 
anterior  parts  thereof.  The  posterior  columns  separate,  V-shape,  and 
continue  on  up  as  the  restiform  bodies  and  inferior  cerebellar  peduncles. 
The  central  canal  of  the  cord  opens  out  into  the  fourth  ventricle,  which 
is  bounded  above  laterally  by  the  superior  cerebellar  peduncles.  The 
central  gray  matter  and  anterior  horns  of  the  cord  sink  backwards  until, 
with  the  widely  separated  remains  of  the  posterior  horns,  they  form  a 
plate  of  gray  matter  just  beneath  the  floor  of  the  fourth  ventricle.     At 


FIGURE  207. 


pjnf.     I       /•/  i>. 


a.m.f. 


Section  of  the  MEDniA 

OBLONGATA    IN    THE  REGION    OP    THE 
SUPERIOR   PYRAMIDAL  DECUSSATION. 

(Schwalbe.)     ^ 

a.m.f.,  anterior  median  fissure ; 
f.a.,  superficial  arcifomi  fibres  emerg- 
ing from  the  fissure  ;  'py. ,  pyramid  ; 
7i.ar.,  nucleus  of  the  arciform  fibres  ; 
f.a'.,  deep  arciform  fibres  becoming 
superficial  ;  o.,  lower  end  of  olivary 
nucleus ;  0'.,  accessory  olivary  nucleus ; 
n.l.,  nucleus  lateralis  ;  f.r.,  formatio 
reticularis  ;f.a.^,  arciform  fibres  pro- 
ceeding from  formatio  reticularis  ;  </., 
substantia  gelatinosa  of  Rolando ; 
a.  v.,  ascending  root  of  fifth  nerve  ; 
n.c,  nucleus  cuneatus  ;  n.c'.,  external 
cuneate  nucleus  ;  f.c,  funiculus  cu- 
neatus ;  n.g.,  nucleus  gracilis  ;  f.g., 
funiculus  gracilis ;  p.m.f,  posterior 
median  fissure;  c.c,  central  canal 
surrounded  by  grey  matter,  in  which 
are,  n.XI.,  nucleus  of  the  spinal 
accessory,  and,  n.XI  I.,  nucleus  of  the 
iypoglossal  :  s.cJ.,  superior  pyramidal 
decussation. 


the  top  of  the  posterior  columns  an  expansion  of  gray  matter  becomes 
the  nuclei  of  the  posterior  columns. 

The  second  great  change  in  the  medulla  to  be  noted  in  relation  to 
the  cord  tracts  is  that  the  pyramidal  tracts  course  ventrally  and  decus- 
sate in  the  well-known  decussation  of  the  pyramids. 

The  third  change  is  that  the  sensory  tracts  in  large  part  decussate 
in  the  fillet. 

With  the  aid  of  the  accompanying  diagrams  and  a  knowledge  of 
the  gross  anatomy,  the  reader  can  easily  trace  every  pathway  and  gray 
deposit  in  the  spinal  cord  up  into  the  medullar.  The  apparent  con- 
fusion is  caused  merely  by  their  rearrangement  and  not  by  any  essen- 
tial change. 

The  cranial  nuclei  are  the  special  points  of  interest  in  the  medulla 
in  clinical  neurology.  These  nuclei  are  the  cause  of  the  special  symp- 
tomatology of  medullary  diseases.  They  are  all  in  the  gray  matter 
making  up'  the  floor  of  the  fourth  ventricle  and  the  aqueduct  of  Sylvius. 


950 


THE   iXON-NEURONIC  DISEASES 


The}'  are  the  remains  of  the  anterior  and  posterior  horns  and  central 
gray  matter  of  the  spinal  cord. 

The  Figure  175  illustrates  more  accurately  than  any  long 
description  can  the  relative  positions  of  these  nuclei.  Being  but  the 
upward  extension  of  the  gray  matter  of  the  cord,  they  are  liable  to  the 
same  sort  of  disease  processes  that  the  latter  is.  They  may  undergo 
primary  and  secondary  degeneration  and  be  subject  to  the  distinctive 
effects  of  hemorrhage,  inflammation,  compression,  etc.  In  this  respect 
medullary  diseases  dift'er  in  nowise  from  spinal  cord  affections. 

The  symptoms  of  disease  of  the  medulla  and  pons  are  both  general 


FIGURE  2c8. 

Section  of  the  me- 
iiulla  oblongata  at  about  the 
middle  of  the  olivary  body. 
(Schwalbe.)     ± 

f.l.a.,  anterior  median  fissure; 
n.ar.,  nucleus  arcifonnis  ;  p., 
pyramid;  XII.,  bundle  of  hypo- 
glossal nerve  emerging  from  the 
surface  ;  at  b,  it  is  seen  coursing 
between  the  pyramid  and  the  c 
olivary  nucleus,  o.  ;  f.a.e.,  exter- 
nal arciform  fibres  ;  n.L,  nucleus 
lateralis;  a.,  arciform  fibres 
passing  towards  restiform  body 
partly  through  the  substantia  gel- 
atir.osa,  f/.,  partly  superficial  to 
the  ascending  root  of  the  5th 
nerve,  a.  V.  ;  X,  bundle  of  vagus 
root,  emerging  ;  /".?•.,  formatio  re- 
ticularis ;  c.r.,  corpus  restiforme, 
beginning  to  be  formed,  chiefly 
by  arciform  fibres,  superficial  and 
deep;  'n.c,  nucleus  cuneatus ; 
5!.y.,  nucleus  gracilis  ;  (. ,  attach- 
ment of  the  ligula  :  /.---'.,  funiculus 
solitarius  ;  71. X.,  /(.X'.,  two  parts 

of  the  vagus  nucleus  ;  v. XII.,  hypoglossal  nucleus  ;  n.i.,  nucleus  of  the  funiculus  teres  : 
n.a'iii.,  nucleus  aml>iguus  ;  r.,  raphe  ;  A.,  continuation  of  anterior  column  of  cord  ;  <^,o", 
accessory  olivary  nuclei ;  p.o,  pedunculus  olivse. 


and  focal.  The  former  are  the  same  as  they  are  in  similar  trouble  in 
other  parts  of  the  nervous  system.  The  focal  symptoms  arc  the  great 
dominant  feature  in  bulbar  and  pontile  disease.  These  have  been  de- 
tailed elsewhere  under  the  head  of  cerebral  localization  and  symptoms 
of  disease  of  the  brain. 

Among  the  cranial  nerves  there  are  two  quite  distinct  groups — 
namely,  those  that  move  the  eyeball  and  those  that  innervate  the  mus- 
cles about  the  orifice  of  the  alimentary  and  respiratory  canals.  The 
nuclei  of  the  third,  fourth  and  sixth  nerves  of  the  first  group  are  scat- 
tered along  the  floor  of  the  aqueduct  of  Sylvius.  When  they  undergo 
primary  degeneration  the  disease  is  known  as  degenerative  ophthal- 
moplegia, described  elsewhere.  Sometimes  they  are  made  the  seat  of 
a  hemorrhagic  inflammation,  which  is  supposed  to  be  of  infectious 
origin  or  toxic,  and  analogous  to  the  same  process  that  takes  place  in 


THE   NOX-XEURONIC   DISEASES 


95^ 


acute  anterior  poliomyelitis  lower  down  in  the  cord.  This  is  Wernicke's 
acute  stipcrior  polioencephalitis. 

When  primary  degeneration  attacks  the  lower  group  of  nuclei  the 


FIGURE  2C9. 


uW 


FIGURE  210. 


Figure  2C9,  section  of  the  medulla  oblongata  just  above  the   pyramidal   decussa- 
tion.    Figure  210,  section  through  the  pyramidal  decussation.   (After  Jakob.) 

condition  is  known  as  chronic  or  progresswc  bulbar  paralysis.  It  may 
continue  as  an  isolated  affection,  but  more  generally  it  is  associated 
with  progressive  muscular  atrophy,  there  being  no  fixed  rule  ot  prece- 


952  THE   NOxV-NEURONIC  DISEASES 

dence  in  regard  to  the  appearance  of  the  bulbar  or  the  spinal  symp- 
toms. I  have  described  this  also  elsewhere.  This  second  group  of 
nuclei,  like  the  first,  can  also  be  subject  to  an  acute  hemorrhagic  in- 
flammatory process,  a  condition  which  is  sometimes  called  acute  in- 
ferior polioencephalitis. 

These  are  all  forms  of  bulbar  paralysis.  They  are  essentially  dis- 
eases of  the  lower  motor  neurones,  with  all  the  characteristics  that 
belong  to  such  diseases  in  regard  to  atrophy,  reflex  action  and  elec- 
trical response.  They  are  homologous  to  the  poliomyelitic  affections. 
The  paralysis  is  flaccid  and  shows  a  tendency  to  pick  out  special  mus- 
cles. Typical  bulbar  palsy  is  bilateral.  Bulbar  symptoms  may,  how- . 
ever,  occur  unilaterally  or  even  in  the  distribution  of  a  single  cranial 
nerve.  Of  course,  in  the  last  case,  it  is  impossible  to  diflierentiate  a 
neurific  from  a  nuclear  palsy.  A  psciido-hulhar  palsy  may  be  observed 
when  a  bilateral  lesion  implicates  the  cortical  centers  that  correspond 
to  the  medullary  nuclei.  Under  these  circumstances  the  disease  being 
in  the  upper  motor  neurones,  the  paralysis  will  be  of  the  spastic  type 
with  increase  of  reflex  actions  and  absence  of  atrophy  and  electrical 
changes. 

APOPLECTIFORM  BULBAR  PARALYSIS. 

Cases  of  a  symmetrical  bulbar  palsy  of  sudden  onset  have  been 
seen.  They  differ  from  the  typical  form  of  the  disease  in  their 
apoplectiform  and  non-progressive  character.  They  occur  in  the  later 
periods  of  life  when  there  is  beginning  arterial  degeneration.  Younger 
persons  have  manifested  the  same  condition  as  the  result  of  trauma. 

The  onset  of  the  symptoms  are  sudden;  usually  zvithout  loss  of 
consciousness;  and  with  vomiting  and  vertigo.  At  first  there  may 
be  motor  and  sensory  disturbances  in  the  limbs,  but  these  quickly  pass 
away  and  leave  only  the  glosso-labio-laryngeal  palsy.  This  even  may 
improve  for  a  time ;  but  finalty  the  condition  becomes  stationary  and 
may  remain  so  for  years.  Late  degeneration  takes  place  and  then  the 
disease  assumes  all  the  characteristics  of  the  progressive  type  of  the 
disease.  Perfect  bilaterality  does  not  alwavs  obtain  in  the  symptoms. 
The  weakness  will  be  more  marked  on  one  side  than  on  the  other, 
or  in  certain  muscles  more  than  in  others. 

In  these  cases,  as  in  typical  progressive  bulbar  palsy,  there  is 
dysarthria  or  anarthria,  difUcult  deglutition  and  embarrassed  respira- 
tion and  voice  production. 

The  pathology  of  these  cases  is  obscure,  though  it  is  probable  that 
there  is  embolic  obstruction  in  or  near  the  middle  line.  In  a  case  re- 
ported by  Gowers  in  which  there  was  no  atrophy  and  no  loss  of  elec- 
trical irritability — i.  e.,  no  evidence  of  damage  of  the  nuclei  themselves 
— it  was  surmised  that  the  paths  from  the  hemispheres  were  injured 
just  above  the  nuclei,  near  their  decussation.  The  close  commissural 
connection  between  the  nuclei  may  easily  account  for  the  occasional 
appearance  of  bilateral  symptoms  from  a  unilateral  lesion. 

The  diagnosis  of  these  cases  is  not  difficult  if  the  suddenness  and 
complete  bulbar  picture  are  present.     Mere  focal  lesions  that  damage 


THE   XOX-XEUROXIC  DISEASES 


953 


suddenly  this  or  that  nucleus  are  not  to  be  confounded  with  this 
disease. 

Pseudo-bulbar  paralysis  may  at  times  closely  simulate  this  affec- 
tion and  cause  serious  mistakes  in  diagnosis.  In  these  cases  the  lesion 
has  for  the  most  part  been  in  the  central  ganglia.  Both  hemispheres 
were  aft'ected,  but  not  simultaneously.  The  bulbar  picture  usually 
appeared  after  the  second  stroke,  which  completed  the  bilateralit}^  of 
the  lesion. 

In  rare  cases  of  pseudo-bulbar  paralysis  there  have  not  been  two 
successive  apoplectiform  attacks.  These  cases  are  extremely  difficult 
to  diagnose  properly  at  times.  The  lenticular  nucleus  has  been  par- 
ticularly frequently  the  seat  of  the  lesion.  It  has  appeared  elsewhere, 
however.  The  proper  explanation  of  these  cases  is  not  yet  forth- 
coming. 

There  is  an  infantile  form  of  pseudo-bulbar  paralysis. 

The  prognosis  of  these  apoplectiform  types  of  bulbar  palsy  is  ex- 
ceedingly serious.  Life  is  constantly  in  danger.  Xot  being  a  primary 
degenerative  disease,  the  later  outlook  is  better  here  than  it  is  in  the 
typical  progressive  t}'pe  of  the  disease.  Sometimes  much  improvement 
occurs  and  complete  recoveries  have  been  several  times  recorded.  If 
after  a  month  there  is  no  more  improvement  observed,  it  is  probable 
that  none  will  occur. 

The  treatment  is  the  same  as  that  for  intracranial  embolism  de- 
scribed in  another  part  of  the  book. 

Bulbar  palsy  of  a  slow  type  may  be  due  to  compressio)i  from  a 
tumor  or  aneurism.  There  is  nothing  distinctive  about  it.  I  have 
mentioned  it  when  treating  of  intracranial  tumors. 

Myasthenia  gravis,  which  by  some  is  called  asthenic  bulbar  paraly- 
sis, is  discussed  in  detail  among  the  neuronic  diseases  of  the  lower 
motor  segment. 

There  is  a  hereditary  and  familial  form  of  progressive  bulbar 
paralysis,  described  by  Fazio.  Charcot.  Londe  and  others,  that  rep- 
resents something  more  than  a  mere  phase' of  progressive  muscular 
atrophy  as  the  common  form  of  progressive  bulbar  paralysis  does.  In 
these  cases  the  parents  have  been  blood-relatives  and  the  children  have 
shown  the  disease.  The  physical  stigmata  of  degeneracy  are  usually 
w^ell  marked  in  them.  The  atrophic  paralysis  usually  begins  in  the 
upper  facial  area,  continues  there  along  with  the  involvement  of  the 
lower  area  and  thus  distinguishes  these  cases  from  the  ordinary  forms 
of  the  disease.  Ptosis  also  occurs  in  these  cases,  showing  the  involve- 
ment of  the  third  nerve  nuclei.  The  extremities  are  not  implicated. 
There  are  other  features  about  these  cases  that  seem  to  distinguish 
them  from  the  adult  type  of  the  trouble.  It  is  supposed  that  there 
is  a  polioencephalitis  underlying  them.  They  seem  to  be  more  nearly 
related  to  the  mysterious  congenital  ocular  and  facial  palsies  than 
to  auA-thing  else,  and  are  to  be  regarded  in  the  light  of  developmental 
anomalies.  Other  forms  of  hereditary  disease  wath  bulbar  symptoms 
have  been  observed,  but  little  is  known  of  their  anatomical  bases. 

The  pons  is  the  seat  of  small  focal  lesions  at  times.  There  local- 
ization diagnosis  is  merely  the  application  of  the  knowledge  of  anatomy. 


954  THE   NOxN"-NEURONIC  DISEASES 

Small  hemorrhages,  spots  of  softening  and  tumor  may  occur  here  as 
elsewhere.  Involvement  of  the  cortico-spinal  tracts,  the  formatio 
reticularis  and  the  roots  of  the  fifth  nerve  constitutes  the  prominent 
features  of  pontile  symptomatology. 

In  pontile  lesions  situated  ventrally,  the  damage  to  the  pyramidal 
tracts  dominates  the  clinical  picture.  This  gives  a  uniform  side  to  it. 
The  other  side  of  the  picture  will  vary  according  as  the  lesion  is  in 
the  upper  (frontad)  or  lower  (caudad)  part  of  the  pons.  The  pyra- 
midal tracts  arc  from  the  cortex  and  distribute  fibres  to  the  cranial 
nuclei,  as  well  as  continuing  on  down  into  the  cord.  As  we  know, 
these  tracts  decussate :  those  fibres  to  the  cranial  nuclei  crossing  above 
and  those  to  the  limbs  crossing  in  the  pyramids.  If  the  lesion  should 
be  in  the  upper  part  of  the  pons,  above  a  line  drawn  approximately 
through  the  points  of  emergence  of  the  fifth  nerves  and  involve  the 
pyramidal  fibres  for  the  trigeminal,  abducens  and  facial  nerves  before 
their  decussation,  the  paralysis  of  the  face  and  extremities  will  be  on  the 
same  side  of  the  body,  but  on  the  opposite  side  from  that  of  the  lesion. 
If,  however,  the  lesion  is  below  this  line  drawn  through  the  trigeminal 
roots,  after  the  pyramidal  fibres  for  the  above-named  cranial  nerves 
have  decussated,  the  hemiplegia  will  be  of  the  alternate  or  crossed  type. 
The  facial  paralysis  will  be  on  the  same  side  as  the  lesion,  the  paraW- 
sis  of  the  extremities  on  the  side  opposite  that  of  the  lesion.  In  the 
former  condition  both  facial  and  limb  paralysis  are  of  the  pure  central 
type ;  ^  in  'the  latter  condition  the  facial  paralysis  is  of  the  peripheral 
type,  while  that  of  the  limbs  is  of  the  central. 

Alternating  anccsthesia  is  occasionally  met  with  in  pontile  lesions. 
According  to  Starr,  a  unilateral  anaesthesia  of  the  face  (not  due  to 
trigeminal  neuritis  or  to  a  cortical  lesion)  is  indicative  of  a  lesion  in 
the  medulla  or  pons,  in  the  outer  third  of  the  formatio  reticularis.  If 
the  lesion  is  high  up  (cephalad)  in  the  pons,  the  anaesthesia  will  be  on 
the  opposite  side;  if  the  lesion  is  low  down  (caudad)  in  the  pons  or 
in  the  medulla,  the  anaesthesia  will  be  on  the  same  side. 

If  anaesthesia  occurs  in  the  limbs  and  is  not  due  to  a  cerebral 
lesion,  the  site  of  the  trouble  is  in  the  medulla  or  pons,  in  the  inner 
two-thirds  of  the  formatio  reticularis  and  on  the  side  opposite  that  of 
the  anaesthesia.    Of  course,  it  may  be  in  the  spinal  cord. 

A  lesion  below  the  point  of  union  of  the  ascending  and  descending 
roots  of  the  fifth  nerve  and  affecting  the  entire  lateral  extent  of  the 
formatio  reticularis,  will  cause  anaesthesia  of  one  side  of  the  face  and 
of  the  limbs  of  the  opposite  side. 

If  the  face  and  limbs  of  the  same  side  are  anjesthetic,  the  lesion 
is  frontad  of  the  point  of  union  of  the  ascending  and  descending  roots 
of  the  fifth  nerve  in  the  pons. 

DISEASES  OF  THE  CEREBELLUM. 

The  anatomy  and  physiology  of  the  cerebellum  have  been  de- 
scribed with  the  brain  at  the  head  of  this  section.  The  results  of  ex- 
perimentation and  pathological  observation  in  regard  to  cerebellar 
lesions  do  not  exactly  coincide.     Our  knowledge  of  this  part  of  the 


THE   NON-NEURONIC  DISEASES  955 

brain  is  ipcomplete.  The  clinical  picture  is  usually  confused  by  the 
symptoms  of  intracranial  pressure,  which  symptoms  may  be  due  to 
parts  entirely  away  from  the  cerebellum. 

According  to  Russell,  experimental  ablation  of  one  half  of  the 
organ,  exclusive  of  the  middle  lobe,  results  in  incodrdination,  rotation, 
Jitvbatwii,  reeling,  a  characteristic  attitude,  disturbed  reflexes,  muscular 
rigidity  and  convulsions,  motor  paresis  and  ocidar  defects.  These  have 
all  been  seen  as  the  result  of  disease  in  man.  Just  how  much  of  the 
symptomatology  is  due  in  man  to  implication  of  the  middle  lobe  of  the 
cerebellum  and  pressure  upon  the  medulla  and  the  great  tracts  running 
through  the  medulla  it  is  not  easy  to  say.  It  is  usually  considered  that 
a  lesion  of  the  cerebellar  hemispheres  in  man  that  does  not  compress 
the  middle  lobe  or  medulla  gives  rise  to  no  symptoms  whereby  it  can 
Jbe  recognized.     There  are  certainly  no  localizing  signs. 

The  reeling  gait  of  the  disease  of  the  middle  lobe  of  the  little 
train  is  almost  pathognomonic.  The  patient  finds  it  difficult  to  stand 
and  every  step  is  accompanied  by  unsteadiness,  like  that  of  a  drunken 
person.  It  is  almost  impossible  to  maintain  equilibrium.  The  walk  is 
:zigzag.  Occasionally  the  movements  of  the  arms  are  jerky.  The  gait 
is  sometimes  spoken  of  as  ataxic,  but  it  is  not  like  the  irregular  ataxic 
gait  of  tabes,  though  the  progression  in  tabes  may  sometimes  approach 
in  appearance  the  progression  of  cerebellar  disease.  In  the  latter  it  is 
distinctly  reeling,  oscillatory,  unsteady  and  due  to  a  distinct  loss  of 
the  sense  of  equilibrium.  This  symptom  may  be  produced  by  disease 
■of  the  lateral  hemisphere  that  compresses  the  middle  lobe. 

Closely  associated  with  this  s3mnptom  are  vomiting  and  vertigo. 
They  are  very  common  signs,  though  they  are  not  of  much  value  as 
localizing  signs,  since  they  occur  in  many  other  intracranial  troubles. 
The  vomiting  is  of  the  pure  cerebral,  projectile  type.  The  vertigo  is  in 
TIG  way  distinctive.  They  occur  only  with  irritative  and  compressing 
lesions  and  hence  are  probably  due  to  implication  of  the  great  longi- 
tudinal tracts  running  between  the  brain  and  the  cord  or  to  dis- 
turbance of  the  vagus  and  other  nuclei  in  the  medulla.  The  vertigo 
is  not  necessarily  related  to  the  incoordination,  for  the  latter  can  be 
extreme  without  the  slightest  sense  of  giddiness.  Vertigo  is  probably 
a  psycho-sensory  phenomenon  :  whereas  the  incoordination  is  more 
intimately  related  to  the  motor  apparatus. 

Titubation  resembles  that  seen  in  disseminated  sclerosis.  The 
liead  is  unsteady  on  the  trunk  and  the  unsteadiness  is  increased  with 
€very  attempt  at  voluntary  movement.  This  is  a  symptom  well  marked 
in  clinical  cases,  though  never  so  much  so  as  the  incoordination  in  the 
extremities. 

The  attitude  is  often  striking.  The  trunk  is  carved,  the  con- 
cavity being  to  the  side  of  the  cerebellar  lesion.  The  head  is  laterally 
inclined  to  the  same  side  and  the  face  is  drawn  towards  the  shoulder. 

In  experimental  lesions  the  tendon-jerks  are  exaggerated.  In 
clinical  cases  in  man  they  arc  usually  diminished  or  lost,  though  they 
may  be  exaggerated  and  long  remain  so.  The  loss  of  the  knee-jerk 
occurs  in  irriteting  lesions  and  is  probably  due  to  some  influence  ex- 
erted upon  the   reflex  spinal   centers.     A'ariations  occur  in  both   the 


cjtO  the  nox-xeuroxic  diseases 

diminished  and  exaggerated  types  of  patella  disturbance  from  time  to 
time. 

Xystag})ius  is  common  in  tumor  of  the  cerebellum.  On  account 
of  the  intracranial  pressure,  ocular  paralyses  are  not  infrequent.  The 
opposite  sixth  nerve  is  especially  liable  to  sufifer  from  pressure.  This- 
causes  an  internal  strabismus  in  the  eye  on  the  opposite  side  to  that 
of  the  cerebellar  lesion.  Nystagmus  with  ocular  displacement  due  to 
pressure  has  no  special  features  to  cause  it  to  indicate  a  cerebellar 
lesion.  \\'hen,  however,  there  is  no  ocular  displacement,  or  when  the 
displacement  is  characteristic  of  removal  of  one-half  of  the  organ,  or 
when  secondary  pressure  is  not  needed  to  explain  the  condition,  the 
nystagmus  is  characteristic  enough  to  be  a  valuable  localizing  sign. 
It  is  lateral.  \Mien  it  is  spontaneous  it  is  intensified  by  the  voluntar}'" 
turning  of  the  eyes  to  the  side  of  the  lesion.  When  it  is  not  spontane- 
ous, it  may  not  be  elicited  at  all  or  it  may  be  observed  slightly  if  the- 
eyes  are  turned  voluntarily  away  from  the  side  of  the  lesion,  or  it  may 
be  very  marked  if  the  eyes  are  turned  voluntarily  to  the  side  of  the- 
lesion. 

\Mien  the  compression  of  the  cerebellar  lesion  implicates  the 
medulla,  other  cranial  nerve  symptoms  ma)^  appear,  such  as  occur  in 
focal  disease  of  the  medulla — namely,  disturbed  articulation,  respira- 
tion and  deglutition. 

A  motor  paresis  occasionally  occurs  as  a  hemiplegia  in  the  limbs- 
on  the  side  of  the  lesion.  The  face  remains  intact.  Very  often  the 
pyramidal  tracts  are  compressed  and  there  is  \Aeakness  in  the  limbs  with 
exaggeration  of  the  tendon-jerks. 

Epileptiform  convidsions  are  rare,  but  have  been  seen  in  disease 
of  the  cerebellum.  As  an  indirect  pressure  symptom  a  tetanoid  rigidit}^ 
with  opisthotonos  has  been  observed.    It  occurs  only  in  tumor. 

Disease  of  the  cerebellar  superior  and  inferior  peduncles  is  rarely- 
isolated.  Rotation,  forced  movements,  vertigo,  asymmetrical  displace- 
ment of  the  eyes  are  among  the  occasional  manifestations.  To  these 
must  usually  be  added  signs  of  involvement  of  the  pons  and  the  fiftlx 
nerve. 

The  cerebellum,  like  any  other  part  of  the  brain,  is  subject  to- 
hemorrhage,  softening,  inflammation,  abscess,  tumor,  atrophy  and 
sclerosis.  Occasionally  it  is  congenitally  under  size  and  is  the  site  of 
an  agenesis.  There  is  a  cerebellar  type  of  infantile  palsy  and  in  some 
cases  of  congenital  atrophy  the  symptoms  have  a  close  resemblance  to 
those  of  Friedreich's  disease. 

^lALFORMATIOXS  OF  THE  BRAIX. 

These  are  of  no  clinical  interest  whatever,  since  they  are  monsters- 
that  never  continue  to  live  long  after  birth.  There  are  many  varieties, 
all  of  which  are  interesting  from  the  embryological  and  developmental 
standpoint. 

Anoicephaly  accompanies  acrania  and  is  a  condition  in  which- 
there  is  no  cranial  cavity  or  contents.  The  cerebellum  and  the  primi- 
tive basal  ganglia  ma}-  be  present  in  some  cases. 


THE   NON-NEURONIC  DISEASES  957 

Micrencephaly  and  'microcephaly  means  a  monstrously  small  head 
snd  brain. 

Porencephaly  is  a  partially  damaged  brain.  I  have  described  it 
xmder  the  head  of  congenital,  infantile  hemiplegia. 

Cyclopia  is  where  the  anterior  cerebral  vesicle  fails  to  separate 
or  divide  and  the  orbits  remain  together  with  a  single  optic  apparatus. 

Meningocele,  encephaloccle  and  hydrencephalocele  are  hernias,  the 
nature  of  which  is  sufftcientlv  indicated  in  the  names. 


SECTION   D. 


GENERALMALADIESWITH  LEADING  NEURO- 
LOGICAL SYMPTOMS. 


ALCOHOLISM. 


Alcohol  seems  to  exert  a  particularly  deleterious  influence  upon 
the  nervous  S3'stem.  Its  effects  are  somewhat  different  when,  taken  in 
large  quantity  occasionally  from  what  they  are  when  it  is  imbibed  in 
small  quantities  for  long  periods  of  time.  It  may  be  studied  therefore 
under  the  heads  of  acute  and  chronic  alcoholism.  In  the  course  of 
chronic  alcoholism  there  are  occasional  outbreaks  of  an  acute  condi- 
t.on,  known  as  delirium  tremens. 

Acute  Alcoholism. — The  ingestion  of  a  large  amount  of  this 
poison  results  in  disturbances  of  coordination,  psychosis  and  narcosis. 
The  condition  is  known  preeminently  as  drunkenness,  intoxication,  and 
is  of  physiological  and  toxicological  interest  rather  than  neurological. 
There  is  a  flushed  or  cyanotic  condition  of  the  face,  the  pulse  is  full, 
the  breathing  labored.  The  pupils  are  dilated.  The  temperature  is 
generally  below  normal.  Unconsciousness  is  present,  but  it  is  not  so 
deep  but  what  the  patient  can  generally  be  aroused  momentarily  with 
a  great  effort.  Muscular  twitchings,  occasional  convulsions  and  great 
stupor  are  not  infrequently  seen.  This  is  the  form  of  alcoholism 
usually  observed  in  the  condition  known  as  dipsomania,  wherein  there 
is  a  strong  hereditary  tendency  toward  drink  and  a  yielding  to  it  by 
the  indulging  in  a  periodical  spree. 

Acute  alcoholism  is  chiefly  of  interest  to  neurology  in  the  role  it 
plays  in  the  differential  diagnosis  of  cerebral  hemorrhage,  epilepsy, 
hysteria,  syncope,  ursemic  coma  and  other  affections  accompanied  by 
unconsciousness. 

Chronic  Alcoholism. — The  constant  drinking  of  alcohol  and  alco- 
hoHc  beverages  in  amounts  that  never  are  sufhcie'nt  to  cause  actual 
drunkenness  produces  changes  of  a  degenerative  character  in  nearly 
all  of  the  tissues  of  the  body.  In  a  work  of  this  sort  we  are  only  con- 
cerned with  the  changes  that  are  established  in  the  nervous  tissues  and 
functions.  I  will  pass  by,  therefore,  with  the  merest  mention,  the  well- 
known  alterations  in  the  digestive  apparatus,  the  heart  and  arteries,  the 
kidneys  and  the  skin. 

The  earliest  manifestations  of  chronic  alcoholic  intoxication  are 


960  GENERAL    INTOXICATIONS 

functional  in  character.  There  is  a  muscular  tremor  which  affects 
principally  the  lips,  the  tongue  and  the  hands.  It  is  also  in  the  legs,  but 
it  is  not  so  observable.  It  is  an  intentional  tremor  in  part,  being  empha- 
sized when  any  voluntary  movement  is  attempted.  It  causes  unsteadi- 
ness and  is  very  obvious  in  the  speech  and  the  writing.  It  is  a  fine  yet 
irregular  oscillatory  tremor,  and  is  most  noticeable  in  the  morning. 
A  dose  of  alcohol  diminishes  or  puts  a  stop  entirely  to  it  for  the  time 
being. 

Insoinnia  is  a  troublesome  symptom  in  these  habitues  and  during 
their  sleep  the  muscles  often  jerk  and  twitch. 

The  mental  state  is  characteristic  of  a  mild  degree  of  degenerative 
encephalitis  or  meningo-encephalitis.  In  the  morning  until  the  ac- 
customed stimulant  is  obtained  there  is  dullness  and  apathy  and  some- 
times confusing  headache.  The  temperament  gradually  undergoes  a 
change.  The  individual  is  irritable,  restless,  forgetful,  morally  low- 
ered. He  may  be  emotionally  depressed  and  maudlin.  He  is  given  to 
silly  sentimentalism  and  is  often  suspicious.  His  judgment  and  reason- 
ing faculties  are  impaired.  His  volition  lacks  force.  Later  on  actual 
dementia  may  supervene.  If  alcohol  is  not  a  cause  of  dementia 
paralytica,  the  clinical  picture  it  induces  is  very  similar  to  it.  Mental 
breakdown,  epilepsy  and  other  serious  results  are  certainly  to  be  at- 
tributed to  it  in  a  certain  percentage  of  cases. 

Delirium  Tremens. — This  is  a  condition  bordering  on  but  not 
classified  as  an  insanity.  It  does  not  follow  an  excessive  ingestion  of 
alcohol  in  "a  person  usually  temperate ;  it  is  liable  to  occur  in  a  habitual 
drinker  who  may  take  an  overdose  of  the  poison.  It  is  therefore  an 
incident  merely  in  the  course  of  chronic  alcoholism.  It  may  even  occur 
as  the  result  of  the  sudden  withdrawal  of  the  poison. 

The  symptoms  appear  gradually  but  rapidly,  attaining  their  maxi- 
mum in  two  or  three  days.  They  may  be  provoked  by  a  shock  in  a 
heavy  drinker,  a  sudden  fright,  an  accident  with  a  profound  mental 
disturbance  following  it.  As  the  attack  approaches  the  individual 
sleeps  badly,  has  horrible  dreams,  is  restless,  depressed  in  spirits  and 
devoid  of  appetite.  Flashes  of  light  appear  before  his  eyes  and  noises 
of  a  disagreeable  character  ring  in  his  ears.  To  overcome  these  he 
takes  more  liquor,  goes  to  bed,  and  at  night  experiences  anew  the 
vivid,  distressing  and  terrifying  dreams,  the  visual  and  auditory  hallu- 
cinations, the  restlessness  and  harassing  motility.  As  the  attack  draws 
on  to  its  climax  absolute  insomnia  occurs,  the  visual  hallucinations 
assume  definite  shapes,  suspicions  and  uneasiness  are  prominent  and  a 
veritable  delirium  is  in  evidence. 

Loquacity  is  enormous.  The  patient  talks  incoherently  without 
cessation.  He  is  in  constant  motion ;  tries  to  get  up  and  go  out ; 
rushes  toward  the  open  window  or  attempts  to  push  past  his  guards  to 
the  door.  He  is  subject  to  all  sorts  of  distressing  and  suspicion-pro- 
voking hallucinations.  At  times  he  trembles  and  cries  out  in  evident 
alarm  and  fright.  He  declares  his  enemies  are  in  the  room ;  that  they 
are  trying  to  injure  him.  He  points  them  out,  though  his  finger  indi- 
cates only  empty  space.  He  thinks  he  is  surrounded  and  overrun 
with  rats  and  mice  and  snakes  and  other  crawling  vermin.     This  of 


GENERAL    INTOXICATIOMS  961 

course  increases   his   terror.      He   is  now   the  victim   of  the  genuine 
"horrors."" 

There  is  great  muscular  tremor  and  to  all  intents  the  poor  fellow 
is  in  the  state  of  a  thoroughly  terrified  animal.  The  countenance  is 
flushed  and  the  conjunctiva  congested.  The  pulse  is  soft,  frequent 
and  easily  compressed.  Perspiration  is  free  and  the  temperature, 
except  in  mild  cases,  is  slightly  raised.  The  average  temperature  is 
about  102  or  103  degrees  F.  When  it  climbs  to  108  or  109  degrees 
it  is  a  most  ominous  sign.  The  tongue  is  coated  heavily  and  there  is 
absolute  want  of  appetite. 

The  insomnia  continues  and  becomes  a  constant  feature.  In  three 
or  four  days,  if  the  case  is  favorable,  the  symptoms  all  aoate;  the  rest- 
lessness subsides ;  the  hallucinations  slowly  vanish  ;  and  the  appetite 
comes  back. 

In  severe  cases  the  delirium  continues,  and  being  less  active  is 
gradually  replaced  by  signs  of  profound  prostration.  Stupor  super- 
venes, the  respirations  grow  shallow  and  the  patient  dies  of  gradual 
heart-failure. 

The  symptoms  caused  by  the  polyneuritis  which  often  constitutes 
a  part  of  the  clinical  picture  of  chronic  alcoholism  will  be  found  de- 
tailed in  the  section  devoted  to  peripheral  nerve  lesions. 

Diagnosis. — The  diagnosis  of  chronic  alcoholism  and  of  delirium 
tremens  is  not  difficult.  The  entire  condition  of  the  patient  must  be 
taken  into  account.  The  cutaneous,  gastric,  circulatory,  renal,  nervous 
and  mental  appearances  must  all  be  given  due  consideration.  If  this 
is  done  it  is  almost  impossible  to  make  a  mistake  ,for  scarcely  any  other 
disease,  in  fact  none,  presents  so  broad  a  picture.  Acute  mania  and 
symptomatic  delirium  certainly  do  not,  for  they  are  wanting  in  the 
characteristic  visual  hallucinations  and  tremor.  The  tremor  may  be 
mistaken  for  the  tremor  of  dementia  paralytica,  but  the  latter  is  accom- 
panied by  a  somewhat  different  psychic  state,  more  of  an  exaltation  and 
with  more  distinct  delusions.  The  lungs  should  always  be  carefully 
examined,  for  in  some  intances  an  overlooked  pneumonia,  especially 
in  a  drunkard,  may  be  the  cause  of  the  delirium  starting.  The  same 
is  to  be  said  in  regard  to  erysipelas  and  trauma. 

Pathology  and  Pathogenesis. — The  changes  observed  in  the 
■nervous  tissues  in  chronic  alcoholism  are  slight  and  never  in  any 
sense  characteristic.  The  dura  may  be  hemorrhagic  and  inflamed. 
The  pia-arachnoid  is  often  opaque  and  thickened  and  chronically 
■changed.  Actual  signs  of  meningitis  are  rare  in  either  membrane. 
The  underlying  convolutions  of  the  brain,  in  old  cases,  are  wasted  and 
•depressed.  Adhesions  with  signs  of  genuine  meningo-encephalitis  may 
be  seen  in  some  protracted  cases.  Berkeley,  Buzzard,  Hoch,  Cole  and 
others  have  found  chromatolytic  and  other  degenerative  signs  in  the 
neurones.     Especially  so  in  alcoholic  neuritis  described  elsewhere. 

Though  these  findings,  as  well  as  others  outside  of  the  nervous 
system,  such  as  the  congestion  of  the  bases  of  the  lungs,  of  the  skin,  of 
the  face  and  of  the  kidneys,  are  highly  suggestiv'  in  chronic  alcohol- 
ism, they  do  not  explain  the  delirium  tremens.  The  latter  is  patholog- 
ically as  much  of  a  mystery  as  ever.    It  is  undoubtedly  due  to  an  acute 


962  GENERAL    INTOXICATIONS 

process  of  some  sort  in  the  cerebral  cortex,  which  disturbs  the  function 
of  the  latter,  runs  a  definite  course  and  then  tends  to  subside.  We 
cannot  even  form  a  guess  of  the  nature  of  that  process.  It  is  more 
than  a  mere  intoxication,  such  as  is  evidenced  in  the  findings  of  simple 
chronic  alcoholic  poisoning. 

Prognosis. — In  private  practice  the  prognosis,  for  obvious  rea- 
sons, is  better  than  it  is  in  hospital  practice.  Many  cases  recover,  but 
relapses  are  common  if  the  use  of  the  poison  is  resumed.  It  is  well 
for  the  patient  to  get  away  from  his  home  and  usual  haunts ;  for  this 
reason  institutional  treatment  is  more  favorable  than  home  treatment. 
Complications  add  to  the  gravity  of  the  prognosis  in  all  cases.  The 
condition  of  the  pulse  is  a  fair  indication  of  the  outlook.  If  some 
improvement  is  detected  after  sleep,  a  favorable  temination  may  be 
expected.  If  the  patient  wakes  up  and  is  as  bad  as  ever,  a  fatal  issue  is 
likely  to  occur  soon.  \'ery  high  temperature,  103  or  105  degrees,  is 
an  unfortunate  sign.  Sudden  rise  in  temperature,  with  old  age,  are 
bad  prognostics.  Associated  pneumonia  and  nephritis  cloud  the  prog- 
nosis ;   so  also  do  traumata,  wounds  and  operative  procedures. 

Treatment. — The  treatment  of  chronic  alcoholism  practically  re- 
solves itself  into  the  removal  of  the  poison.  This  had  better  be  done 
absolutelv.  Only  in  very  exceptional  cases  will  it  ever  be  found  nec- 
essary, on  account  of  the  pulse  or  tendency  to  delirium  tremens,  to 
allow'  a  little  alcohol  or  to  attempt  to  reduce  it  gradually.  The  craving 
for  the  liquor  should  be  suppressed  as  much  as  possible.  Capsicum 
is  efifective  sometimes.  General  tonics  like  strychnine,  quinine,  iron  and 
the  bitters  generally  are  always  in  order.  Abundant  nourishing  diet 
also  must  be  prescribed,  and  all  other  measures  that  tend  towards 
reconstruction  and  the  health  of  the  organism.  All  of  this  can  be 
carried  out  best  in  an  institution. 

The  special  manifestations  call  for  no  particular  consideration  here, 
for  their  management  will  be  found  described  under  the  various  dis- 
eases and  disorders  throughout  the  book. 

The  deliriiini  tremens  needs  careful  management.  The  patient 
must  be  put  under  restraint  and  vigilantly  watched  night  and  day. 
His  strength  and  violence  is  such  that  two  male  nurses  will  usually  be 
required  to  handle  him.  No  open  window  should  be  allowed  and  all 
dangerous  articles  and  medicines  by  which  he  might  injure  himself 
should  be  removed.  It  is  rarely  necessary  to  resort  to  a  "strait- 
jacket."  Other  means  can  sometimes  be  devised  by  which  he  can 
be  strapped  and  confined  to  his  bed.  Broad  straps  may  be  attached 
to  his  wrists  and  ankles  and  then  fastened  to  the  sides  of  the  bed.  A 
sheet,  long  and  strong,  may  be  wrapped  around  him  and  the  bed  at  the 
same  time.  If  the  hallucinations  are  increased  by  darkness  or  a  dim 
light,  the  room  had  better  be  kept  well  illuminated. 

The  alcohol  should  be  withdrawn  at  once,  except  in  those  few  cases 
in  which  there  is  a  dangerous  feebleness  of  the  pulse.  S<jfnetimes  even 
in  these  cases  ammonia,  ether,  cofifee  or  other  stimulant  may  be  found 
available.  Digitalis,  at  one  time  so  much  used,  is  now  not  considered 
safe,  as  it  accomplishes  little  in  the  mild  cases  and  has  often  proved 
disastrous  in  the  severe  ones. 


GENERAL    IXTOXICATIOXS  963 

Xourishment  is  of  supreme  importance.  It  should  be  fostered  as 
rapidly  as  possible,  and  in  as  thorough  a  manner  as  the  condition  of  the 
organs  will  permit.  Hence  it  is  well  to  use  a  liquid  diet  for  a  time  and 
give  it  every  two  or  three  hours.  Beef  tea,  milk,  lightly  beaten  eggs  are 
available. 

The  bowels  should  be  gently  and  promptly  moved,  but  severe 
purgation  must  be  avoided. 

Ware  has  shown  that  a  simple  expectant  treatment  gives  as  a 
rule  better  results  than  that  with  medicines.  However,  though  de- 
lirium tremens  usually  runs  its  course  without  being  affected  by  medi- 
cines, a  certain  amount  of  medicinal  treatment  is  in  order.  The  object 
to  be  attained  by  this  is  the  sedation  of  the  nervous  system,  the  produc- 
tion of  sleep  and  the  supporting  of  the  strength. 

Bromides  are  usually  disappointing.  They  may  produce  a  certain 
amount  of  quietude,  but  they  rarely  cause  sleep.  Full  doses  are  neces- 
sary. 

Paraldehyde  was  and  to  some  extent  is  still  popular.  Bromides 
with  tincture  of  capsicum  are  sometimes  verv^  effective.  Chloral,  unless 
markedly  contra-indicated  by  the  condition  of  the  heart,  is  the  most 
general  available  drug  in  this  condition.  Sixty  grains  can  be  given 
by  the  mouth  and  in  many  cases  a  refreshing  sleep  thus  be  secured. 
The  hypodermic  use  of  hyoscine,  gr.  i-ioo,  or  of  morphine,  gr.  %, 
cautiously  repeated,  is  second  in  value  only  to  chloral.  Opium  itself 
must  be  used  with  great  circumspection.  Aloreover,  it  tends  to  lock 
up  the  secretions.  Pilocarpine  has  been  recommended,  but  it  is  dan- 
gerous to  the  heart.  Cannabis  indica  has  effected  a  desirable  sedation 
in  a  few  cases.  Cold  douching,  cold  bathing  and  a  cold  pack  may  be 
tried  if  the  heart  can  bear  the  shock.  A  word  of  caution  is  necessary 
in  the  drug  treatment  of  delirium  tremens.  Ofttimes  in  spite  of  the 
most  heroic  administration  of  hypnotics  and  sedatives  the  patient  con- 
tinues wide  awake.  It  is  risky  to  go  on  plying  the  remedies  under 
such  circumstances,  for  as  they  accumulate  in  the  system  they  may 
suddenly  exhibit  a  poisonous  effect  and  the  patient  die  in  complete 
stupor. 

THE  OPIOI  AXD  KIXDRED  HABITS. 

There  are  certain  drugs  which  are  taken  medicinally  at  first,  rarely 
as  a  luxury,  and  producing  certain  pleasurable  or  unpleasurable  effects 
upon  the  nervous  system,  are  continued  until  the  disastrous  hab!t  is 
formed.  After  alcohol,  opium  and  its  alkaloid  morphia  are  most  abused 
in  this  way.  Then  follows  the  use  oi  chloral,  cocaine,  ether,  chloro- 
form, paraldehyde,  cannabis  indica.  Acute  poisoning  by  these  various 
drugs  is  a  subject  of  special  interest  to  physiology  and  toxicolog}* 
more  than  to  neurology.  Chronic  poisoning  is  pretty  nearly  the  same,, 
differing  more  in  degree  than  in  kind,  in  all  of  them.  A  description 
of  chronic  opium  poisoning  will  cover  more  or  less  the  clinical  picture 
produced  by  all  of  the  others.  As  in  the  discussion  of  chronic  alcohol- 
ism, I  will  briefly  consider  only  the  neurological  manifestations. 

Opium  Habit. — Morphinomania.  Morphinism.  In  certain  coun- 
tries where  opium  is  used  regularly  there  is  established  a  partial  im- 


964  GENERAL   INTOXICATIONS 

niunity  against  its  deleterious  effects.  The  eft'ects  are  present,  but  they 
are  not  so  obvious  as  they  are  with  us.  In  this  country  the  habit  is 
generally  started  by  the  use  of  morphia  to  relieve  pain.  A  headache 
or  an  old  sciatica,  the  pains  of  chronic  rheumatism  or  of  tabes  are  re- 
lieved for  the  nonce  by  the  drug,  even  upon  the  prescription  of  the 
medical  attendant.  When  the  pains  return  the  patient  acquires  the 
drug  for  himself,  learns  how  to  use  it  hypodermically  and  so  starts 
the  habit.  The  use  of  chloral  for  insomnia,  and  in  fact  all  of  the 
above-named  drugs,  is  started  in  this  way.  Women  and  physicians 
themselves  are  the  leading  victims  of  these  habits.  Gradually  the  dose 
has  to  be  increased  to  obtain  the  desired  relief,  not  from  the  pains  so 
much  now  as  from  the  depressing  after-effects  of  the  drug  itself,  so 
that  ere  long  the  patient  has  lapsed  completely  into  the  ranks  of  the 
habitues.  The  origin  of  the  habit  should  enforce  the  lesson  upon  the 
profession  to  be  chary  in  the  use  of  these  drugs,  especially  in  chronic, 
painful  states.  I  have  seen  several  lives  ruined  by  the  injudicious  use 
of  morphine  by  a  physician  at  the  beginning  of  a  simple  ailment.  When 
the  ailment  returned  the  patient  repeated  the  prescription  upon  his  own 
responsibility  until  he  found  himself  in  the  grip  of  the  habit. 

Symptoms. — There  has  never  been  written  a  more  vivid  account 
of  the  symptomatology  of  chronic  opium  poisoning  than  De  Quincey's 
"Confessions  of  an  Opium  Eater."  Every  physician  should  be  familiar 
with  this  masterly  essay.  It  both  teaches  and  warns  in  terms  that 
cannot  be  mistaken. 

The  symptoms  at  first  are  not  at  all  significant  and  sometimes 
whole  months  may  go  by  without  the  health  showing  much  deteriora- 
tion. Sooner  or  later,  however,  except  in  the  most  rare  instances,  the 
physical  and  mental  signs  of  breakdown  declare  themselves.  These  are 
subjectively  noticed  most  as  the  effect  of  the  drug  wears  off.  There  is 
a  feeling  of  weariness,  lassitude,  apathy,  depression  and  distress. 
Sometimes  there  is  nausea  and  gastric  discomfort.  The  mind  is  so 
depressed  and  the  patient  feels  generally  so  bad,  that  he  resorts  to  the 
drug  again  to  get  relief.  As  this  dose  wears  off  he  experiences  the 
same  depression  in  a  little  more  marked  degree.  And  thus  the  evil 
grows.  Physically  he  becomes  sallow  in  appearance,  emaciated,  gray 
and  aged.  His  appetite  is  deranged  or  gone  entirely.  His  pupils  are 
dilated  or  unequal,  except  when  under  the  direct  influence  of  the  drug. 
A  general  condition  of  asthenia  and  extreme  physical  debility  ultimately 
obtains. 

Showing  the  degenerative  effects  upon  the  nervous  system,  these 
patients  are  immoral,  irresponsible,  unreliable,  liars  and  cheats.  Los- 
ing their  higher  psychic  inhibitions,  they  .fall  a  step  toward  the  mon- 
key ;  hence  they  are  silly,  cunning,  without  a  manly  sense  of  obliga- 
tion, selfish,  maudlin  and  sentimental.  Their  mental  stamina  is  gone 
and  they  lack  initiative  force  and  self-control.  They  are  restless, 
irritable  and  emotional.  They  are  sometimes  the  victims  of  most  vivid 
and  terrifying  visual  and  auditory  hallucinations.  I  once  saw  a  pa- 
tient reach  out  to  put  her  hand  into  the  pocket  of  her  brother,  who 
she  thought  was  standing  beside  the  bed,  but  who  had  been  dead  many 
years.     Itching  and  other  paraesthesise  are  complained  of.     There  are 


GENERAL    INTOXICATIONS  965 

occasional  chills,  followed  by  profuse  sweats.  Sometimes  marked 
hysterical  and  neurasthenic  symptoms  dominate  the  clinical  picture. 
Some  of  the  profoundest  neurasthenia  I  have  ever  witnessed  was  in 
morphine  users.  Unless  the  case  is  not  too  far  gone,  so  that  under 
heroic  treatment  recovery  can  be  obtained,  these  patients  usually  go  on 
increasing  the  dose  of  the  drug  until  they  become  complete  physical 
wrecks   and  mental  dements,  and  die  of  inanition  and  heart   failure. 

There  is  nothing  to  be  said  of  the  pathology^  of  the  condition.  It 
is  a  progressive  degeneration  of  wide  extent,  toxic  in  origin. 

The  treatment  is  practically  impossible  outside  of  an  institution. 
The  patient  must  be  isolated,  systematically  fed  and  deprived  of  all 
possible  means  of  securing  the  drug.  In  mild  cases  the  drug  may  be 
withdrawn  abruptly  and  completely ;  in  severe  cases  only  a  gradual 
withdrawal  had  better  be  attempted.  For  the  first  week  or  so  the 
patient  had  better  be  kept  in  bed  and  the  drug  gradually  diminished. 
In  the  meantime,  with  the  aid  of  baths,  moral  suasion,  massage,  etc., 
the  restlessness,  insomnia,  nausea,  vomiting  and  even  the  abdominal 
pains  should  be  alleviated  as  much  as  possible.  The  bowels  should 
be  moved  gently  and  regularly.  The  diet  should  be  plain,  nourishing 
and  frequently  given.  It  should  consist  of  meat  broths,  milk,  whipped 
eggs,  matzoon,  koumys  and  other  light,  semi-fluid  articles. 

If  the  pulse  calls  for  it,  stimulation  with  aromatic  spirits  of  am- 
monia may  be  given.  Sleep  should  be  fostered  by  warm  baths,  w'arm 
drinks  and  other  measures ;  but  sometimes  sulphonal,  hyoscine  or  even 
morphia  itself  may  have  to  be  temporarily  resorted  to. 

Rapid,  forced  nourishment,  with  gradual  withdrawal  of  the  drug, 
is  the  sum  total  of  the  treatment  in  these  cases.  In  this  respect  it 
follows  along  the  same  lines  as  that  for  chronic  alcoholism.  In  spite 
of  the  occasional  complete  restoration  to  health,  these  patients  too 
often  lapse  back  into  their  old  habit ;  which  makes  the  treatment  of 
them  a  discouraging  and  thankless  task. 

TETANUS. 

This  is  sometimes  called  lockjan'.  It  is  a  most  virulent  form  of 
infection  in  which  there  are  severe  tonic  spasms  in  the  muscles  of  the 
body. 

'Etiology. — The  cause  of  this  disease  is  the  tetanus  bacillus  dis- 
covered by  Nicolaier  and  studied  by  Rosenbach,  Kitasato  and  others. 
The  gerrn  enters  the  body  through  an  open  wound  in  the  skin  or 
mucous  membrane.  It  is  found  in  the  earth.  It  has  been  isolated  and 
cultivated.  In  appearance  it  is  a  slender  rod  which  may  grow  into 
long  threads,  with  one  end  swollen  and  occupied  by  a  spore.  It  is  an- 
aerobic, motile  and  develops  at  ordinary  temperatures.  The  bacillus 
itself  does  not  enter  the  blood  or  organs,  but  at  the  site  of  the  woun.l 
it  produces  a  tox-albumin.  which  is  the  most  virulent  form  of  poison 
that  is  known  to  enter  the  body. 

Pathology  and  Pathogenesis. — There  are  no  distinctive  patho- 
logical findings.  The  congestions  observed  in  different  parts  of  the 
body,  the  perivascular  exudations  and  beginning  chromatolytic  changes 


966  GENERAL    INTOXICATIONS 

in  the  neurones  may  be  the  result  rather  than  the  cause  of  the  symp- 
toms. There  are  local  manifestations,  as,  for  instance,  in  and  about  the 
wound  and  the  inflammation  of  the  umbihcus  in  tetanus  neonatorum, 
and  constitutional  symptoms. 

Symp'i-qms. — We  speak  of  a  puerperal  tetanus,  a  tetanus  ncono- 
torum  and  of  endemic  and  cpideniic  attacks  of  the  disease.  Essentially 
they  are  all  the  same. 

The  symptoms  do  not  develop  immediately  after  the  invasion  of 
the  bacillus,  but  gradually.  It  has  been  suggested  that  this  is  because 
the  toxin  undergoes  a  still  further  change  in  the  system.  In  about 
ten  days  the  ea'rliest  signs  begin  to  appear.  The  first  are  a  little 
stiffness  in  the  neck,  slight  rigidity  in  the  jazv  and  difficulty  in  mastica- 
tion. General  toxic  symptoms,  such  as  chills,  fever  and  malaise,  may 
accompany  these  early  troubles.  Gradually  trismus  occurs,  or  tonic 
contraction  of  the  muscles  of  the  lower  jaw.  This  cardinal  symptom 
has  given  the  name  lockjaw  to  the  malady.  As  the  eyebrows  are  ele- 
vated and  the  corners  of  the  mouth  are  stretched  laterally,  the  counte- 
nance assumes  a  horrible  sort  of  a  grimace,  risus  sardoiiicus. 

In  children  the  symptoms  remain  thus  in  the  face  often,  but  in  adults 
the  musculature  of  the  body  is  generally  affected  also.  The  muscles 
of  the  back  are  most  frequently  involved  after  the  jaw  muscles.  This 
causes  a  bowing  of  the  neck  and  back,  so  that  the  patient  rests  on  his 
heels  and  occipit.  So  violent  is  this  opisthotonos  at  times  that  the 
abdominal  muscles  have  been  torn  directly  across.  If  the  entire  body 
and  limbs  are  rigid,  the  condition  is  known  as  orthotonos.  A  lateral 
bending  of  the  spine  causes  pleurothotonos.  In  rare  instances  the  ab- 
dominal muscles  are  so  violently  spasmodic  that  the  body  is  curved 
forward  into  a  condition  known  as  emprosthotonos.  Sometimes  the 
chest  is  compressed,  the  glottis  thrown  into  spasm,  the  respirations 
diminished  and  the  patient  almost  completely  asphyxiated. 

There  is  excruciating  pain  with  all  this  violent  spasm  and  the 
patient,  silent  and  immovable  as  if  clamped  in  a  vise,  is  bathed  in  a 
profuse  perspiration  and  reveals  untold  agony.  The  paroxysms  are 
variable  in  duration  and  are  easily  excited.  The  intervals  between 
the  paroxysms  are  usually  very  brief. 

The  temperature  is  usually  normal,  though  just  before  death  it 
may  rise  to  no  degrees  F.  Even  higher  temperatures  have  been  seen. 
Heart-failure,  asphyxia  or  exhaustion  puts  a  grateful  termination  to 
the  patient's  sufferings,  usually  in  a  paroxysm. 

What  is  called  head-tetanus  is  the  unilateral  stift'ness  of  the  jaw 
and  facial  muscles,  from  a  wound  on  that  side  of  the  head,  usually  near 
the  fifth  nerve. 

Diagnosis. — The  characteristic  clinical  picture  and  the  history 
of  a  wound  make  the  diagnosis  of  tetanus  a  matter  of  no  great  diffi- 
culty. The  similarity  between  this  form  of  toxaemia  and  strychnine 
poisoning  is  obvious.  There  is  no  history  of  a  wound,  however,  in 
the  latter,  and  trismus  does  not  lead  in  the  symptomatology.  In  tetany 
the  tonic  spasms  begin  in  and  are  usually  limited  to  the  ends  of  the 
extremities,  especially  the  fingers  and  hands.    Doubtful  cases  of  tetanu.s 


GENERAL    INTOXICATIONS 


967 


can  always  be  decided  by  a  bacteriological  examination  of  the  secre- 
tions in  the  wound. 

Prognosis. — This  is  decidedly  bad  in  the  traumatic  cases,  at  least 
80  per  cent,  dying  in  three  or  four  days.  In  the  so-called  idiopathic 
cases  the  mortality  ranges  about  50  per  cent.  Childoen  offer  the  worst 
prognosis.  If  the  symptoms  are  late  in  coming  on,  if  they  confine  them- 
selves to  the  jaw  and  face,  and  if  there  is  little  or'  no  fever,  hope  of 
recovery  may  be  entertained. 

Treatment. — Strict  attention  to  the  wound  is  the  first  requisite. 
It  should  be  thoroughly  excised,  antiseptically  washed  and  according 
to  Tizzoni  treated  with  nitrate  of  silver  to  destroy  the  germ  in  situ. 

A  dark  and  perfectly  still  room  should  be  the  domicile  of  the  pa- 
tient. Extraordinary  care  should  be  exercised  to  avoid  every  possible 
sort  of  irritation.     Noise,  light,  drafts  of  air,  change  of  nurses  should 

FIGURE  211. 


Tetanus.     (After  Sir  Charles  Bell.) 

be  guarded  against.  Even  such  strenuous  efforts  will  not  forestall  the 
paroxysms  in  most  cases. 

Feeding  is  a  problem  on  account  of  the  locked  condition  of  the 
jaws.  A  tube  may  be  passed  through  the  nostrils  into  the  gullet  or 
into  the  rectum  and  liquid  diet  adrninistered  in  that  way. 

The  control  of  the  spasms  is  best  secured  with  full  doses  of  mor- 
phia. Chloroform  inhalations  and  such  drugs  as  the  bromides,  chloral, 
cannabis  indica,  calabar  bean,  curare  are  available  agents.  Recovery 
has  sometimes  followed  their  employment. 

Blood-scrum  therapy  seems  to  hold  out  some  hopes  in  this  disease. 
By  Tizzoni  and  Cantani  the  blood-serum  of  immunized  animals  has 
been  used  with  some  degree  of  success.  Behring  and  Roux  have  each 
prepared  an  antitoxine  serum.  That  of  Tizzoni  seems  to  be  the  most 
successful.  It  is  recommended  that  2.25  grammes  of  the  Tizzoni  anti- 
toxine be  employed  for  the  first  dose  and  0.6  grammes  for  subsequent 
doses. 

From  the  observations  of  Marie  and  Morax,  of  Meyer  and  Ransom 


968  GICNERAL    INTOXICATIONS 

and  of  Rogers,  it  would  seem  to  be  advisable  to  expose  the  nerves  of 
the  part  in  which  the  primary  infection,  lies  as  near  the  cord  as  possible 
and  to  inject  directly  into  the  substance  of  each  nerve  the  antitoxine. 
This  prevents  the  absorption  of  more  poison  from  the  wound.  An 
injection  should  then  be  made  low  down  in  the  spinal  cord  or  in  several 
places.    The  injection  may  be  made  as  in  an  ordinary  lumbar  puncture. 

HYDROPHOBIA. 

This  is  sometimes  called  lyssa  and  rabies.  It  is  an  acute  disease 
of  warm-blooded  animals ;  is  dependent  upon  a  specific  virus ;  and  is 
characterized  by  marked  nervous  symptoms. 

Etiology. — The  poison  that  causes  rabies  is  found  chiefly  in  the 
nervous  system  and  in  some  secretions  such  as  the  saliva.  We  know 
nothing  of  its  essential  nature.  Many  animals  are  susceptible  to  it, 
namely,  man,  the  dog,  the  wolf,  the  cat  and  by  inoculation  the  ox, 
horse,  pig  and  skunk. 

The  period  of  incubation  is  shorter  in  children  than  it  is  in  adults. 
Bites  are  more  dangerous  in  exposed  parts  of  the  body,  like  the  face 
and  hands,  than  they  are  in  covered  parts  like  the  trunk  and  legs. 
Large,  punctured  wounds  afford  the  most  ready  entrance  to  the  poison. 
According  to  Horsley,  only  15  per  cent,  of  those  bitten  by  dogs  be- 
come affected  with  the  disease.     Wolf  bites  give  a  higher  percentage. 

The  incubation  period  in  man  ranges  from  two  weeks  to  three 
months.     The  average  time  is  about  six  or  eight  weeks. 

Pathology  and  Pathogenesis. — The  blood  vessels  of  the  cere- 
bro-spinal  nervous  system  are  congested,  particularly  in  the  medulla. 
There  is  an  exudation  of  leucocytes  in  the  perivascular  spaces  and 
minute  hemorrhagic  extravasations.  The  virus  is  found  abundantly 
in  the  brain,  spinal  cord  and  nerves,  but  not  in  the  kidneys,  spleen  or 
liver.  Congestions  are  observed  in  the  stomach,  larynx,  trachea  and 
bronchi. 

Symptoms. — These  appear  after  a  variable  interval  after  the  in- 
oculation. For  the  sake  of  practical  convenience,  they  are  divided 
into  those  of  the  premonitory,  excitable  and  paralytic  stages. 

The  earliest  signs  of  the  malady  are  irritability,  restlessness,  mental 
depression,  fear  of  impending  trouble,  pain  and  numbness  near  the 
bite,  headache,  loss  of  appetite  and  insomnia.  Often  there  is  a  general 
hypercesthesia  to  all  forms  of  sensation.  Light  and  noise  irritate  the 
patient.  The  larynx  being  congested,  the  z'oice  grows  husky  and 
deglutition  becomes  embarrassed.  The  pulse  is  somewhat  rapid  and 
the  temperature  is  slightly  elevated. 

Gradually  the  hypersesthesia  increases,  the  restlessness  grows, 
worse,  the  dejection  passes  into  alarm  and  general  spasms  begin  to 
develop.  This  is  the  beginning  of  the  stage  of  excitement.  As  this 
advances,  every  sort  of  external  stimulation,  a  noise,  a  bright  light,  a 
mere  verbal  suggestion,  a  draught  of  air  may  provoke  a  most  violent 
spasm.  The  spasms  are  strikingly  in  the  areas  supplied  by  nerves  from 
the  medulla,  namely,  the  muscles  of  the  larynx  and  mouth.  Thev 
are  reflex  spasms  and  are  exceedingly  painful.     An  attempt  to  drink 


GENERAL    INTOXICATIONS  969 

water  sets  up  the  spism  so  violently  that  the  patient  dreads  the  very 
thought  of  drinking,  hence  the  name  of  the  malady,  hydrophobia. 

The  mind  is  usually  affected  along  with  this  spasmodic  condition. 
The  patient  is  maniacal,  though  between  the  spasms  he  may  be  calm 
and  rational.  He  is  usually  harmless  and  even  takes  care  not  to  hurt 
any  one  unless  his  mania  is  furious.  The  temperature  is  generally  ele- 
vated in  this  stage. 

After  a  few  days  the  paralytic  stage  comes  on,  terminating  in 
coma  and  death  in  a  few  hours.  Heart  failure  and  syncope  close  the 
distressing  scene. 

Pseudo-hydrophobia  or  lyssophobia  is  in  all  probability  a  hysteroid 
trouble,  developed  upon  a  background  of  fear  and  dread.  An  indi- 
vidual who  has  been  bitten  may  undergo  and  simulate  all  the  phenome- 
na of  true  rabies  in  a  mild  degree.  The  condition  lasts  longer  than  in 
the  genuine  disease  and  the  patient  always  recovers. 

Diagnosis. — This  is  easy  in  view  of  the  history  of  a  bite  and  the 
characteristic  symptomatology.  In  cases  of  doubt,  or  better  still,  in 
all  cases,  so  as  even  to  forestall  any  possible  doubt,  the  animal  that 
has  bitten  the  patient  should  be  made  to  furnish  inoculations  from  the 
region  of  the  medulla.  If  these  be  tested  upon  other  animals,  especially 
the  rabbit,  the  paralytic  form  of  the  disease  will  appear  in  from  fifteen 
to  twenty  days.  This  will  tell  us  what  to  expect  in  the  patient  and 
confirm  the  diagnosis. 

Treatment. — This  is  not  the  place  to  discuss  the  general  prophy- 
laxis of  hydrophobia  and  the  laws  that  should  be  passed  in  regard  to 
the  muzzling  of  dogs.  The  preventive  inoculations  of  Pasteur  do  cer- 
tainly seem  to  be  effective  in  man,  if  we  are  to  judge  from  the  sta- 
tistics sent  out  by  the  various  Pasteur  Institutes  throughout  the 
world,  and  especially  by  the  one  in  Paris. 

The  management  of  a  case  of  hydrophobia  is  a  most  unsatisfactory 
task.  There  is  no  specific  remedy  and  so  the  treatment  must  perforce 
be  entirely  symptomatic.  It  must  also  be  heroic.  The  wound,  of 
course,  should  be  antiseptically  washed,  cauterized  and  kept  open  for 
several  weeks. 

When  the  disease  has  developed  it  is  absolutely  incurable.  Chloro- 
form and  morphia  are  about  the  only  agents  at  our  command  to  assist 
in  alleviating  the  patient's  sufferings.  Chloral,  bromides,  hyoscine 
are  practically  useless.  Cocaine  may  be  painted  on  the  throat,  enabling 
the  patient  to  swallow  somewhat.  Rectal  nutrient  enemata  as  a  rule, 
however,  will  have  to  be  resorted  to. 

Arthritis  Deformans. — Under  this  name  are  probably  masking 
a  number  of  conditions,  so  that  we  are  only  justified  in  regarding  the 
term  as  merely  representing  a  symptom-complex.  The  view  is  gaining 
ground  that  an  infection  or  toxaniia  underlies  the  manifestations.  The 
microbic  origin  of  the  disease  is  not  satisfactorily  established  yet, 
though  Schiiller,  Bannatyne  and  Blaxall  and  others  have  found  micro- 
organisms in  the  fluids  of  the  joints.  The  affection  is  often  associated 
with  previous  infections,  as  shown  by  the  statistics  of  Stewart  and 
others.  This  local  infection  theory  is  accepted  by  Baumler,  but  not  by 
Osier  and  others. 


970 


GENERAL    INTOXICATION'S 


An  attempt  is  being  made,  and  I  think  somewhat  successfully,  to 
bring-  the  old  neurotic  theory  of  the  origin  of  arthritis  deformans  in 
line  "with   the  infection  or  toxemic  theory.     There  can  be  no  doubt 


FIGURE  212. 


Arthritis    deformans.      (From    a   photograph  in  the  Pathological  Museum  of 
the  Med.  Depart,  of  the  Universitj-  of  Illinois.) 

of  the  tropho-neurotic  nature  of  the  malady  in  some  of  its  phases  at 
least.  We  are  familiar  with  the  acute  and  chronic  forms  of  arthritis 
that  often  accompany  gross  disease  of  the  cord.    The  arthropathies  of 


GENERAL    INTOXICATIONS 


97  L 


tabes  are  among  the  latter's  cardinal  symptoms.  In  dementia  para- 
lytica, syringomyelia,  hemiplegic  conditions  and  diseases  of  the 
peripheral  nerves,  atrophy  and  other  changes  not  infrequently  occur  in 
the  bones  and  in  and  about  the  jomts.  Hence  the  dependence  of 
trophic  joint  troubles  upon  disease  of  the  central  nervous  system  can- 
not be  gainsaid. 

There  are  several  features  in  rheumatoid  arthritis  that  suggest 
most  forcibly  a  central  nervous  explanation  of  the  trouble.  The 
changes  in  the  joints  are  all  but  identical  with  those  that  occur  in  the 
spinal  arthropathies  just  mentioned.  Similar  changes  of  a  trophic 
nature  occur  in  various  tissues  in  arthritis  deformans,  just  as  they  do 
in  many  spinal  diseases.  The  skin  becomes  glossy,  the  nails  get  brittle, 
the  bones  and  muscles  undergo  dystrophic  alterations.  The  muscles 
sometimes  markedly  atrophy.  The  distribution  of  the  joint  and  other 
changes  is  S3anmetrical,  thus  suggesting  a  central  cause  for  them. 
And  finally  neuritis  is  often  found  clinically  and  pathologically  in  the 
disease.  Osier  notes  that  in  a  case  of  chronic  arthritis  from  Dejerine's 
service,  Triboulet  and  Thomas  found  upon  post  mortem  a  sclerotic 
condition  of  the  posterior  columns  of  the  cord.  Puerperal  infection 
seems  to  have  been  the  primary  cause  of  the  trouble. 

Llewelyn  Jones  has  recently  called  attention  to  the  relationship 
of  rheumatoid  arthritis  to  some  other  neurotic  affections,  particularly 
tetany,  Raynaud's  disease  and  exophthalmic  goitre.  In  all  of  these 
troubles  there  is  more  or  less  similarity  in  the  vasomotor  phenomena, 
the  muscular  cramps  and  the  periarthritic  swellings.  As  Jones  sug- 
gests, these  diseases  may  all  pass  insensibly  into  each  other  as  members 
of  one  family  group,  owning  one  common  parent  origin,  a  cerebro- 
spinal toxmnia.  Macalister  has  adopted  views  similar  to  those  of 
Jones. 

Upon  these  and  other  grounds,  I  am  inclined  to  regard  arthritis 
deformans  as  a  cerebro-spinal  tropho-neurosis,  dependent  upon  some 
obscure  form  of  toxaemia.  I  have  not  classified  the  malady  among  the 
tropho-neuroses  in  the  earlier  part  of  the  volume,  because  there  are 
needed  more  data,  especially  from  examination  of  the  central  nervous 
system,  to  positively  affirm  that  the  disease  is  solely  of  neurotic  origin. 

Other  Toxmnic  Troubles. — There  are  many  other  neurotic  mani- 
-festations  and  symptom-complexes  that  are  not  sufficiently  sui  generis 
to  warrant  giving  them  the  dignity  of  a  special  nosological  position 
among  nervous  diseases.^  Such,  for  instance  are  the  nervous  types  of 
intluensa,  with  their  severe  headache,  profound  prostration,  pains  in 
the  back  and  joints,  depression  of  spirits,  melancholia  and  even  de- 
mentia ;  pertussis,  with  its  spasmodic  spells ;  and  many  cutaneous  ex- 
Iiibitions,  such  as  urticaria,  herpes,  pruritis  and  other  parcesthesicc. 
Most  of  these  symptom-groups  can  be  referred  to  neuritis,  poliomyelitic 
processes,  disease  of  the  posterior  root  ganglia  and  other  disorders  of 
the  lower  or  peripheral  neurones. 


Finis. 


GENERAL  INDEX. 


Abdomen,  scaphoid,  803 
Abiotrophy,  352 
Aboulia,   106 
Abscess,  cerebellar,  871 

pontile,  871 

bulbar,  871 

of  the  spinal  cord,  555 

cerebral,  867 
Abnormal  emotional   states,  759 

intellectual  states,  756 
Accommodation  reflex,  63 
Acoustic  striae,  704 
Acquired  diseases,  100 
Acromegaly,   339 
Acute  delirium,  874 

ascending  paralysis,  431 
Acroparsesthesia,  316 
Actinomycosis,    910 
Acrania,  956 
Adiposis  dolorosa,  345 
^sthesiometer,  49 
Afferent  diseases,  367 

path,  98 
Ageusia,  658 
Agenesis,  general,  422 
Agitans,  paralysis,  299 
Agraphia,   767,   769 
Age  in  etiology,  30 
Agoraphobia,  163 
Ainhum,  350 
Akinesia  algera,   iii 
Akinesia,  51 
Akatama,    590,    603 
Alopecia,  170 
Allorhythmia,  169 
Alcoholism,  959 
Alcoholic  coma,  761 

polyneuritis,  592 
Allocheiria,  48 

Alternate  hemiplegia,  jy~,  924 
Alternating  anaesthesia,  954 
Alexia,  762,  767,  770 
Amblyopia,   787 
Ambiguous  layer,  683 
Amyelinic  neuroma.  609 
Amimia,  771 


Amnesia,  595,   762 

Amnesic  aphasia,  767,  7651 

Amyelia,  570 

Amnestic  aphasia,  769 

Amyotrophic  lateral  sclerosis,  395,  401 

Amaurotic  family  idiocy,  451 

Anterior  fundamental  root  zone,  476 

radicular  zone,  475 

fossa,  tumor  of,  925 

poliomyelitis,  acute,  541 

commissure,  472 
Antero-lateral  tract,  476,  484 
Anode,  65 
Aphasia,  762,  767 

sensory,  769 

pressure.  771 

visual,   770 

amnestic,  769 

tactile,  771 
Aphonia,  766 

hysterical,  124 
Apoplexy,   hemorrhagic,   828 

ingravescent,   837 

spinal,  529 
Apoplectiform  bulbar  paralysis,  952 
Apoplexia  parva,  188 
Apoplexie  foudroyante.  830 
Apoplectic   coma,   762 
Apparatus,  nervous,  97 
Area,  auditory,  722 

olfactory,   722 
Analgesia,  48 
Analgesic  paralysis,  623 
Anaesthesia,  47 

crossed,  779.  954 
Anaesthetic  leprosy,  568 
xAngular  curvature.  501 
Angioneurotic   oedema,   318 
Aneurism,   intracranial,  934 
Animal,  a  vertebrate,  459 
Ankle  clonus,  61 

reflex,  61 
Aneurisms,  miliary,  828 
Aneurismal  erosion  of  vertebrae,  50Q 
Anaemia,  spinal,  527 

cerebral,   822 

hydrocephaloid,  824. 


974 


GENERAL    INDEX 


Anosmia.  779 
Anencephaly,  956 
Angioneuroses,  306 
Anarthria,  766 
Anidrosis,  74 
Area,  gustatory,   722 

visual,  722 
Areas,  motor,  723 
sensorial,   719 
Argentic  polyneuritis,  598 
Arthropathy,  383 
Arthritic  palsy,  617 
Arteriosclerosis,   828 
Arterial  system,  cortical,  711 
ganglionic,    713 

choroidal,  714     , 
Arteritis,   degenerative,   829 

syphilitic,  881 
Arthritis  deformans,  969 

of  spine,  510 
Arterise  sulci,  465 
Articular  hydrops,  322- 
Articulate  animal,  an,  459 
Argyria,   598 
Arthralgia,  596    . 
Arrhythmia,  169 
Arachnoid,  462,  667 
Arachnoidal  granulations,  667 
Arborization,  91 
Arm  palsy,  lower,  616 

upper,  616 
Argyll-Robertson  pupil,  63,  376 
Architecture,  neuronic,  96 
Arbor  vitse,   707 
Arsenical  polyneuritis,  597 
Ascending  current,  85 

neuritis,  582 
Asterion,  679 
Astereognosis,   48 
Astasia  abasia,  107 
Association  centers,  747 

tracts,  472,  735 
Associated  movement,  52,  776 
Astrophobia,   163 
Asphyxia,  local,  310 
Aspiration  pneumonia,  660 
Asymmetrical  cord,  570 
.Atavism,  28 
Ataxia,  377,  48,  54,  779 

hereditary,  444 

cerebellar,  444,  447 

of  thought,  449 

locomotor,   367 
Ataxic  paraplegia,  439 

aphasia,  767,  768 

hemiplegia,  836 


Atrophy,  74 

deuteropathic,  393 

optic,  784,  787 

lipomatous  muscular,  416 

occupation  muscular,  430 

progressive  muscular,  392 

protopathic,  393 
Atrophic  spinal  paralysis,  541 
Attitude,  45 
Atelomyelia,  570 
Atheroma,  arterial,  828 
Athyrea,  334 

Athetosis,  53,  425,  777,  778 
Aurium,  tinnitus,  166 
Aura,  198 
Auditory  symptoms,   792 

area,  722 
Aural  vertigo,  153 
Automatic  reflex  action,  476 
Automatism,  142 
Autohypnosis,   145 
Axis — cylinder,  91 

B 

Babinski    reflex,    56 
Baths,   79 

Basedow's  disease,  322 
Baillarger,  line  of,  683 
Basilar  meningitis,  814 
Bechterew,  striae  of,  6S3 
Betz,  giant  cells  of,  685 
Bell's  mania,  874 

palsy,  653 
Beriberi,  590,  603 
Biot's   respiration,   753 
Bifida,  spina,  569 
Bladder  crises,  382 
Blepharospasm,    167 
Blindness,  word,  762,  770 

psychic,  791 
Blushing,  167 
Blind   spot,   781 
Body,  pineal,  739 

pituitary,  739 
Bodies,  olivary,  705 

Pacchionian,  667 
Borborygmi,  168 
Brain,  diseases  of,  662 

anatomy,  662,  668 

diseases,  symptoms  of,  662 

weight   of,   664 

microcephalic,   664 

megalocephalic,  664 

membranes   of,  665 

conducting  tracts  of,  710,  735 

circulation  of,  710 


GEXERAL   INDEX 


975 


symptoms  of  disease  of,  749 

localization  sj'mptoms,  750 

general  symptoms,  751 

tumor  of,  gcg 

tumor  of  the  base  of,  925 

vesicles,  668 

membranes,   diseases   of,  793 

circulatory  diseases  of,  821 

the,  460,  663,  714 

veins  of,  714 

malformations  of,   956 

sand,  696 

structure,    680 
Bregma,  679 
Broca's  center,  724 
Brown-Sequard  syndrome,  492,  530 
Brachypnoea,   382 
Brachial  plexus,  614 
Bradycardia,  169 
Bulbar  paralysis,  apoplectiform,  952 

paralysis,  hereditary,  953 

paralysis,  progressive,  395,  406,  951 

abscess,  871 
Burdach's   column,   475,   484 
Bursitis,  633 


Capsule,  internal  and  external,  689 

internal,  functions,  736 
Cannabis  indica  habit,  963 
Caisson'  disease,  570 
Cauda  equina,  diseases  of,  S73 
Case-book  chart,  44 
Caries  of  the  vertebrae,  499 
Catalepsy,  146 
Calcaneus,  pes,  548 
Cajal,  cells  of,  685 
Cardiac  crises,  382 
Cavities  of  spinal  cord,  '562 
Cathode,  65 

Canals,  semicircular,  149 
Carcinoma  of  the  brain,  910 
Caudate  nucleus,  690 
Cauda  equina,  463 

tumor  of,  557,  559 
Causalgia,   48 

Cerebro-spinal  meningitis,  epidemic,  808 
Cerebral  anaemia,  822 

hypersemia,  825 

hemorrhage,  828 

embolism,  845 

thrombosis,  845 

palsy  of  childhood,  854 

diplegia,  854 

paraplegia,  854 

abscess,  867 


Cerebral — 

syphilis,  877 

localization,  662,  714 

cortex,  672,  681,  717 

concussion  coma,  761 

epiphysis,  695 
Cerebro-spinal  fluid,  495 
Cerebellar  agenesis,  450 

cortex,  707 

abscess,  871 

tract,  direct,  475,  484 
Cerebellum,  705,  740 

tumor   of,   922 

diseases  of,  954 
Center,  Broca's,  724 
Centers,  cortical,  717 

spinal,  480 

association,  higher,  747 

psychomotor,  729 
Central  convolutions,  tumor  of,  920 

myelitis,  537 

scotoma,  787 

ganglia,  tumor  of,  921 
Cells  of  Purkinje,  707 
Cervico-brachial  neuralgia,  251 
Cervical   enlargement,  463 

opisthotonos  of  infants,  S20 

myelitis,   536 

hypertrophic  pachymeningitis,  514 
Cephalic  flexures,  670 
Cephalcea,  234 
Cephalalgia.  234 
Chemosis,   811 
Choked  disc,  784 
Choroidal  arterial  system,  714 
Chloroform  habit,  963 
ChromophylHc    substance,   93 
Cheyne-Stokes    respiration,   753 
Chromatol3-sis,  36 
Chorea,  286 

habit,  265 

procursive,  299 

magna,  132,  299 

corpuscles,  289 

festinans,  299 

hysterical,  132,  299 
Chronic  chorea,  297 

infantile  meningitis.  820 

meningitis,  820 
Chiasm,  optic,  694,  7S8 
Cholesteatoma  of  the  brain,  910 
Chorda  tympani,  701 
Chloral  habit,  963 
Chvostek's  sign,  260 
Cincture  pain,  535 
Ciliary  body,  707 


976 


GENERAL    IXDEX 


Circle  of  Willis,  711 
Circulation  of  the  brain,  710 
Circulatorj-  diseases  of  brain,  821 
Claustrum,  689 

Clarke's  vesicular  column,  469 
Clonus,  ankle,  61 

jaw,  62 
Clonic  spasm,  52 
Climate  in  etiologj^  32 
Climato-therapy,  87 
Classitication  of  diseases,  22 
Claustrophobia,   163 
Clavus.  109 
Cocaine  habit,  963 
Coccydynia,  251 
Conarium,  695 
Collateral,  91 
Colonies,  epileptic,  215 
Coccj'geal  neuralgia,  251 
Conus  medullaris,  463 
Cornual   myelitis,    541 
Cord,  the,  460 

tumor  of,  555 

abscess  of,  555 

malformations  of,   569 

spinal,  diseases  of,  526 

spinal,  anatomy,  etc.,  459 
Cortex,  cerebellar,  707 

cerebral,  672,  681,  717 
Cortical  layers  684 

arterial  system,  711 

deafness,  723 
Corticopetal  path,   jss 
Conjugate  deviation,  j/j 
Conducting  tracts  of  the  brain.  710 
Compression  paralysis,  619 

myelitis,   537 
Compressed  air  paralysis,  570 
Corpus  callosum,  tumor  of,  922 
Corpus  dentatum,  707 
Consciousness,  74S 

loss  of.  760 

double,  762 
Concussion,   spinal,   574 
Congenital   myotonia,   284 
Conduction,  spinal.  476,  481 
Convulsion,   52,  772 
Convolutions,  cerebral,  672 
Corticofugal  path,  723 
Coma,  761 

Communicantes,  rami,  308 
Comma  tract,  descending,  475 
Commissure,  gray,  460 

anterior,  472 
Contraction  of  visual  field,  780 
Contracture,  53,  776 


Confabulation,  595 
Coprolalia,  270 
Corpus  callosum,  736 
Corpora  geniculata,  692,  738 

subthalamica.  692.  695,  738 

albicamia,  692,  739 

quadrigemina,  692.  695,  738 

striata,  689,  737 

quadrigemina,  tumor  of,  922 
Coxitis,  550 
Coxalgia,  633 
Cramp,  52,  167 

writer's,  273 
Cranial  nerves,  diseases  of,  643 

nerve  nuclei,  698 
Cranio-cerebral  topography,  677 
Craft  palsy,  430 

paral3'sis,   581.  621 
Cretinism,  334,  337 
Cremasteric  reflex,  56 
Crossed  pj^ramidal  tracts,  472,  483 

paralysis,  655 

paralysis,  924 

paralysis,  51 

anaesthesia,  779,  954 
Cross-legged  progression,  424 
Crises,  381 

Cry,  hydrocephalic,  817 
Crutch  palsy,  581,  620 
Crura  cerebri,  739 
Curs'ature,  angular,  501 

lateral,   509 
Cup,  phj-siological,  784 
Cyclopia,  957 
Cjtoplasm,  93 

Cysticercus  of  the  brain,  910 
Cyrtometer,  678 

D 
Deafness,  hysterical,  124 

cortical,  723,  762 

word,  723,  762,  769 
Deep  reflexes,  57 
Deformans,  arthritis,  969 

osteitis,  343 
Delirium,  760 

hallucinatory,  107 

acute,  874 

grave,  874 

tremens,  960 
Dentate  body,  707 

nucleus,   739 
Depression,  760 
Deuteropathic  atrophy,  393 
Degeneration,  36,  584 

reaction  of,  170 

primar}',  580 


GENERAL  INDEX 


977 


Degeneration,  secondary,  458, 
Descending  current,  85 

comma  tract,  475 
Demarche  tabeto-cerebelleuse, 
Degeneracy,  29 
Decentralization,  36 
Dercum's  disease,  345 
Dentate  ligament,  462 
Deviation,  conjugate,  'j'j'] 
Delusion,   758 
Dendrite,  91 

Dementia  paralytica,  888 
Dermographia,   74 
Diatheses  in  etiology,  2)2> 
Diagnosis,  general,  41 
Diabetic  polyneuritis,  603 
Digiti  mortui,  311 
Dietetics,  78 
Dipsomania,   959 
Direct  pyramidal  tracts,  472 
Diplegia,  774 

cerebral,  854 
Diplegic  facial  palsy,  654 
Diseases,  neuronic,  89 

primary,  20 

secondary,  21,  458 
Disorientation,  595 
Disseminated  sclerosis,  901 

nodal  neuritis,  584 

myelitis,  537 
Dislocations  of  vertebrae,  496 
Disc,   choked,  784 
Diplomyelia,   570 
Diphtheritic  polyneuritis,  599 
Direct  cerebellar  tract,  475,  48;; 
Diencephalon,  668 
Diastematomyelia,  570 
Diaphragmatic   paralysis,   613 
Diaphragm  sellje,  666 
Diplopia,  647,  792 
Diuresis,  74 
Diver's  paralysis,  570 
Doctrine,  the  neurone,  89 
Dolorosa,  adiposis,  345 

puncta,  629 

tubercula,  611 
Double  consciousness,  762 
Dorsal  nerves,  624 

myelitis,  536 
Dolorous  paraplegia,  508 
Dorsalis,  tabes,  367 
Dreaming,  141 
Dropsy,   sleeping,   148 
Drunkard's  paralysis,  581 
Dura  mater,  461,  665 
Dysthyroidation,  323 


580 


448 


Dysarthria,  407,  766 

Dystrophy,  progressive  muscular,  409 

Dyskinesis,  53 

Dysphagia,  658 

Dyspepsia,  nervous,  168 

Dynamometer,  52 


Echinococcus   of  the  brain,  910 
Echolalia,  270 
Echokinesis,  270 
Eclampsia,  252 

infantum,  252 

parturientium,  254 

urjemica,   255 
Efferent  diseases,  392 

path,  98 
Efferentes,  rami,  308 
Electric  chorea,  299 
Electro-diagnosis,  64 

therapy,  85 
Elephantiasis  mollis,  610 
Embolism,  spinal,  528 

cerebral,  845 
Emissive  centers,  717 
Emission,  seminal,   170 
Emprosthotonos,  966 
Emotional  states,  abnormal,  759 
Encephalomalacia,  845 
Encephalometer,  678 
Encephalitis,  864 

hemorrhagic,  865 

suppurative,  867 
Encephalocele,  957 
Encephalon,  663 
Encephalopathia  saturnina,  596 
Endoneuriuni,  577 
Endogenous  diseases,  25 
Endemic  polyneuritis,  603 
Endarteritis,  spinal,  528 
Enlargement,  cervical  and  lumbar,  463 
Epineurium,  577 
Epilepsy,   188 

hystero,  120 

Jacksonian,   206 

symptomatic,  206 

traumatic,  190 

reflex,  191 

senile,  191 
Epileptic  fit,  200 

coma,  761 

face,  209 

colonies,  215 
Epileptic  equivalent,  205 
Epilepticus,   status,   189,  207 
Epiphysis  cerebri,  695,  739 


978 


GENERAL   INDEX 


Epidemic  cerebrospinal  meningitis,  808 

Equivalent,  epi'.eplic,  205 

Equivalents,  hemicranial,  230 

Equino-varus.  548 

Erythromelalgia,   314 

Erigentes,  ner\ri,  308 

Erosion  of  vertebrae,  aneurismal,  509 

Erythrophobia,  167 

Erb's  sign  in  tetany,  260 

palsy,  616 

spinal  paralysis,  523 
Essential  contracture,  256 
Etiology,  general,  25 
Ether  habit,  963 
Examination  of  patient,  41 
Excitation,  reaction  of,  260 
Exaltation,  759 
Exudative,  inflammation,  39 
Exogenous  diseases,  25 
Exercise,  physical,  79 
External  pachymeningitis,  512 
Exophthalmos,  324 
Exophthalmic  goitre,  322 

F 
Facts,  184 

Facies  epileptica,  209 
Facial  hemiatrophy,  348 

tic,  265 
Factitia,  urticaria,  168 
Failure,  mental,  762 
Familial  diseases,  29 
Falling  sickness,  188 
Fasciculus,  solitary,   704 
Fear  neuroses,  163 
Fetichism,  170 
Fever,  spotted,  808 
Fibroma  moUuscum  multiplex,  609 
Fissures,  cerebral,  672 
Fibres,  tangential,  683 
Fibrillary  tremor,   53 
Fibroma  of  the  brain,  910 
Fit,  epileptic,  200 
Filum  terminale,  461,  463 

diseases  of,  573 
Flaccid  paralysis,   51 
Fluid,  cerebro-spinal,  495 
Flexures,  cephalic,  670 
Forced  movement,  53 
Focal  neuritis,  629 
Frankel's  exercises,  391 
Folic  musculaire,  291 
Folic  de  grandeur,  894 
Frontal  lobes,  tumor  of,  918 
Friedreich's  disease,  444 
Fractures  of  the  vertebrae,  496 


Frontal   lobes,   functions  of,  719 
Functional  diseases,  40 
Funiculus,  577 

gracilis,  475 

cuneatus,  475 


GaLeni,    venae,    714 
Ganglia,  auditory,  698 

Gasserian,  698 

jugular,  658,  698 

geniculate,   698 

petrous,  658,  698 
Ganglionic  arterial  system,  713 
Ganglion  habenulae,  691,  696 
Gastric  crises,  381 
Gait,  45 

herniplegic,  834 
Gangrene,  symmetrical,  310 
Gelatinous  substance  of  Rolando,  469 
General  paresis,  888 
Genius,   29 
Gesture  aphasia,  767 
General  tic,  269 

Gilles  de  la  Tourette's  disease,  269 
Gland,  pineal,  695,  739 
Globus  hystericus,  119 

pallidus,  690 
Glomerulus,  olfactory,  688 
Glabella,  679 
Glioma  of  the  cord,  568 

of  the  brain,  910 
Gliosis,  40,  457,  563 
Gliomatosis,  40 
Glossodynia,  250 
Giant  swelling,  318 

cells  of  Betz,  685 
Gigantism,  343 
Girdle  pain,  535 
Goitre,  exophthalmic,  322 
Goll's  column,  475,  484 
Gowers'  tract,  476,  484 
Grand  mal,  188,  200 
Gray  matter,  97 

commisure,  460 
Giant  urticaria,  320 
Granulationes  arachnoideales,  667 
Granular  meningitis,  815 
Grave's  disease,  322 
Grave,  delirium,  874 
Gratiolet,  radiations  of,  694 
Graphospasm,  273 
Grandeur,  folic  de,  894 
Gustatory  symptoms,  792 
area,  722 


GENERAL   INDEX 


979 


Gummatous  meningitis,  878 

neuritis,  521 

meningitis,  521 
Gymnastics,  83 
Gyri,  cerebral,  676 

H 

Habenulse,  ganglion,  6gi,  696 
Habit  chorea,  265 
Haematoma,  794 
Hasmoglobinuria,  312 
Hasmic  headache,  235 
Hallucinatory  delirium,  107 
Hallucination,  757 
Hand,  preacher's,  515 
Head-tetanus,  966 
Headache,  234,  751 

paroxysmal,  226 
Heart,  tobacco,   169 
Hematomyelia,  528 
Hematorrhachis,    524 
Hematomyeloporosis,   529 
Hemicranicus,  status,  230 
Hemiachromatopsia,   789 
Hemiageusia,  655 
Hemichorea,  776 
Hemiatrophy,  facial,  348 
Hemianopsia,  782,  789 
Hemicranial  equivalents,  230 
Hemiplegia,  51,  724,  T]2, 
•  progressive,  885 

infantile,  854 

alternate,  "JTJ,  924 

ataxic,  836 
Hemiplegic,  a,  833 

gait,  834 
Hemicrania,  221 
Hemihypertrophy,  343 
Hemispasm,  772 
Hemiansesthesia,  TJ"] 
Hemorrhage,  spinal  meningeal,  524 

spinal,  528 

cerebral,  828 

ventricular,   836 
Hemorrhagic  encephalitis,  865 

pachymeningitis,  794 
Hephaestic  hemiplegia,  281 
Hereditary  chorea,  297 

trophcedema,   321 

ataxic  paraplegia,  443 

ataxia,   444 

cerebellar  ataxia,  444 

bulbar  paralysis,  953 
Heredity,  26 
Herpes,  970 
Heterotopia.  570 


Hysterogenic  zones,  iii 
Higher  centers,  747 
Hoffmann's  sign,  260 
Homonymous  hemianopsia,   783,  7? 
Horrors,  961 
Huntington's  chorea,  297 
Hydatid,    spinal,    509 
Hydromyelia,  563 
Hydrorrhachis  externa,  569 
Hydrocephalus,   938 

acute,  814 
Hydrocephalic  cry,  817 
Hydrocephaloid  anaemia,  824 
Hydrops,  articular,  321 
Hydrophobia,  968 
Hydrotherapy,  82 
Hydroencephalocele,  957 
Hyperesthesia,  47 
Hypaesthesia,  47 
Hyperalgesia,  48 
Hyperosmia,  780 
Hyperthyroidation,  323 
Hypertrophy,   74 
Hypertrophic  pachymeningitis,  514 

osteo-arthropathy,   345 
^     neuritis  of  infants,  454 
Hypertemia,  spinal,  527 

cerebral,  825 
Hyperkinesis,  52  , 

Hyperidrosis,  74 
Hypoglossal  tic,  266 
Hypochondriasis,  173 
Hypophysis  cerebri,  739 
Hypnotism,   142,   143 
Hypnosis,  145 
Hysteria,  102 

Hysterical  chorea,  132.  299 
Hystero-epilepsy,   120 
Hystericus,  status,   122 

globus,  119 


Ideas,  764 

Idiocy,   amaurotic   family,  451 

Idiopathic  reflex  irritability,  63 

Illusion,  756 

Incoordination,  53 

Indirect  pyramidal  tracts,  472 

Infection,  33 

Infantile  hemiplegia,  854 

palsy,  541 

meningitis,  chronic,  820 

convulsions,  252 
Influenza,  971 

Ingravescent   apoplexy,  837 
Inherited  diseases,  100 


98o 


GENERAL   INDEX 


Inhibition,    746 
Inhibiting  lobe,   747 
Inhibitory  functions,  721 
Inion,  679 
Inference,  184 
Infectious  polyneuritis,  599 
Incisures,  Lantermann's,  579 
Inflammation,  38 

interstitial,   579 

parenchymatous,  579 
Internal  capsule,  736 
Intermittent  incontinence  of  urine,  480 
Intercostal  neuralgia,  251 
Interstitial  hypertrophic  neuritis,  454 
Interstitial   nervous   diseases,  457 

inflammation,  579 

neuritis,   581 
Intracranial  aneurism,  934 

sinuses,  661 

veins,  thrombosis  of,  850 

sinuses,  thrombosis  of,  850 
Intoxication,  33 

vertigo,   155 

lead,    595 
Intermittent  articular  hydrops,  321 
Intentional  tremor,  905 
Intellectual  states,  abnormal,  756 
Insomnia,  146 
lodothyrin,  323 
Irritation,  spinal,  505 

sensory,  779 
Irritability,   19 

Iridochoroiditis,  purulent,  811 
Ischuria  paradoxa,  480 
Ischiadic   neuralgia,  627 


Jaw,  reflex,  62 
clonus,  62 
Jacksonian  epilepsy,  188,  206 


Kakke,  590,  603 

Karyochrome,  93 

Keratitis,  neuroparalytic,  651 

Kernig's  sign,  517,  803 

Knies'  obstructive  optic  neuritis,  870 

Korsakoff's  syndrome,  594 

Kubisagara,   156 

Kyphosis,  341,  501,  508 

L 
Latah,  270 
Laryngeal  crises,  382 
Lambda,  679     . 
Lancisi,  nerves  of,  687 
Labile  current,  85 


Lateral  curvature,  509 

limiting  layer,  476 
Language,  disturbances  of,  763 
Laryngeal  paralysis,  660 
Lantermann's  incisures,  579 
Landry's  paralysis,  431 
Lancinating  pains,  375 
Layer,  ambiguous,  683 
Lead  palsy,  619 

intoxication,  595 
Lenticular  nucleus,  690 
Lesser  zone,  475 
Leprosy,  anaesthetic,  568 
Leontiasis  ossea,  343 
Lethargy,   146 
Leptomeningitis,  intracranial,  798 

spinal,  516 
Leprous  polyneuritis,  604,  611 
Lipoma  of  the  brain,  910 
Lipomatous  muscular   atrophy,  416 
Little's  disease,  421,  425,  854 
Ligamentum  dentatum,  462 
Lissauer's  zone,  476 
Lobar  sclerosis,  857 
Lobes,   cerebral,  672 
Lobe,  inhibiting,  747 
Local   asphyxia,  310 

thermometry,  74 
Lockjaw,  965 
Locomotor  ataxia,  367 
Localization  schools,   716 

cerebral,  662,  714 

spinal,  459,  485 
Longitudinal  fasciculus,  posterior,  699 
Lordosis,  417 
Lower  arm  palsy,  616 
Loss  of  consciousness,  760 
Lumbo-sacral  myelitis,  536 
Lumbar  neuralgia,  251 

enlargement,  463 

puncture,  459,  493,  8c6 

plexus,  624 
Luy's  body,  695 
Lyssophobia,  969 
Lyssa,  968 

M 

Macrojesthesia,    48 
Mortui,  digiti,  311 
Macropodia,  343 
Macrocheiria,  343 
Magrums,  297 
Mai,  petit,   188,  204 
grand,  188,  200 
Malignant  meningitis,   Sit  | 

Malingering,   133,   1S6 


GENERAL   INDEX 


98i 


Malum  cotunnii,  627 
Malformations  of  the  brain,  956 

of  the  cord,  569 
Malarial  coma,  762 
Mania,   Bell's,  874 
Main-en-griff e,  515,  623 
Marriage,  "/j 
Marrow,  spinal,  461 
Marantic  thrombosis,  850 
Mariotte,  blind  spot  of,  781 
Mastodynia,  251 
Masochism,  170 
Masticator\-  tic,  266 
Masturbation,   169 
Alassage,  84 
Matter,  nerv'ous,   17 

gray  and  white,  97 
Mater,  dura,  461,  665 

pia,  462,  667 
Mechanico-therapy,  83 
Medulla  oblongata,  740 

oblongata,  diseases   of,  948 

oblongata,  tumor  of,  923 

olfactorius.  687 

spinalis,  461 
Medullary  substance,  91 
Medicinal  treatment,  87 
Megalopsia,  792 
Megalocephalic  brain,  664 
Magalocephaly.  343 
Megrims,   297 
Melancholia,  162,  174 
Membranes,    spinal,    diseases    of,    511 

of   brain,   665 

of  the  brain,  diseases,  793 
Mental  failure,  '/62 

paralysis,  776 
^Meniere's  disease,  153,  657 
Meningitis,  granular,  815 

chronic,  820 

syphilitic   spinal,   519 

gummatous,  521,  878 

pneumococcus,  813 

tuberculous,  814 

serous,  820,  939 

malignant,  811 

ossifying,   chronic,  820 

epidemic  cerebrospinal,  808 

chronic  infantile,  820 

spinal,  512 

basilar,  814 
Meningeal  hemorrhage,   spinal,   524 
Meningo-myelitis,  syphilitic,  523 
Meningomyelocele,   569 
Meningo-encephalitis.   864 
Meningocele,  569,  957 


Meningomyelitis,  531 

Mesencephalon,  668 

A'leriatschenje,  270 

Mercurial  polyneuritis,  598 

Aletasyphilis,  367 

Metencephalon,  668 

Metatarsalgia,  Morton's,  633 

Micromegaly,   343 

Micropsia,   792 

Microcephalic  brain.  664 

Microgyria,  857 

Micrencephaly,  957 

Micromyelia,  570 

Microcephaly,  957 

Middle  fossa,  tumor  of,  926 

Migraine,  221 

Mitral   cells,  688 

Miliary  aneurisms,  828 

Alinor  chorea,  287 

Mind,  the,  129,  140,  754 

Miryachit,  270 

Mode  of  life,   31 

Mogiphonia,  282 

]\Iogigraphia,   273 

Monroe,  groove  of,  669 

Monospasm,  724,  772 

Monocular  diplopia,  792 

Monoplegia,  51,  773 

Morphinomania,  963 

^lorphinism,  963 

Morphine  habit,  963 

Morton's  fluid,  570 

Morvan's  disease,  568,  623 

INIorbus  sacer,  188 

Motor  projection  paths,  359,  483.  710 

segment,  361 

symptoms,  50 

areas,  723 

aphasia,  767,  768 
Movements,  associated.  776 
Multiplex,  paramyoclonus,  271 
Multiple   sclerosis,   901 

neuritis,  589,  454 

neuromata.  609 
Musca;  volitantes,  166 
Muscles  and  their  functions,  636 

rubber,  621 
Muscular  sense,  721 

insanity,  291 
Mutism,  hysterical,   124 
Myasthenia   gravis,   429 
Myelencephalon,  668 
Myelo-encephalitis,  864 
Myelitis,  531 

syphilitic,  522 
Mvelinic  neuroma,  609 


982 


GENERAL   INDEX 


Myelocele,  569 
Myelomalacia,  500 
Myokymia,  167.  264 
Myoclonus-epileps}',  207 
Myoclonia,   264,   271 
Myospasia,  271 
Myospasm.  262 
Myotatic  irritability,  60 
Myositis  of  the  diaphragm,  613 
Myospasia  impulsiva,  269 
Myotonia  congenita,  284 
Myosclerosis,  411 
Myxoedema,   335 
Myxoma  of  the  brain,  910 

N 

Narcosis,  opium,  762 
Nausea,  752 

Nationality  in  etiology,  31 
Necrobiosis,  39,  846 
•Nerves,  spinal,  diseases  of,  613 

dorsal,  624 

phrenic,  613 

posterior  thoracic,  614,  617 

suprascapular,  614,  618 

rhomboid,  614 

subclavian,   614 

anterior   thoracic,   614 

musculo-cutaneous,  614,  618 

median,  614,  621 

of  Wrisberg,  614 

internal   cutaneous,   614 

ulnar,  614,  622 

subscapular,  614 

circumflex,  614,  618 

musculo-spiral,  614,  619 

dorsal,  624 

obturator,  626 

anterior  crural.  626 

external  cutaneous,  626 

superior  gluteal,  626 

external  popliteal,  634 

internal  popliteal,  635 

tibialis  posticus,  635 

plantar,  635 

cranial,  diseases  of,  643 

olfactory,  643,   688 

optic,  643 

oculomotor,  or  third,  646 

trochlear,  patheticus,  fourth,  648 

abducens,   or   sixth,   648 
■  trifacial,  trigeminal,  fifth,  649 

pudic,  626 

sciatic,  626 

peroneal,  627,  634 

facial,  or  seventh,  652 


Nerves — 

artist's,  653 

auditory,  or  eighth.  657 

glossopharyngeal,  or  ninth,  658 

pneumogastric,   tenth,  659 

accessorius,  eleventh.  660 

hypoglossal,  twelfth,  661 

of  Wrisberg,  700 

energy,  specific,  243 

diseases  of,  576 

anatomy  of,  576 

tumors  of,  609 

the.  460,  577 

sympathetic,   306 
Nervous  system,  the,  17 

matter,  17 

organ,  20 

apparatus,  97 

dyspepsia^  168 
Nervi  erigentes,  308 
Neuroses,  102 
Neuroses,  traumatic,   182,   575 

fear,    163 

occupation,  272 
Neuralgia,  242 

sciatic,  633 
Neuro-retinitis,   784 
Neurone,  the,  91 
Neurone  doctrine,  the,  89 
Neuronic  diseases,  89 

functions  and  symptoms,  460 
Neural  tube,  668 
Neuralgia  ischiadica,  627 
Neuroma,  plexiform,  610 

true  and  false,  609 
Neuromata,  609 

multiple,  609 
Neurolization,  585 
Neuritis,  581 

optic,  784,  787 

retrobulbar,  787 

Knies'   obstructive,   870 

multiple  syphilitic,  886 

sciatic,  633 

focal,  629 

multiple  gummatous,  521 

hj'pertrophic,  454 

multiple,  454,  589 
Neuroglia,  95,  457 
Neuromyelitis,   454 
Neuroparalytic  keratitis,  651 
Neurofibromatosis,  612 
Neuropathy,  28 
Neuropathic  headache,  236 
Neuronic  architecture,  96 
Neurotic  vertigo,    155 


GENERAL   INDEX 


98: 


Neurasthenia,   157 
Neuraxone,   91 
Neurilemma,  91 
Neighborhood    symptoms,    718 
Negro  lethargy,  148 
Nocturnus,  pavor,   141 
Nigra,  substantia,  695 
Non-neuronic   diseases,   457 
Nocturnus,  favor,  141 
Node  of  Ranvier,  578 
Nodal  neuritis,  disseminated,  584 
Nucleus,  motoroculi,  699 

trigeminal,  699 

of  Dieter,  703 

dentatus,  739 

emboliformis,  707 

fastigium,  707 

globosus,  707 

caudate,  690 

lenticular,  690 

red,  692,  695,  739 

tegmenti,  695,  739 

of  Bechterew,   704 

accessorius,    704 

vago-glosso-pharyngeal,  704 

ambiguus,  705 

hypoglossal,  705 

facial,  700 
Nuclei,  auditory,  703 

pontile,  741 

nodal,  705,  741 

cranial  nerve,  698,  741 

gracilis  and  cuneatus,  475 
Nutans,  spasmus,  268 
Nymphomania,  381 
Nystagmus,  449,  905 


Obstetrical  palsy,  617 
Obsession,   163,   759 
Occipital  neuralgia,  250 

lobes,  tumor  of,  921 
Occupation  muscular  atrophy,  430 

neuroses,   272 

in  etiology,  31 
Ocular  palsy,  periodical,  647 

vertigo,   152 
Qidema,  angioneurotic,  318 
Olfactory  paraesthesia,   780 

hallucinations,  780 

area,  722 

lobes,  686 

glomerulus,  688 

symptoms,  779 
Olivary  bodies,  705,  741 
Ophthalmoplegia,  427,   950 


Opisthotonos,  810 

cervical,  of  infants,  820 
Opium  habit,  963 

narcosis,  762 
Optic  thalami,  691,  737 

tracts,  692 

chiasm,  694,  788 

neuritis,  784,  787 

atrophy,  784,  787 

symptoms,  780 
Operculum,  675 
Oppenheim's  reflex,  57 
Organ,  the  nervous,  20 
Organo-therapy,  88 
Organic  headache,  237 

diseases,  loi 
Orthotonos,  810 
Ossea,  leontiasis,  343 
Ossifying  meningitis,  820 
Osteoma  of  the  brain,  910 
Osteomyelitis,  550 
Osteitis  deformans,  343 
Osteo-arthropathy,   hypertrophic,   345 


Pachydermatocele,  610 
Pachymeningitis,  793 

interna,  794 

externa,  512,  794 

cervical  hypertrophic,  514 
Pacchionian  bodies.  667 
Pachyakria,  339 
Paget's  disease,  343 
Pain,  242 
Palpitation,   168 
Palmus,  269 
Palmar  reflex,  56 
Pallidus,  globus,  690 
Palsy,   infantile,  541 

craft,  430,  621 

professional,  430,  621 

arthritic,  617 

obstetrical,  617 

serratus,  617 

lead,  619 

cerebral,  of  childhood,  854 

Erb's,  616 

upper  arm,  616 

Klumpke's,  616 

lower  arm,  616 

facial,  653 

Bell's,  653 

rheumatic,  653 

refrigeratory,  653 

crutch,  581,  620 

recurrent  ocular,  647 


984 


GENERAL   INDEX 


Pantophobia,  163 
Pantomimic  aphasia,  767,  771 
Pantomime,  77r 
Panophthalmitis,  651 
Papillitis,  784 
Paralysis,  51 

compression,  619 

analgesic,  623 

apoplectiform   bulbar,   952 

diver's,  570 

atrophic  spinal,  541 

craft,  581 

drunkards,  581 

acute  ascending,  431 

Landry's,  431 

agitans,  299 

periodical,  436 

hereditary  bulbar,  953 

crossed,  924 

compressed  air,  570 

crossed,  655 

psychic,  776 

pseudo-bulbar,  766,  774 

laryngeal,  660 

diaphragmatic,  613 
Paralytic  chorea,  291 

vertigo,   156 
Paralytica,  dementia,  888 
Parry's  disease,  322 
Partial  epilepsy,   188,  206 
Paroxysmal  headache,  226 
Parkinson's  disease,  299 
Paresis,  51 

general,  888 
Parietal  lobes,  tumor  of,  919 
Parenchymatous   neuritis,  581 
Paraldehyde  habit,  96 
Parasyphilis,  367 
Parturient  convulsions,  254 
Paramyoclonus   multiplex,   271 
Paraplegia,  51 

dolorosa,   508 

syphilitic,  522 

cerebral,  854 

spastic,  421 

ataxic,  439 
Paradoxical  ischuria,  480 

muscular  contraction,  64 
Paraphasia,  767 
Parjesthesia,  47 
Paramimia,  771 

Parenchymatous  inflammation,  579 
Paraplasm,  93 
Para^sthesise,  971 

Pars  intermedia  of  Wrisberg,  652 
Patella  reflex,  58 


Pathology,  general,  35 
Patient,   examination  of,  41 
Path,  corticopetal,  733 

corticofuga!,   733 
Paths,  afferent  and  efferent,  98 
Pavor  nocturnus,  141,  757 
Pederasty,  170 
Peripheral  nerves,  diseases  of,  576 

nerves,  anatomy  of,  576 
Perforating  ulcer,  383 
Perineuritis,   581 
Pertussis,  971 
Periodical  paralysis,  436 

ocular  palsy,  647 
Perversion,  sexual,  170 
Peripheral   nerves,  pathology  of,  579 
Peroneal  atrophy,  399 
Perimeter,  780 
Periependymal  myelitis,  537 
Perikaryon,  93 
Perineurium,   577 
Pes   equino-varus,   548 

calcaneus,  548 

anserinus.   653 

pedunculi,  697 
Petit  mal,  188,  204 
Pharyngeal  crises,  382 
Phobia,  107,  163,  759 
Phlebitis,  851 
Phrenic  nerve,  613 
Physiology  of  the  brain,  714 
Physiological  cup,   784 

scotoma,  781 
Ph3'sical  exercise,  79 
Pia  mater,  462,  667 
Pineal  gland,  695,  739 
Pianist's  cramp,  273 
Pied-en-griffe,  634 
Pituitary  body,   739 
Plexus,  brachial,  614 

palsy,  brachial,  616 

lumbar,  624 

sacral,  626 

coccygeal,  626 
Plexiform  neuroma,  610 
Plantar  neuralgia,  252 
Pleurothotonos,  966 
Pneumonia,  aspiration,  660 
Pneumococcus  meningitis,  813 
Pododynia,  252 
Polyneuritis,  589 

senile,  590 

alcoholic,   592 

toxic,  592 

lead,   595 

saturnine,   595 


GENERAL   INDEX 


985 


Pclyneuritis — 

arsenical,  597 

argentic,  598 

mercurial,  598 

syphilitic,  598 

infectious,  599 

diphtheritic,  599 

rheumatic,  602 

puerperal.  602 

diabetic,  603 

endemic,  603 

leprous,  604,  611 
Poliomj'elitis,  532 

anterior  acute,  541 

of  adults,  552 
Poliomyelitis,  532 
Polioencephalitis,  409,  855,  864 

acute  inferior,  951 

acute  superior,  951 
Polyclonia,  271 
Polysesthesia,  48 
Pons  Varolii,  740 

tumor  of,  923 

diseases  of,  948 
Pontile  abscess,  871 
Porencephaly,  856,  957 
Postero-median  tracts,  475,  484 
Postero-lateral  tracts,  475,  484 
Postero-internal  radicular  zone,  475 
Posterior  longitudinal  fasciculus,  699 

fossa,  tumor  of,  926 

spinal  sclerosis,  2>^y 
Post-hemiplegic  chorea,  297 
Pott's  disease,  499 
Potamophobia.  163 
Precuneus,  676 
Pre-hemiplegic  chorea,  297 
Pressure  aphasia,  771 
Preacher's  hand,  515 
Progressive  stupor,  883 

hypertrophic  neuritis,  454 

muscular  atrophy,  392 

bulbar  paralysis.  395.  406,  951 

muscular  dystrophy,  409 

hemiplegia,    885 
Progression,  cross-legged,  424,  858 
Protopathic  atrophy,  393 
Proto-albumose,  495 
Prosencephalon,  668 
Procursive   chorea,   299 
Projection  path,  motor,  359.  483,  710 

tracts,  472,  710 
Professional  palsy,  430 
Protoplasm,  93 
Protoplasmic  process,  91 
Primary  diseases,  20 


Pruritis,  971 
Prophylaxis,  yy 
Prosopalgia,  248 
Prosopoplegia,  653 
Prostatorrhaa,   170 
Primary  degeneration,  61 
Pseudoclonus,  61 

tetanus,  256 

tabes,  384,  597,  605 

ptosis,  124 

hypertrophy,  74 

hypertrophic  paralysis,  416 

atrophy,  74 

hydrophobia,   969 

bulbar  paralysis,  766,  774,  952 

meningitis,  806 

paralysis,   51 

reminiscence,  595 
Psychosis,   717,   754 
Psychic  headache,  237 

epileps}^  188 

blindness,  791 

paralysis,  ^^6 

symptoms,  45,  753 
Psychoneuroses,  102 
Psj'chomotor  centers,  729 
Psychology^  voluntaristic,  754 
Psyclampsia,  759 
Psychalgia,  162,  760 
Psammoma  of  the  brain,  910 
Ptosis,  647 
Pterion,  679 

Puncture,  lumbar,  459,  493,  806 
Pupillary  reflex,  63,  780 
Pulvinar,  691,  738 
Puncta  dolorosa,  629 
Purkinje,  cells  of,  707 
Putamen,  690 
Pulse,  752 

Purulent   inflammation,  39 
Pyramidal  tracts,  472 
Pyrosis,  168 
Pj^rocatechin.  495 


Quadriplegia,  536,  604 
Quadrigemina,  corpora,  692,  695,  738 


Rabies,  968 
Rachischisis,  569 
Rachitis,  550 

Radiations  of  Gratiolet,  694 
Radicular  zones,  475 


986 


GENERAL   INDEX 


Rami  efferentes,  308 

communicantes,  308 
Ranvier,  node  of,  578 
Raynaud's  disease,  310 
Reaction  of  degeneration,  70 

a  distance,  585 

of  excitation,  260 
Rectal  crises,  382 
Rectus  clonus,  442 
Receptive  centers,  717 
Red  nucleus,  692,  695 
Reflex  action,  spinal,  476,  477 

headache,  236 

epilepsy,  191 

causes  of  disease,  34 

action,  automatic,  476 

action,  55 
Refrigeratory  palsy,  653 
Reinforcement,   59 
Regeneration,  39,  585 
Regio  subthalamica,  695 
Renal  crises,  382 

symptoms,  753 
Respiration,  753 
Respiratory  tic,  266 

crises,  382 
Rest-cure,  178 
Retina,  692 

Retrobulbar  neuritis,  787 
Rheumatic  palsy,  653 

polyneuritis,  602 
Rhinencephalon,  686 
Ring  scotoma,  117 
Rinne's  test, 
Risus  sardonicus,  966 
Root-zone,  anterior  fundamental,  476 
Rodagen,  331 
Rubber  muscles,  621 


Sacral  plexus,  626 
Sadism,  170 
Salivation,  74 
Saltatoric  spasm,  120 
Sand,  brain,  696 
Sardonic  grin,  966 
Sarcoma  of  the  brain,  910 
Saturnine  encephalopathy,  596 
Satyriasis,  381 
Scanning  speech,  "jG"] 
Scapulo-humeral  reflex,  62 
humeral  dystrophy,  418 
Scaphoid  abdomen,  803 
Schools,  localization,  716 
Sciatica,  251,  627 


Sclerosis,  disseminated,  901 

lobar,  857 

multiple,  901 

amyotrophic  lateral,  395,  401 
Sclerosis,  39 

posterior  spinal,  367 
Sclerodactylia   347 
Scleroderma,   346 
Scoliosis,  631 
Scotoma,  781,  782 

physiological,  781 

central,  787 

ring,  117 
Scrivener's  palsy,  273 
Secondary  diseases,  21,  458 

spastic  paralyses,  426 

degenerations,  458,   580 
Secretory   symptoms,   74 

reflexes,  d^ 
Segment,  motor,  361 
Self-nutrition,   19 
Semicircular  canals,   149 
Seminal  emission,  170 
Sense,  muscular,  721 

stereognostic,  721 

sphere,  728 
Sensitive-motor  zone,  739 
Senile  epilepsy,  191 
Sensory  symptoms,  46 

aphasia,  769 

irritation,   779 

projection  path,  363,  710 
Sensorial  areas,  719 
Serum-therapy,  88 
Serous  meningitis,  820,  939 
Serratus  palsy,  617 
Sex  in  etiology,  31 
Sexual  perversion,  170 
Shoemaker's  spasm,  256 
Shaking  palsy,  299 
Sinuses,  intracranial,  666 
Simulation,    186 
Sinus  thrombosis,  850 
Skin  reflexes,   56 , 
Skiagraphy,  75,  561,  929 
Sleep,  141 

Sleeping  sickness,  148 
Solitary   fasciculus,    704 
Softening,   39 
Spasmus  nutans,  268 
Spasmodic   torticollis,   267 
Spastic  paralysis,  51 
Spasm,  52,  262,  772 
Spasmodic  tic,  264 

paraplegia,   421 
Space,  subarachnoid,  462 


GEXERAL   INDEX 


987 


Speech,  45,   763 
scanning,  767 
staccato,  767  . 
voluntary,  769 
disturbances  of,  763 
Specific  nerve-energy,  243 
Spermatic  neuralgia,  252 
Spermatorrhoea,    170 
Spinal  hydatid  disease,  509 

arthritis  deformans,  510 

membranes,  diseases  of,  511 

meningitis,  512 

leptomeningitis,  516 

paralysis,  Erb's,  523 

meningeal  hemorrhage,  524 

cord  diseases,  526 

anaemia,  527 

hypersemia,  527 

as^Tnmetr}-,   570 

concussion,   574 

centers,  480 

column,  diseases  of,  496 

marrow,  461 

cord  cavities,  562 

embolism,   528 

thrombosis,  528 

endarteritis,    528 

Tiemorrhage,  528 

apoplexy,  529 

paralysis,  atrophic,  541 

cord  abscess,  555 

cord  tumor,  555 

cord,  anatomy,  etc.,  459 

localization,  459,  485 

topography,  459,  485 

nerves,  diseases  of,  613 

irritation,  505 

syphilis,  519 
Spina  bifida,  569 
Spotted  fever,  808 
Spondylitis,  tubercular,  499 
Spontaneous  movements,  379 
St.  Vitus'  dance,  287 
Static  ataxia,  377 
■Status  hystericus,  122 

epilepticus,  189,  207 

hemicranicus,  230 
Staccato  speech,   767 
Stabile  current,  85 
Stammering,  282 
Stephanion,  679 
Stellwag's   symptom,  328 
Striae  of  Bechterew,  683 

acusticae,   704 
Striate  bodies, '689,  7Z7 
Struma,   324 


Stupor  progressive,  883 
Stuttering,  266,  282 

hysterical,  124 
Substantia  gelatinosa,  469 

nigra,  695 
Subthalamic  region,  695 
Suggestion,  143 
Sulci,  cerebral,  672 

arterize,  465 
Suspension  treatment,  390 
Sydenham's  disease,  287 
Sympathetic  nerves,  306 

disease  symptoms,  309 
Symptoms,  psychic,  45 

motor,  50 

sensory,  46 

vasomotor,  72 

secretory,  74 

trophic,  74 

neighborhood,  718 

of  spinal  cord  disease,  459 
S3'mptomatolog\',  general,  41 
Symptomatic  epilepsy,  206 
Symbol,  764 

Symmetrical  gangrene,  310 
Synapse.  91 
Somatochrome,  93 
Syphilis,  cerebral,  877 

spinal,  519 
Sj'philitic  myelitis,  522 

paraplegia,  522 

meningo-myelitis,  523 

polyneuritis,   598 

disease  of  vertebrae,  509 

spinal  meningitis,   519 

pseudo-tabes,  384 
Syphiloma  of  the  cord,  522 

of  the  brain,  910 
Suppurative  encephalitis,  867 
Sj^stem  diseases,  350,  356 

the  nervous,  17 
Syringomyelocele,  569 
Syringomyelia,    563 
Swelling,  giant,  318 


Tabes  dorsalis,  ibj 
Tache  cerebrale,  804 

bleuatre,  517,  74 
Tactile  aphasia,  771 
Tachj'Cardia,  324 
Talipes  calcaneus,  635 

valgus,   548 
Tangential  fibres,  683 
Tegmentum.   697 


988 


GENERAL   INDEX 


Telodendrion,  91 
Telegrapher's  cramp,  273 
Telencephalon,  668 
Temperature  crises,  382 
Temporal  lobes,  tumor  of,  921 
Temperature,  752 
Tendon  reflexes,  57 
Tetany,  256 
Tetanilla,  256 
Tetanus,  965 

pseudo,  256 
Thermo-ansesthesia,  377 
Thermometry,  local,  74 

general,   75 
Therapy,   symptomatic,   81 
Thermanjesthesia,  48 
Thrombosis,  cerebral.  845 

of  the  sinuses,  850 

spinal,  528 
Thalamencephalon,  668 
Thalami,  optic,  691,  TZ"; 
Thomsen's  disease,  284 
Thyroiodin,  323 
Tic  impulsif,  269 

de  pensee,  270 

spasmodic,   264 

convulsif,  264 

facial,  265 

douloureux,  248 
Tinnitus  aurium,   166 
Titubation,  955 
Tobacco  heart,  169 
Tonic  spasm,  52 

influence,  spinal,  476,  481 
Topoalgia,  48 
Topography,  spinal,  459,  485 

cranio-cerebral,  677 
Torticollis,   spasmodic,  267 
Toxic  headache,  236 

polyneuritis,   592 
Traumata,  33 
Traumatic  neuroses,  182,  575 

epilepsy,  190 
Tracts,  optic,  692 
Tractus  tegmento-cerebellaris,  695 

cortico-spinalis,  698 
Tremor,  53 

intentional,  905 
Tremens,  delirium,  960 
Treatment,  general,  75 
Triceps  reflex,  62 
Trigeminal  neuralgia,  248 
Trismus,  966 
Trophic  symptoms,  74 

influence,  spinal,  476,  481 
T'ophoedema,  hereditary,  320 


Trousseau's  sign,  260 
Trophoneuroses,  74,  306 
Tube,  neural,  668 
Tubercular  spondylitis,  499 
Tubercula  dolorosa,  611 
Tuberculous  meningitis,  814 
Tuberosa,   urticaria,  318 
Tubercle  of  the  brain,  910 
Tubular  vision,  112 
Tumor  of  the  spinal  cord,  555 

of  the  Cauda,  557,  559 

of  the  brain,  909 

of  the  vertebrae,  507 
Tumors  of  the  nerves,  509 
Turck's  column,  472 
Tussis  hysterica,   119 
Tympani,  chorda,  701 

U 

Ursemic  convulsions,  255 

coma,  761 
Uncrossed  pyramidal  tracts,  472,  483; 
Upper  arm  palsy,  616 
Urticaria,  970 

tuberosa,  318 

giant,  320 

factitia,   168 
Urethrodynia,  252 


Vacuolation,  36 
Valleix's  points,  586,  629 
Vasomotor  symptoms,  "jz 

reflexes,  63 

action,  476 
Vasocorona,  465 
Veins  of  the  brain,  714 
Venae  Galeni,  714 
Ventricular  hemorrhage,  836 

zone,  475 
Ventral  cerebro-spinal  fasciculus,  476. 
Vertebrate  animal,  459 
Vertebrae,  diseases  of,  496 

caries  of,  499 

tumors  of,  507 

syphilis  of,  509 

erosion  of,  509 
Vertigo,  55,  149,  752 

ocular,  152 

aural,   153 
Vermis,    705 
Vesicular  columns,  469 
Vesicles  of  the  brain,  668 
Vicq  d'Azyr,  line  of,  682 
Visceral  reflexes,  63 

neuralgia,  252 


GENERAL   INDEX 


989 


Vision,   tubular,   112 
"Visual  disturbances,  780 
aphasia,  770 

field,    contraction   of,    780 
area,    722 
^'''itae,  arbor,  707 
Vita  sexualis,   191 
'Volitantes,  niuscas,   166 
\"oluntar3'  speech,  169 
Voluntaristic  psychology-,  754 
A'omiting,  751 
Von  Grsefe's  sign,  327 

W 

Wallerian  degeneration,  37.  351,  584 

AVeber's  test,   792 

"Weight  of  brain,  664 

Weir  Mitchell  treatment,  178 


Weigert-Edinger   hypothesis,   357 
Wet  brain,  806 
White  matter,  97 
Willis,  circle  of,  711 
Word- deafness,  723,  762,  769 

blindness,  762,  770 
Wrist  reflex,  62 

drop,  566,  619 
W^risberg,  nerve  of,  700 
Wryneck,  spasmodic,  267 
Writer's  cramp,  275 


Zone,  hysterogenic,  iii 
sensitive-motor,  729 
Zones,  radicular,  475 
Zona  molecularis,  707 
granulosa,  707 


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A  treatise  on, diseases  of  the 
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